Saturday, December 27, 2008
Many patients in pain also have diabetes and they should be aware of dangerous hypoglycemic (low levels of blood glucose) episodes.
To prevent hypoglycemia there is a need for maintaining normal blood glucose levels, education, decision strategies, volitional control, and avoid hyper and hypoglycemia, with the latter defined as plasma glucose less than 60 mg/dl.
Glucose levels must be controlled continuously and without holidays. Failure to maintain normal glucose levels results from biological factors and psychosocial factors including overmedication and/or inappropriate choices regarding food, drink, and, in certain cases, exercise. Diabetic patients, especially those treated with insulin, are at risk for developing hypoglycemia. Treatment, even with oral agents such as sulfonylureas, increases this risk.
Asymptomatic episodes of hypoglycemia may constitute up to 10% of a 24-h period in diabetic patients. Individuals with type 1 diabetes average 43 symptomatic episodes annually; insulin-treated individuals with type 2 diabetes average 16 episodes. As for severe hypoglycemic episodes, patients with type 1 diabetes experience up to two episodes annually, whereas patients with type 2 diabetes experience about one episode over 5 years.
The risk increases with a history of hypoglycemia and an increased number of years of insulin treatment. Hypoglycemia deprives the brain of the constant supply of glucose needed for energy. Such low levels of blood glucose are sensed by the ventromedial hypothalamus. Within the body there is spontaneous re-adjustment to rapidly restore normal glucose levels by:
1. Inhibition of insulin secretion.
2. Release of glucagon and epinephrine elevates glucose production through increased breakdown of carbohydrates within the liver as well as production of glucose from the liver and kidneys.
3. Release of growth hormone and cortisol are slow-acting adjustments to prolonged hypoglycemia.
Hypoglycemia may promote neuronal cell death. Counterregulatory responses also stimulate the sympathetic autonomic nervous system, resulting in symptoms of sweating, trembling, anxiety, hunger, and nervousness.
Deprivation of glucose triggers can produce confusion and irritability.Severe hypoglycemic episodes often occur during sleep, when the intensity and recognizability of counterregulatory responses tend to be diminished, thereby depriving individuals of the adequate stimulus to counteract hypoglycemia.
These episodes, termed nocturnal hypoglycemia, may result in part from insufficient food intake and/or inappropriate insulin dosage the previous evening. Asymptomatic nocturnal hypoglycemia is a relatively common phenomenon affecting up to 50% of adults and 78% of children and lasting as long as several hours.
Individuals may also fail to recognize hypoglycemic episodes during the day. Such desensitization is due to decreased neuroendocrine responses to hypoglycemia that dampen symptomatic responses. Men are more prone to desensitization, whereas women inherently exhibit decreased counterregulatory responses to hypoglycemia. Thus, in both sexes, the warning signs and symptoms of hypoglycemia are typically not exhibited until blood glucose drops to dangerously low levels.
Even two episodes of moderate hypoglycemia are sufficient to decrease counterregulatory hormonal responses to hypoglycemia. Hence, hypoglycemia begets hypoglycemia.
Hypoglycemia-associated autonomic failure may also result from intense physical activity. Those who have been ill and when beginning rehabilitation are most prone to sever hypoglycemia if insulin dosages are not re-adjusted to the new levels of physical activity. Exercise-induced hypoglycemia occurs up to 17 h after cessation of physical activity and can result from increased insulin sensitivity and glucose utilization. Furthermore, counterregulatory responses may be reduced by 50% during hypoglycemia following moderately intense exercise.
The stability of blood glucose levels is complicated by several factors, including circadian rhythms, stress, insulin sensitivity, and time of day). In addition, certain genetic factors can predispose diabetic patients to severe hypoglycemia. Furthermore, a recent study has shown that current smokers have an increased risk for severe hypoglycemia, due to the decreased insulin clearance associated with smoking.
Short-term consequences:The acute sequela of mild hypoglycemic episodes includes decrements in motor skills, visual acuity, auditory processing, mood, and a variety of cognitive processes. It is unclear whether age moderates the level of decline exhibited with mild hypoglycemic episodes.The rate at which glucose decreases in acute hypoglycemia also affects cognition. A fast decline in blood glucose following rapid-acting insulin injection reduced the counterregulatory response and increased cognitive dysfunction.
