Hyperosmolar non ketotic coma - Clinicals, Diagnosis, and Management

Emergency Medicine

Clinicals - History

Fact Explanation
Generalized weakness Hyperosmolar non ketotic coma (HONK) is a rare and serious complication that predominantly occurs in elderly type 2 diabetic patients. Hyperosmolar non ketotic coma is characterized by severe hyperglycemia and hyperosmolarity in the absence of ketosis or acidosis.
HONK is a result of decrease in insulin to glucagon ratio. Due to relative or absolute reduction of insulin with an increment of counter regulatory hormones. This biochemical change keeps glucose in the intravascular compartment preventing them to enter into cells. This is applicable to most of the cells in the body except brain and renal cells where glucose intake is not dependent on insulin. This causes energy starvation of the cells leading to generalized body weakness. As the condition progresses, patients become bed-bound and lethargic. These features occur insidiously in contrast to diabetic ketoacidosis where the symptoms are very rapid in onset.
Generalized weakness
Hyperosmolar non ketotic coma (HONK) is a rare and serious complication that predominantly occurs in elderly type 2 diabetic patients. Hyperosmolar non ketotic coma is characterized by severe hyperglycemia and hyperosmolarity in the absence of ketosis or acidosis.
HONK is a result of decrease in insulin to glucagon ratio. Due to relative or absolute reduction of insulin with an increment of counter regulatory hormones. This biochemical change keeps glucose in the intravascular compartment preventing them to enter into cells. This is applicable to most of the cells in the body except brain and renal cells where glucose intake is not dependent on insulin. This causes energy starvation of the cells leading to generalized body weakness. As the condition progresses, patients become bed-bound and lethargic. These features occur insidiously in contrast to diabetic ketoacidosis where the symptoms are very rapid in onset.
Visual problems Decreased renal clearance and decreased peripheral utilization of glucose leads to hyperglycemia. Hyperglycemia and hyperosmolarity cause osmotic diuresis. The eventual dehydration, cellular level glucose starvation and derangement of electrolytes. Patient may complain of transient visual impairment or blurring of vision. Visual problems
Decreased renal clearance and decreased peripheral utilization of glucose leads to hyperglycemia. Hyperglycemia and hyperosmolarity cause osmotic diuresis. The eventual dehydration, cellular level glucose starvation and derangement of electrolytes. Patient may complain of transient visual impairment or blurring of vision.
Muscle cramps A muscle cramps are involuntarily. The forcibly contracted muscle does not relax. Loss of electrolytes, such as sodium and potassium during diuresis causes hyponatremia which in turn leads to muscle cramps. Muscle cramps
A muscle cramps are involuntarily. The forcibly contracted muscle does not relax. Loss of electrolytes, such as sodium and potassium during diuresis causes hyponatremia which in turn leads to muscle cramps.
Frequent urination Hyperosmolarity in the intravascular compartment causes increased volume in it. So the renal perfusion and glomerular filtration increase making the urination more frequent and profuse. Frequent urination
Hyperosmolarity in the intravascular compartment causes increased volume in it. So the renal perfusion and glomerular filtration increase making the urination more frequent and profuse.
Extreme thirst/hunger Osmotic diuresis which in return causes osmotic shift of fluid to the intravascular space. Intracellular dehydration activates osmoreceptors and increases thirst as a compensatory effect and a protective measure. Extreme thirst/hunger
Osmotic diuresis which in return causes osmotic shift of fluid to the intravascular space. Intracellular dehydration activates osmoreceptors and increases thirst as a compensatory effect and a protective measure.
Nausea and vommiting Can develop as a result of decreased mesenteric perfusion. This is less common in HONK than in DKA. Nausea and vommiting
Can develop as a result of decreased mesenteric perfusion. This is less common in HONK than in DKA.
Difficulty in swallowing Loss of tissue turgor in the esophageal epithelium related to the dehydration. Difficulty in swallowing
Loss of tissue turgor in the esophageal epithelium related to the dehydration.
Neurological symptoms (eg : lethargy, confusion, hemiparesis) If the rehydration does not take place further diuresis leads to hypovolemia and hypotension. Tissue perfusion becomes depleted. Decreased brain perfusion along with electrolyte imbalance leads to neurological symptoms. In the most severe form this causes coma. Neurological symptoms may also be due to severe electrolyte imbalance. These ranges from lethargy, confusion, hemiparesis, hemiballism, chorea to seizures, or coma occasionally. These symptoms are transient and reversible with prompt management. Neurological symptoms (eg : lethargy, confusion, hemiparesis)
If the rehydration does not take place further diuresis leads to hypovolemia and hypotension. Tissue perfusion becomes depleted. Decreased brain perfusion along with electrolyte imbalance leads to neurological symptoms. In the most severe form this causes coma. Neurological symptoms may also be due to severe electrolyte imbalance. These ranges from lethargy, confusion, hemiparesis, hemiballism, chorea to seizures, or coma occasionally. These symptoms are transient and reversible with prompt management.
Proceeding infection and other triggering factors Infections (cellulitis, dental infections, pneumonia, sepsis, urinary tract infection) are the commonest triggers for developing Hyperosmolar non ketotic coma in an an individual who is diagnosed to have type 2 diabetes mellitus. Diabetes can also present as Hyperosmolar non ketotic coma in an undiagnosed individual.
Some co-existing diseases can be the trigger. Namely : Acute myocardial infarction, pheochromocytoma, cerebrovascular accident, Cushing’s syndrome, hyper/hypothermia, mesenteric thrombosis and pancreatitis.
Calcium channel blockers, diuretics, cimetidine, glucocorticoids
Loop/ thiazide diuretics, phenytoin and propranolol are among causative drugs. Non compliance of the diabetic patient or substance abuse are some common causes.
Proceeding infection and other triggering factors
Infections (cellulitis, dental infections, pneumonia, sepsis, urinary tract infection) are the commonest triggers for developing Hyperosmolar non ketotic coma in an an individual who is diagnosed to have type 2 diabetes mellitus. Diabetes can also present as Hyperosmolar non ketotic coma in an undiagnosed individual.
Some co-existing diseases can be the trigger. Namely : Acute myocardial infarction, pheochromocytoma, cerebrovascular accident, Cushing’s syndrome, hyper/hypothermia, mesenteric thrombosis and pancreatitis.
Calcium channel blockers, diuretics, cimetidine, glucocorticoids
Loop/ thiazide diuretics, phenytoin and propranolol are among causative drugs. Non compliance of the diabetic patient or substance abuse are some common causes.

