How long hypoglycemic brain damage

Behar, K. Effect of hypoglycemic encephalopathy upon amino acids, high-energy phosphates, and pHi in the rat brain in vivo: Detection by sequential 1 H and 31 P NMR spectroscopy. Eisenberg, S. The cerebral metabolic effects of acutely induced hypoglycemia in human subjects. Metabolism 11 — Fazekas, J. Irreversible posthypoglycemic coma. Feise, G. Effect of insulin hypoglycemia upon cerebral energy metabolism and EEG activity in the rat.

Brain Re s. Harris, R. Cerebral extracellular calcium activity in severe hypoglycemia: Relation to extracellular potassium and energy state. Kalimo, H. Effect of severe hypoglycemia on the human brain. Acta Neurol. LaManna, J. Regional comparisons of brain glucose influx. Brain Res. Mayer-Gross, W. Insulin coma therapy of schizophrenia: Some critical remarks on Dr. Sakel's report. McIlwain, H. Glucose level, metabolism, and response to electrical impulses in cerebral tissues from man and laboratory animals.

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Sakel, M. Neue Behandlungsart Schizophreniker und verwirrter Erregter. The methodical use of hypoglycemia in the treatment of psychoses. Psychiatr y 94 — Sandberg, M. Extracellular overflow of neuroactive amino acids during severe insulin-induced hypoglycemia: In vivo dialysis of the rat hippocampus.

Ikeda et al. Furthermore, 1-week follow-up was probably too short to fully evaluate this pathology. The retrospective study by Witsch et al. Six of them died, two were lost to follow-up, five had a long-term good outcome and two had a poor outcome.

These outcomes are consistent with the findings of the present study. However, the series was too small to identify outcome predictive factors. As already known, hypoglycemic encephalopathy is more common in diabetic patients and diabetes was associated with poor outcome in univariate, but no longer in multivariate analysis.

These data are consistent with findings of previous studies [ 1 , 2 , 7 , 8 ]. Duration of hypoglycemia was a significant predictor of outcome in univariate analysis, but was not included in the multivariate analysis due to several missing data.

For many patients, time between hypoglycemia onset and first glucose administration was impossible to precisely assess. In the paper by Ikeda et al. These differences may be explained by both different criteria of good outcome and a very earlier outcome assessment than in the present study.

Nevertheless, both studies strongly suggest that duration of hypoglycemia should be a major determinant of outcome. Occurrence of seizures, most of them being observed early, was identified as a factor of good prognosis in univariate analysis.

This issue has not been studied in the previous main hypoglycemic encephalopathy series [ 1 , 2 ]. Our findings are not consistent with the results of a recent rodent hypoglycemic model study, showing that seizures and especially their frequency were associated with increased mortality [ 11 ]. Interestingly, a retrospective study about patients with subarachnoid hemorrhage found that patients who presented early-onset seizures had a final good outcome, despite initial poor mRS [ 12 ].

Whatever the explanation of our findings, early-onset seizures should not be considered at least as adding more clinical severity in prolonged hypoglycemic encephalopathy. Brain imaging has been evaluated as a prognosis tool [ 6 , 7 , 8 , 13 , 14 , 15 , 16 ]. Yanagawa et al. Johkura et al. The absence of lesions on the first early diffusion MRI was associated with good outcome. Conversely, Witsch et al. In the present study, lesion localization at first imaging including MRI and CT scan was not predictive of outcome but normal early imaging that was mostly observed in brain CT scans was considered as a factor of good outcome.

In contrast to Ikeda et al. This discrepancy may be explained by several reasons. Thereby, patients with moderate disability but independent in daily living were considered as poor outcome patients, while they would have been included in our good outcome group.

Furthermore, even if Ikeda et al. Therapeutic limitation was decided in 22 patients. All of them further displayed a poor outcome. Decisions of therapeutic limitation were mostly based on the clinical severity of neurological insult and the expected absence of significant improvement with time. A similar reasoning is usual in anoxic—hypoxic encephalopathy. However, mechanisms of brain damage are different [ 17 , 18 ], so that clinical prognostic tools used for decades in hypoxic encephalopathy have yet to be validated in hypoglycemic encephalopathy.

On the one hand, patients with therapeutic limitations had a longer time under mechanical ventilation and stay in the ICU, a longer duration of hypoglycemia, and survivors did not improve their outcome over time as compared with not limited patients. Taken together, these findings suggest that decisions to withhold or withdraw care should be taken very cautiously, obviously not prematurely after ICU admission.

Ten to fifteen days with no clinical improvement could be a minimal threshold, based on the minimal time from admission to decision of therapeutic limitation among the patients who survived their ICU stay.

In addition, normal brain imaging, especially using RMI, could help to further postpone a decision to limit care. Our study has several limitations. Several data such as duration of hypoglycemia were missing.

Selection biases cannot be excluded regarding the non-responding invited ICU centers. Our population was small due to the scarcity of this disease, and a larger population would have allowed a more robust multivariate analysis. In addition, several patients did not undergo brain MRI, a more sensitive tool than CT scan, and four of them had no imaging at all.

Continuous EEG monitoring, never performed here could have been more relevant to rule out subclinical status epilepticus or better delineate patterns with prognosis value. Finally, mRS assessment was not based on a standardized questionnaire, which could have led to possible mistakes.

This multicenter study confirms that prolonged hypoglycemic encephalopathy is a severe condition leading to a poor long-term outcome. Factors of good outcome were a low mRS prior to admission and normal brain imaging, while the hypothesis of a long duration of hypoglycemia as a predictor of poor outcome is suggested.

However, some patients with severe impairment at ICU discharge may improve later, suggesting that therapeutic limitation should not be decided early. Finally, the present findings offer prognostic tools, which need to be further delineated in larger, prospective investigations.

Hypoglycemic encephalopathy: a case series and literature review on outcome determination. J Neurol. Article PubMed Google Scholar. Predictors of outcome in hypoglycemic encephalopathy. Diabetes Res Clin Pract. Cryer PE. Mechanisms of sympathoadrenal failure and hypoglycemia in diabetes.

J Clin Invest. Group IHS. Minimizing hypoglycemia in diabetes. Diabetes Care. Article Google Scholar. A case of hypoglycemic coma with good outcome despite sustained unconsciousness and widespread leukoencephalopathy.

Early diffusion MR imaging findings and short-term outcome in comatose patients with hypoglycemia. Am J Neuroradiol. You bet! Good old fashioned trial and error. So get out your dart board or your Ouija Board. Use it to pick one of the likely causes of cramps.

Treat that cause for a few weeks and see if your cramps get better. If not, go on to the next most likely cause. Now if you want to be a real scientist, once you think you found the cause, stop the treatment and see if the cramps come back. If so, quod erat demonstrandum — meaning you found the cause. But to stop the pain immediately during an acute cramp attack, most people have good results hoping around on one foot, swearing, trying to massage the cramp and praying for a swift death.

Sorry, I have no real science to offer on this one. My mother read about it somewhere and has sworn by it for years. I frequently get nasty cramps during sharp blood sugar excursions the cause of which is no mystery: equal parts gluttony and stupidity in the kitchen and, for me, popping a couple of calcium pills quickly resolves cramps. Of course, I still observe the hoping and swearing ritual, too. Just to be on the safe side.

So maybe a shot of calcium mellows out the excited nerves again. Oh, and one last dose of save-your-bacon myth busting: For many years the malaria drug quinine also present in tonic water, interestingly was believed to help nighttime leg cramps.

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