Long-term consequences:It has been suggested that the medial temporal lobe, involved in memory, is particularly sensitive to hypoglycemic insult. Declarative memory (factual memory) and spatial memory have been shown to inversely correlate with the number of severe hypoglycemic episodes in children. Even mild hypoglycemia during sleep impaired consolidation of declarative memory. Thus, in children, hypoglycemia may have both an immediate and long-term effect on declarative memory.
Mechanisms secondary to hypoglycemia: adults and children
In addition, acute hypoglycemia may temporarily affect the cardiovascular system; however, in those with endothelial dysfunction, these changes can trigger major cardiovascular events, including myocardial and cerebral ischemia. Hypoglycemia also induces distinct modifications in cardiac repolarization (decreases in the height and width of the T-wave and/or lengthened corrected QT interval), which may heighten susceptibility to cardiac arrhythmias.
Anxiety and depression:Hypoglycemia adversely alters mood. Recurrent hypoglycemia elevates anxiety, depression, and lack of energy. Of particular importance is that in depression, selective serotonin reuptake inhibitors are associated with a progressively increased risk of severe hypoglycemia. Other types of antidepressants may be more appropriate for diabetic individuals with high risk of severe hypoglycemia.
Interacting effects of multiple treatment methods:Additionally, several medications have been shown to increase the risk of hypoglycemia. A selective review of the literature indicates that levothyroxine was associated with an increased risk of hypoglycemia in Japanese patients with liver impairment. ACE inhibitors may increase the risk of hypoglycemia in diabetic individuals compared with other antihypertensive drugs, possibly by increasing insulin sensitivity. Short-acting insulin analogues (lispro, aspart, and glulisine) have better postprandial glycemic control without intensifying the risk of hypoglycemia compared with human insulin. Finally, the insulin pump appears to improve glycemic control, reduce episodes of hypoglycemia, and increase quality of life more effectively than multiple-daily-injection therapy.
Perlmuter, LC , Flanagan BP Shah PH Singh SP:Hypoglycemia. Is the loser the winner?Diabetes Care31:2072-2076, 2008
hypoglycemia,
insulin,
pain,
rehabilitation
Saturday, December 27, 2008
Many patients in pain also have diabetes and they should be aware of dangerous hypoglycemic (low levels of blood glucose) episodes.
To prevent hypoglycemia there is a need for maintaining normal blood glucose levels, education, decision strategies, volitional control, and avoid hyper and hypoglycemia, with the latter defined as plasma glucose less than 60 mg/dl.
Glucose levels must be controlled continuously and without holidays. Failure to maintain normal glucose levels results from biological factors and psychosocial factors including overmedication and/or inappropriate choices regarding food, drink, and, in certain cases, exercise. Diabetic patients, especially those treated with insulin, are at risk for developing hypoglycemia. Treatment, even with oral agents such as sulfonylureas, increases this risk.
Asymptomatic episodes of hypoglycemia may constitute up to 10% of a 24-h period in diabetic patients. Individuals with type 1 diabetes average 43 symptomatic episodes annually; insulin-treated individuals with type 2 diabetes average 16 episodes. As for severe hypoglycemic episodes, patients with type 1 diabetes experience up to two episodes annually, whereas patients with type 2 diabetes experience about one episode over 5 years.
The risk increases with a history of hypoglycemia and an increased number of years of insulin treatment. Hypoglycemia deprives the brain of the constant supply of glucose needed for energy. Such low levels of blood glucose are sensed by the ventromedial hypothalamus. Within the body there is spontaneous re-adjustment to rapidly restore normal glucose levels by:
1. Inhibition of insulin secretion.
2. Release of glucagon and epinephrine elevates glucose production through increased breakdown of carbohydrates within the liver as well as production of glucose from the liver and kidneys.
3. Release of growth hormone and cortisol are slow-acting adjustments to prolonged hypoglycemia.
Hypoglycemia may promote neuronal cell death. Counterregulatory responses also stimulate the sympathetic autonomic nervous system, resulting in symptoms of sweating, trembling, anxiety, hunger, and nervousness.
Deprivation of glucose triggers can produce confusion and irritability.Severe hypoglycemic episodes often occur during sleep, when the intensity and recognizability of counterregulatory responses tend to be diminished, thereby depriving individuals of the adequate stimulus to counteract hypoglycemia.