Clinicals - Examination

Fact Explanation
Signs of dehydration Dehydration is more pronounced in Hyperosmolar non ketotic coma than in Diabetes ketoacidosis.
Dry buccal mucosa, sunken eye balls, poor skin turgor, tachycardia, hypotension and shock are some of the signs indicating moderate to severe dehydration. Postural hypotension when present, suggests severe dehydration.
Signs of dehydration
Dehydration is more pronounced in Hyperosmolar non ketotic coma than in Diabetes ketoacidosis.
Dry buccal mucosa, sunken eye balls, poor skin turgor, tachycardia, hypotension and shock are some of the signs indicating moderate to severe dehydration. Postural hypotension when present, suggests severe dehydration.
Low grade fever This is usually due to underlying infection which proceeds Hyperosmolar non ketotic coma. Patients can be normothermic or
even hypothermic primarily because of peripheral vasodilation.
Low grade fever
This is usually due to underlying infection which proceeds Hyperosmolar non ketotic coma. Patients can be normothermic or
even hypothermic primarily because of peripheral vasodilation.
Abdominal distention This is due to transient gastroparesis induced by hypertonicity of the gastrointestinal tract which resolves quickly following adequate rehydration. Abdominal distention
This is due to transient gastroparesis induced by hypertonicity of the gastrointestinal tract which resolves quickly following adequate rehydration.
Changes in the mental status ranging from complete lucidity, disorientation, lethargy to coma. The level of neurologic impairment is related directly to the effective serum osmolarity. Patient is at risk of coma once the serum osmolarity is more than 350 mOsm/kg. Changes in the mental status ranging from complete lucidity, disorientation, lethargy to coma.
The level of neurologic impairment is related directly to the effective serum osmolarity. Patient is at risk of coma once the serum osmolarity is more than 350 mOsm/kg.
Seizures Seizures are present in 25% cases. Seizures can be generalized, focal, myoclonic jerking, or movement induced. Seizures
Seizures are present in 25% cases. Seizures can be generalized, focal, myoclonic jerking, or movement induced.
Hemiparesis Gradually developing hemiparesis is also a result of the reduced brain perfusion secondary to hypotension. It is easily reversible with adequate rehydration.
The same pathophysiology causes several other neurological abnormalities such as hemianopsia, aphasia, paresis, a positive Babinski sign and myoclonic jerks.
Hemiparesis
Gradually developing hemiparesis is also a result of the reduced brain perfusion secondary to hypotension. It is easily reversible with adequate rehydration.
The same pathophysiology causes several other neurological abnormalities such as hemianopsia, aphasia, paresis, a positive Babinski sign and myoclonic jerks.

