Hypoglycemia
Hypoglycemia is defined as any blood glucose value below 60 mgs per cent; it inay be accompanied by clinical signs and or symptoms, or may be asymptomatic.It is a common acute complication in diabetics under treatment with both oral hypoglycemic agents as well as on insulin. 'The symptoms of hypoglycemia are commonly divided into autonomic and "neuro-glycopenic".The autonomic symptoms are mainly due to stimulation of sympathetic system and manifest as tremor, nervousness, sweating, palpitations, anxiety and pallor. These serve as waning symptoms and are useful to patients so that they can take remedial action to increase glucose level. These symptoms are not present in patients with long-standing diabetes who have neurologic damage. The elderly people in general have lower awareness of hypoglycemia because autonomic nervous system is less active.
Neuroglycopenic symptoms are confusion, dificulty in thinking, poor coordination,headache, hunger, weakness, dizziness, faintness, drowsiness, irritability, nightmares,abnormal belligerent behavior, sonmolence, seizures, and coma.Some focal neurologic symptoms are also recognized as due to hypoglycemia and they are blurred or double vision, slurred speech, paresthesias, tinnitus, and hemiplegia.
Hypoglycemia unawareness is common in the elderly and in patients with long-standing diabetes who have develope neuropathy.Hypoglycemia is common in patients with renal failure if it is not realized by the physician that doses of hypoglycemic agents should be reduced. In renal failure, some improvement in diabetic status occurs partly due to the fact that insulin is normally degraded in the kidney, and this function is affected in renal insufficiency.Biochemical counter-regulatory hormones are activated as blood glucose drops below 60 mgs per cent, and these are initiated by the stimulation of the sympathetic nervous system. Release of cortisol, glucagon and epinephrine result in glucose production through gluconeogenesis.
Management
Hypoglycemia should be considered in every unconscious person specially if there is a history of diabetes. A sample of blood should be drawn for blood glucose assessment and sent to the labobratory, and a bolus dose of 20 ml of 25-50 per cent glucose should be given and a 10 per cent glucose drip should be maintained, If aglucometer is at hand then this can be used for immediate documentation. In elderly patients who have been on oral hypoglycemics, the glucose infusion should be kept going for 48 hours because of the long half life of these drugs in the elderly. If the hypoglycemia is due to excessive insulin, then 4 to 6 hours of treatment is usually sufficient once the patient has regained consciousness. Thereafter, a detailed history should be taken to ascertain the cause of the episode and a proper education about prevention of a similar attack needs to be done.
Diabetic Keto-acidosis
This is a medical emergency. When there is a severe deficiency of insulin relative to the needs of the body, there is an inability to utilize glucose for fuel.A correspondingly elevated level of glucagon initiates fatty acid mobilization and this undergoes P-oxidation in the mitochondria of the hepatocytes. The energy released is used in leiu of glucose--derived energy; the brain is able to utilize glucose even in the absence of insulin. Fatty acids are metabolized to ketone bodies (aceto-acetate,p hydroxybutarate, and acetone). These ketone bodies are not able to be removed effectively due to excessive production. Being highly acidic they result in acidosis and the blood pH may fall to levels below 7.0. Acidosis causes vomiting and coma.Meanwhile the high blood sugar is, often as high as 500-600 mgs per cent, exceeds the renal threshold for glucose and gets filtered out in the kidney. This results in osmotic diuresis and dehydration and electrolyte imbalance, mainly of sodium and potassium.
Clinical Abnormalities in Diabetic Keto-acidosis
Hypoglycemia is defined as any blood glucose value below 60 mgs per cent; it inay be accompanied by clinical signs and or symptoms, or may be asymptomatic.It is a common acute complication in diabetics under treatment with both oral hypoglycemic agents as well as on insulin. 'The symptoms of hypoglycemia are commonly divided into autonomic and "neuro-glycopenic".The autonomic symptoms are mainly due to stimulation of sympathetic system and manifest as tremor, nervousness, sweating, palpitations, anxiety and pallor. These serve as waning symptoms and are useful to patients so that they can take remedial action to increase glucose level. These symptoms are not present in patients with long-standing diabetes who have neurologic damage. The elderly people in general have lower awareness of hypoglycemia because autonomic nervous system is less active.
