Early Hyperglycemia and Intravenous Insulin—The Rationale and Management of Hyperglycemia for Spontaneous Intracerebral Hemorrhage Patients: Is Time for Change?

Godoy, Daniel A.; Piñero, Gustavo; Svampa, Silvana; Papa, Francesca; Napoli, Mario Di

doi:10.1007/s12028-008-9098-3

Cited by 8 publications

(4 citation statements)

References 24 publications

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“…In our opinion, we should not abandon insulin therapy in neurocritical patients, but a less intensive target should be implemented 11,29,30 . Rigorous studies need to be conducted to ascertain the value of insulin therapy and to define the optimal blood glucose targets in patients with acute cerebrovascular disease.…”

Section: Discussionmentioning

confidence: 99%

Hyperglycemia in nondiabetic patients during the acute phase of stroke

Godoy¹,

Soler²,

Videtta³

et al. 2012

Arq. Neuro-Psiquiatr.

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OBJECTIVE: To determine patterns of hyperglycemic (HG) control in acute stroke. METHODS: Anonymous survey through Internet questionnaire. Participants included Latin-American physicians specialized in neurocritical care. RESULTS: The response rate was 74%. HG definition varied widely. Fifty per cent considered it when values were >140 mg/dL (7.8 mmol/L). Intravenous (IV) regular insulin was the drug of choice for HG correction. One fifth of the respondents expressed adherence to a protocol. Intensive insulin therapy (IIT) was used by 23%. Glucose levels were measured in all participants at admission. Routine laboratory test was the preferred method for monitoring. Reactive strips were more frequently used when monitoring was intensive. Most practitioners (56.7%) monitored glucose more than two times daily throughout the Intensive Care Unit stay. CONCLUSIONS: There is considerable variability and heterogeneity in the management of elevated blood glucose during acute phase of stroke by the surveyed Latin-American physicians.

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Section: Discussionmentioning

confidence: 99%

Hyperglycemia in nondiabetic patients during the acute phase of stroke

Godoy¹,

Soler²,

Videtta³

et al. 2012

Arq. Neuro-Psiquiatr.

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“…Hyperglycemia has been found to be independently associated with increased mortality and poor functional outcome after acute ischemic stroke with and without thrombolytic treatment [3,12,[16][17][18][19][76][77][78][79][80][81][82], ICH [4,7,21,22,83,84], SAH [2,5,10,85,86], severe TBI [8,9,13,20,87], and severe SCI [23]. Despite lacking a uniform definition of HyperG, the results across multiple studies and disease entities have consistently confirmed this association.…”

Section: Hyperglycemia: Poor Prognostic Factor In Critical Brain Diseasementioning

confidence: 99%

Treating Hyperglycemia in Neurocritical Patients: Benefits and Perils

Godoy

Napoli²,

Rabinstein

2010

Neurocrit Care

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There is growing debate over the value of intensive insulin therapy (IIT) in critically ill patients. Available trials have been performed in general medical or surgical intensive care units, and the results may not be directly applicable to patients with severe acute brain disease because these patients may have heightened susceptibility to hyperglycemia (HyperG) and hypoglycemia. Our objective was to review the pathophysiology and effects of HyperG and hypoglycemia in neurocritical patients and to analyze the potential role of IIT in this population. Source data were obtained from a PubMed search of the medical literature combining the terms HyperG, hypoglycemia, insulin, stroke, intracerebral hemorrhage (ICH), subarachnoid hemorrhage (SAH), traumatic brain injury (TBI), spinal cord injury (SCI), and related diagnoses. Brain metabolism is highly dependent on constant supply of glucose. As a consequence, the acutely injured brain is particularly sensitive to hypoglycemia, which can induce a state of energy failure (metabolic crisis). Meanwhile, neurocritical patients have a high prevalence of HyperG, and its occurrence is associated with poor outcome after acute ischemic stroke, ICH, SAH, and TBI. It is unclear whether this association is due to direct detrimental effects exerted by HyperG or simply represents a marker of severe brain injury. Insulin has been shown to have various potentially pleiotropic neuroprotective properties in experimental models. However, the safety and efficacy of IIT in patients with critical brain disease have not been well studied. Available results do not support the use of IIT to maintain strict normoglycemia in this population. Patients with critical brain disease should have frequent glucose monitoring because severe HyperG and even modest hypoglycemia may be detrimental. Careful use of insulin infusion protocols appears advisable, but maintenance of strict normoglycemia cannot be recommended. Rigorous studies must be conducted to assess the value of insulin therapy and to determine the optimal blood glucose targets in patients with the most common acute vascular and traumatic brain insults.

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“…Moreover, although over 50% of patients with stroke have hyperglycemia15, the clinical benefit of glucose normalization in the acute stroke setting is controversial16–17. Data on the clinical benefit of glucose lowering in ICH are limited and the potential therapeutic window for glucose lowering is unknown4,18–19. Recent guidelines suggest a judicious approach to the management of hyperglycemia in people with spontaneous ICH until additional clinical information is available20.…”

mentioning

confidence: 99%

Hyperglycemia-induced cerebral hematoma expansion is mediated by plasma kallikrein

Liu

Gao

Clermont

et al. 2011

Nat Med

113

110

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Hyperglycemia is associated with increased hematoma expansion and worse clinical outcomes following intracerebral hemorrhage. We demonstrate that cerebral hematoma expansion triggered by intracerebral infusion of autologous blood is increased in diabetic rats and mice, and this response is ameliorated by plasma kallikrein (PK) inhibition and deficiency, respectively. Both diabetes and hyperglycemia induced in nondiabetic rats increase hematoma expansion following intracerebral injection of purified PK, a response not observed with bradykinin, plasmin, or tissue plasminogen activator. This response is rapid, prevented by co-injection of the glycoprotein VI (GPVI) agonist convulxin, and mimicked by GPVI inhibition or deficiency. We show that PK binding to collagen and PK-mediated inhibition of collagen-induced platelet aggregation is enhanced by hyperglycemia. Hyperosmotic mannitol also increases hematoma expansion induced by blood and PK, and increases PK-mediated inhibition of platelet aggregation. These findings suggest that hyperglycemia increases cerebral hematoma expansion by PK-mediated osmotic-sensitive inhibition of hemostasis.

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Early Hyperglycemia and Intravenous Insulin—The Rationale and Management of Hyperglycemia for Spontaneous Intracerebral Hemorrhage Patients: Is Time for Change?

Cited by 8 publications

References 24 publications

Hyperglycemia in nondiabetic patients during the acute phase of stroke

Hyperglycemia in nondiabetic patients during the acute phase of stroke

Treating Hyperglycemia in Neurocritical Patients: Benefits and Perils

Hyperglycemia-induced cerebral hematoma expansion is mediated by plasma kallikrein

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