Investigations - Diagnosis

Fact Explanation
Blood glucose Reduced insulin to glucagon ratio prevents glucose uptake from the insulin dependent cells. This process along with increased gluconeogenesis result in severe hyperglycemia. The plasma glucose level is as high as 600 mg per dL (33.3 mmol per L) or above. Blood glucose
Reduced insulin to glucagon ratio prevents glucose uptake from the insulin dependent cells. This process along with increased gluconeogenesis result in severe hyperglycemia. The plasma glucose level is as high as 600 mg per dL (33.3 mmol per L) or above.
Serum sodium The serum sodium level may be low or normal. It may even be elevated in patients who are severely dehydrated even though total body sodium is depleted.
The reported sodium level should be corrected when the patient’s glucose level is markedly elevated. True sodium concentration (millimolar ) can be obtained by multiplying excess glucose above 100 mg/dl by 1.6 /100.
Serum sodium
The serum sodium level may be low or normal. It may even be elevated in patients who are severely dehydrated even though total body sodium is depleted.
The reported sodium level should be corrected when the patient’s glucose level is markedly elevated. True sodium concentration (millimolar ) can be obtained by multiplying excess glucose above 100 mg/dl by 1.6 /100.
Serum potassium Serum potassium levels at presentation may be high, normal, or low even though total body potassium may be depleted. The initial depletion is due to diuresis. Later the levels may be low or normal owing to the dehydration. Serum potassium
Serum potassium levels at presentation may be high, normal, or low even though total body potassium may be depleted. The initial depletion is due to diuresis. Later the levels may be low or normal owing to the dehydration.
Calculated effective serum osmolality Effective serum osmolarity is calculated by adding the serum sodium level in mEq per L multiplied by 2 to serum glucose (mg per dL) devided by 18. Effective serum osmolality is 320 mOsm/kg or greater in HONK. (normal = 290 +/- 5) Calculated effective serum osmolality
Effective serum osmolarity is calculated by adding the serum sodium level in mEq per L multiplied by 2 to serum glucose (mg per dL) devided by 18. Effective serum osmolality is 320 mOsm/kg or greater in HONK. (normal = 290 +/- 5)
Arterial blood gas Serum pH is greater than 7.30 while bicarbonate concentration is greater than 15 mEq/L. This helps to differentiate HONK from DKA where a marked acidosis is noted. Vomiting and use of thiazide
diuretics may cause a metabolic alkalosis that could mask the severity of acidosis.
Arterial blood gas
Serum pH is greater than 7.30 while bicarbonate concentration is greater than 15 mEq/L. This helps to differentiate HONK from DKA where a marked acidosis is noted. Vomiting and use of thiazide
diuretics may cause a metabolic alkalosis that could mask the severity of acidosis.
Full blood count Hemoglobin & hematocrit values are usually high because of volume contraction. Leukocytosis is evident in some cases due to probable proceeding infection, stress or dehydration. Leukocytosis is usually in the range of 10.0–15.0 × 109/L. Full blood count
Hemoglobin & hematocrit values are usually high because of volume contraction. Leukocytosis is evident in some cases due to probable proceeding infection, stress or dehydration. Leukocytosis is usually in the range of 10.0–15.0 × 109/L.
Urinalysis TO exclude urinary tract infection as an trigger for developing HONK. Apart from that elevated specific gravity suggests dehydration. Urinalysis
TO exclude urinary tract infection as an trigger for developing HONK. Apart from that elevated specific gravity suggests dehydration.
Chest X-ray A chest radiograph is almost always advisable during the initial assessment to exclude pneumonitis. Chest X-ray
A chest radiograph is almost always advisable during the initial assessment to exclude pneumonitis.
Urine/serum ketone bodies Levels are very low or negative. Though the low insulin to glucagon ratio triggers gluconeogenesis, lipolysis and ketogenesis from the liver, hyperosmolar non ketotic coma (HONK) does not show significant lipolysis or ketogenesis as in Diabetic Ketoacidosis. Though the exact cause for this is not known, it is thought that the low insulin to glucagon ratio in HONK is sufficient to trigger gluconeogenesis, though not enough for lipid lysis. Urine/serum ketone bodies
Levels are very low or negative. Though the low insulin to glucagon ratio triggers gluconeogenesis, lipolysis and ketogenesis from the liver, hyperosmolar non ketotic coma (HONK) does not show significant lipolysis or ketogenesis as in Diabetic Ketoacidosis. Though the exact cause for this is not known, it is thought that the low insulin to glucagon ratio in HONK is sufficient to trigger gluconeogenesis, though not enough for lipid lysis.
Blood urea and serum creatinine Initially, blood urea and creatinine concentrations are likely to be elevated due to prerenal azotemia. If these values do not come back to normal after treatment, it suggests an underlying renal involvement related to diabetes mellitus. Blood urea and serum creatinine
Initially, blood urea and creatinine concentrations are likely to be elevated due to prerenal azotemia. If these values do not come back to normal after treatment, it suggests an underlying renal involvement related to diabetes mellitus.