Neuroglycopenic symptoms are confusion, dificulty in thinking, poor coordination,headache, hunger, weakness, dizziness, faintness, drowsiness, irritability, nightmares,abnormal belligerent behavior, sonmolence, seizures, and coma.Some focal neurologic symptoms are also recognized as due to hypoglycemia and they are blurred or double vision, slurred speech, paresthesias, tinnitus, and hemiplegia.
Hypoglycemia unawareness is common in the elderly and in patients with long-standing diabetes who have develope neuropathy.Hypoglycemia is common in patients with renal failure if it is not realized by the physician that doses of hypoglycemic agents should be reduced. In renal failure, some improvement in diabetic status occurs partly due to the fact that insulin is normally degraded in the kidney, and this function is affected in renal insufficiency.Biochemical counter-regulatory hormones are activated as blood glucose drops below 60 mgs per cent, and these are initiated by the stimulation of the sympathetic nervous system. Release of cortisol, glucagon and epinephrine result in glucose production through gluconeogenesis.
Management
Hypoglycemia should be considered in every unconscious person specially if there is a history of diabetes. A sample of blood should be drawn for blood glucose assessment and sent to the labobratory, and a bolus dose of 20 ml of 25-50 per cent glucose should be given and a 10 per cent glucose drip should be maintained, If aglucometer is at hand then this can be used for immediate documentation. In elderly patients who have been on oral hypoglycemics, the glucose infusion should be kept going for 48 hours because of the long half life of these drugs in the elderly. If the hypoglycemia is due to excessive insulin, then 4 to 6 hours of treatment is usually sufficient once the patient has regained consciousness. Thereafter, a detailed history should be taken to ascertain the cause of the episode and a proper education about prevention of a similar attack needs to be done.
Diabetic Keto-acidosis
This is a medical emergency. When there is a severe deficiency of insulin relative to the needs of the body, there is an inability to utilize glucose for fuel.A correspondingly elevated level of glucagon initiates fatty acid mobilization and this undergoes P-oxidation in the mitochondria of the hepatocytes. The energy released is used in leiu of glucose--derived energy; the brain is able to utilize glucose even in the absence of insulin. Fatty acids are metabolized to ketone bodies (aceto-acetate,p hydroxybutarate, and acetone). These ketone bodies are not able to be removed effectively due to excessive production. Being highly acidic they result in acidosis and the blood pH may fall to levels below 7.0. Acidosis causes vomiting and coma.Meanwhile the high blood sugar is, often as high as 500-600 mgs per cent, exceeds the renal threshold for glucose and gets filtered out in the kidney. This results in osmotic diuresis and dehydration and electrolyte imbalance, mainly of sodium and potassium.
Clinical Abnormalities in Diabetic Keto-acidosis
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| Biochemical Abnormalities in Keto-acidosis |
Clinical Features of Diabetic Keto-acidosis
As a result of the abnonnal metabolism described above the patient with diabetic Keto-acidosis has the following features:
1 ) Coma, or drowsiness.
2)Dehydration, with possible hypotension and renal failure.
3) Acidotic breathing, kusslnauls deep sighing breathing.
Factors Precipitating Keto-acidosis
In type one diabetes, mere stoppage of insulin for 12 to 24 hours is sufficient to cause keto-acidosis. However, in type two diabetes, the following precipitating factors are usually the cause, and need to be identified to prevent the patient from slipping back into it.
Causes of.ketoacidosis are as follows:
- Infection,
- Pregnancy,
- Surgery,
- Trauma, and
- Malignancy (sometimes).
- Diagnosis of Keto-acidosis
.
Diabetic .keto-acidosis shoul'd be suspected .in any of the followillg conditions:
1) Any drowsy or comatose patient, especially if known to be diabetic and having acidotic breathing.
2)Any patient who has a blood glucose of greater than 350 mgs.