These episodes, termed nocturnal hypoglycemia, may result in part from insufficient food intake and/or inappropriate insulin dosage the previous evening. Asymptomatic nocturnal hypoglycemia is a relatively common phenomenon affecting up to 50% of adults and 78% of children and lasting as long as several hours.
Individuals may also fail to recognize hypoglycemic episodes during the day. Such desensitization is due to decreased neuroendocrine responses to hypoglycemia that dampen symptomatic responses. Men are more prone to desensitization, whereas women inherently exhibit decreased counterregulatory responses to hypoglycemia. Thus, in both sexes, the warning signs and symptoms of hypoglycemia are typically not exhibited until blood glucose drops to dangerously low levels.
Even two episodes of moderate hypoglycemia are sufficient to decrease counterregulatory hormonal responses to hypoglycemia. Hence, hypoglycemia begets hypoglycemia.
Hypoglycemia-associated autonomic failure may also result from intense physical activity. Those who have been ill and when beginning rehabilitation are most prone to sever hypoglycemia if insulin dosages are not re-adjusted to the new levels of physical activity. Exercise-induced hypoglycemia occurs up to 17 h after cessation of physical activity and can result from increased insulin sensitivity and glucose utilization. Furthermore, counterregulatory responses may be reduced by 50% during hypoglycemia following moderately intense exercise.
The stability of blood glucose levels is complicated by several factors, including circadian rhythms, stress, insulin sensitivity, and time of day). In addition, certain genetic factors can predispose diabetic patients to severe hypoglycemia. Furthermore, a recent study has shown that current smokers have an increased risk for severe hypoglycemia, due to the decreased insulin clearance associated with smoking.
Short-term consequences:The acute sequela of mild hypoglycemic episodes includes decrements in motor skills, visual acuity, auditory processing, mood, and a variety of cognitive processes. It is unclear whether age moderates the level of decline exhibited with mild hypoglycemic episodes.The rate at which glucose decreases in acute hypoglycemia also affects cognition. A fast decline in blood glucose following rapid-acting insulin injection reduced the counterregulatory response and increased cognitive dysfunction.
Long-term consequences:It has been suggested that the medial temporal lobe, involved in memory, is particularly sensitive to hypoglycemic insult. Declarative memory (factual memory) and spatial memory have been shown to inversely correlate with the number of severe hypoglycemic episodes in children. Even mild hypoglycemia during sleep impaired consolidation of declarative memory. Thus, in children, hypoglycemia may have both an immediate and long-term effect on declarative memory.
Mechanisms secondary to hypoglycemia: adults and children
In addition, acute hypoglycemia may temporarily affect the cardiovascular system; however, in those with endothelial dysfunction, these changes can trigger major cardiovascular events, including myocardial and cerebral ischemia. Hypoglycemia also induces distinct modifications in cardiac repolarization (decreases in the height and width of the T-wave and/or lengthened corrected QT interval), which may heighten susceptibility to cardiac arrhythmias.
Anxiety and depression:Hypoglycemia adversely alters mood. Recurrent hypoglycemia elevates anxiety, depression, and lack of energy. Of particular importance is that in depression, selective serotonin reuptake inhibitors are associated with a progressively increased risk of severe hypoglycemia. Other types of antidepressants may be more appropriate for diabetic individuals with high risk of severe hypoglycemia.
Interacting effects of multiple treatment methods:Additionally, several medications have been shown to increase the risk of hypoglycemia. A selective review of the literature indicates that levothyroxine was associated with an increased risk of hypoglycemia in Japanese patients with liver impairment. ACE inhibitors may increase the risk of hypoglycemia in diabetic individuals compared with other antihypertensive drugs, possibly by increasing insulin sensitivity. Short-acting insulin analogues (lispro, aspart, and glulisine) have better postprandial glycemic control without intensifying the risk of hypoglycemia compared with human insulin. Finally, the insulin pump appears to improve glycemic control, reduce episodes of hypoglycemia, and increase quality of life more effectively than multiple-daily-injection therapy.
Perlmuter, LC , Flanagan BP Shah PH Singh SP:Hypoglycemia. Is the loser the winner?Diabetes Care31:2072-2076, 2008
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hypoglycemia, insulin, pain, rehabilitation