3) Any diabetic patient who begins to vomil, and has severe abdominal pain.
The diagnosis is confirmed by perfoming a urine test for acetone using a urine dipstick, or the Rothera's test in urine.Other mandatory tests include the following: serum creatinine, serum sodium an& potassium and bicarbonate. A blood gas analysis is usefulto check blood pH, but this may not be available widely.
Steps in Management of Diabetic Keto-acidosis
The main focus of management is to correct dehydration and electrolyte imbalance,and rdturn blood sugar to normal. Tlie acidosis will usually correct itself automatically, and it is specifically recommended that intravenous bicarbonate should not be given. The precipitating cause of DKA has to be ascertained and treated.Steps in the Management of Diabetic Keto-acidosis The management of DKA is intensive with frequent monitoring of response to treatment. A comprehensive flow chart has to be maintained to keep track of the serial blood glucose tests. This helps to see the response to treatment, and this in turn aids in altering treatment.Fluids are administered rapidly along with intravenous insulin, and blood glucoses are checked hourly. Table 1.2 gives an idea of the management strategy. A similar chart should be used to enter results of lab values and the action taken to give an overall.Avcrage fluid deficit is six litres: tI11.c~ litrcs linm extra cellular comp;u.tmcnt; replace with 0.9 per cent snlinc. 3litrcs is from the intri~ccllular compartment; replace with 5 per cent dexttase.
Urinary cnthe~erizatioll if no urine is passed after Lhlcc hours.Nasogastric tube if patient cctlnatose Lo prevent aspiration. Central vcnous line if in shock or pulmonary cdenla.Plaslna expander ( hc~nmaccel or hacstril) if BP low alter saline infusion.
Diabetic .keto-acidosis shoul'd be suspected .in any of the followillg conditions:
1) Any drowsy or comatose patient, especially if known to be diabetic and having acidotic breathing.
2)Any patient who has a blood glucose of greater than 350 mgs.
3) Any diabetic patient who begins to vomil, and has severe abdominal pain.
The diagnosis is confirmed by perfoming a urine test for acetone using a urine dipstick, or the Rothera's test in urine.Other mandatory tests include the following: serum creatinine, serum sodium an& potassium and bicarbonate. A blood gas analysis is usefulto check blood pH, but this may not be available widely.
Steps in Management of Diabetic Keto-acidosis
The main focus of management is to correct dehydration and electrolyte imbalance,and rdturn blood sugar to normal. Tlie acidosis will usually correct itself automatically, and it is specifically recommended that intravenous bicarbonate should not be given. The precipitating cause of DKA has to be ascertained and treated.Steps in the Management of Diabetic Keto-acidosis The management of DKA is intensive with frequent monitoring of response to treatment. A comprehensive flow chart has to be maintained to keep track of the serial blood glucose tests. This helps to see the response to treatment, and this in turn aids in altering treatment.Fluids are administered rapidly along with intravenous insulin, and blood glucoses are checked hourly. Table 1.2 gives an idea of the management strategy. A similar chart should be used to enter results of lab values and the action taken to give an overall.Avcrage fluid deficit is six litres: tI11.c~ litrcs linm extra cellular comp;u.tmcnt; replace with 0.9 per cent snlinc. 3litrcs is from the intri~ccllular compartment; replace with 5 per cent dexttase.
Urinary cnthe~erizatioll if no urine is passed after Lhlcc hours.Nasogastric tube if patient cctlnatose Lo prevent aspiration. Central vcnous line if in shock or pulmonary cdenla.Plaslna expander ( hc~nmaccel or hacstril) if BP low alter saline infusion.
Antibiotic if infection suspected.Monitor electrolytes and glucose every hour for 3-4 hours i~nd thereafter every 2-4 haul-s.Soluble insulin only can be i~sed and n conlinuc~us infusion with the hclp of an infusion pump is ideal. However, if an infirsion pump is not nvni1;tble then intramuscular insulin every l~our in the deltoid lnusclc using a one and a half inch needle is equally good. Thc reason for not using the gluteal site is bccnuse it is important that subcutaneous'injection should not inadvertently occur as this will cause a slower and lower insulin peak than with IM injection. Once tllc glucose level has fallen to below 250 mgs. Ule rate of infusion can be reduced to 1-4 units per hour, and once the patient is conscious, zind able lo eat, subcutaneous insulin can be started. The 5 per cent glucose drip call be continued for n fluither 24 hours to cover for volliiling and anorexia.
Hyperosmolar Non-ketotic Coma (HONK)
In some situations the gl~icosc levels rise dra~n~tically to levels as high as l0OO1ngscausing increased blood osmolarity, resulting in leakage of fluid from intracellular compartment to the extracellular compartment. Usually this situation arises when the insulin levels are not too low as to cause ketosis, but there is extieme insulin resistance, as well as dehydration. The levels of glucagons and other counter-regulatory levels are not as high as in DKA. Elderly diabetics under the following situations are most likely to experience this complication which carries a mortality as high as 50 per cent:
1) elders living alone.
2) after a cerebro-vascular accident.
3) diuretic treatment.
4) phenytoin treatment.
A diagnosis of HONK coma is made by the following biochemical profile:
1) plasma glucose econcentration >600mgs
2) serum osmolarity ~ 3 3 mOsrn/kg
3) absence of ketones .
4)arterial pH >7.3
5) serum bicarbonate>20 meq/L
Serum osmolarity can be calculated according to the formula given below:Serum bsmolarity = 2 x [Na + K]'+ Glucose in mgs percent118 Normal blood osmolarity is usually 290 n7OsmlKg water.In Hyperosmolar Non-ketotic the serum osmolarity is usually 320 mOsmols/Kg of water.
Management of Hyperosmolar Non-ketotic is based on hydration and smaIl doses of TV continuous insulin. The solution used for hydration is half normal saline (0.45 per cent). Though it is easier to correct the blood glucose value, the coma does not always improve, resulting in a poor prognosis. The reason lies in the fact that prolonged cellular dehydration causes irreversible changes. Cerebral oedema can b e precipitated by too rapid correction of hyperosmolarity. Hyperosmolar Non-ketotic can be re vented by ensuring that oIder diabetics get timely and appropriate care for diabetes as soon as they fall ill.
Hyperosmolar Non-ketotic Coma (HONK)
In some situations the gl~icosc levels rise dra~n~tically to levels as high as l0OO1ngscausing increased blood osmolarity, resulting in leakage of fluid from intracellular compartment to the extracellular compartment. Usually this situation arises when the insulin levels are not too low as to cause ketosis, but there is extieme insulin resistance, as well as dehydration. The levels of glucagons and other counter-regulatory levels are not as high as in DKA. Elderly diabetics under the following situations are most likely to experience this complication which carries a mortality as high as 50 per cent:
1) elders living alone.
2) after a cerebro-vascular accident.
3) diuretic treatment.
4) phenytoin treatment.
A diagnosis of HONK coma is made by the following biochemical profile:
1) plasma glucose econcentration >600mgs
2) serum osmolarity ~ 3 3 mOsrn/kg
3) absence of ketones .
4)arterial pH >7.3
5) serum bicarbonate>20 meq/L
Serum osmolarity can be calculated according to the formula given below:Serum bsmolarity = 2 x [Na + K]'+ Glucose in mgs percent118 Normal blood osmolarity is usually 290 n7OsmlKg water.In Hyperosmolar Non-ketotic the serum osmolarity is usually 320 mOsmols/Kg of water.
Management of Hyperosmolar Non-ketotic is based on hydration and smaIl doses of TV continuous insulin. The solution used for hydration is half normal saline (0.45 per cent). Though it is easier to correct the blood glucose value, the coma does not always improve, resulting in a poor prognosis. The reason lies in the fact that prolonged cellular dehydration causes irreversible changes. Cerebral oedema can b e precipitated by too rapid correction of hyperosmolarity. Hyperosmolar Non-ketotic can be re vented by ensuring that oIder diabetics get timely and appropriate care for diabetes as soon as they fall ill.
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