Management - Supportive

Fact Explanation
Management of an unconscious patient If the patient presents unconscious; airway,breathing and circulation should be assessed. If they are not normal, the first step of the management should be establishing those basic components. Airway management plays an important role. Patient should be turned in to left lateral position.Any foreign body (including dentures) should be removed. Secretions are sucked out and an oropharyngeal airway is inserted. Ambu bag ventilation should be started with high flow oxygen. If the breathing does not pick up, intubation and mechanical ventilation should be considered in an intensive care setting. Management of an unconscious patient
If the patient presents unconscious; airway,breathing and circulation should be assessed. If they are not normal, the first step of the management should be establishing those basic components. Airway management plays an important role. Patient should be turned in to left lateral position.Any foreign body (including dentures) should be removed. Secretions are sucked out and an oropharyngeal airway is inserted. Ambu bag ventilation should be started with high flow oxygen. If the breathing does not pick up, intubation and mechanical ventilation should be considered in an intensive care setting.
Diet Patient should be kept nil by mouth for at least 6 hours. Intravenous rehydration should not be delayed for any reason. All patients should be provided with adequate nutritional support. If the patient is unable to tolerate orally ,parentaral nutrition is recommended. Diet
Patient should be kept nil by mouth for at least 6 hours. Intravenous rehydration should not be delayed for any reason. All patients should be provided with adequate nutritional support. If the patient is unable to tolerate orally ,parentaral nutrition is recommended.
Treatment for the proceeding infection Antibiotic therapy is not routinely recommended for all patients. But individuals who are suspected to have an infection are entitled to empirical antibiotic therapy. Associated fever should be treated with antipyretics. Treatment for the proceeding infection
Antibiotic therapy is not routinely recommended for all patients. But individuals who are suspected to have an infection are entitled to empirical antibiotic therapy. Associated fever should be treated with antipyretics.
Withhold offending medications Patient's drug history should be thoroughly reviewed. If he/she is using any precipitating/ aggravating drug, it is advisable to discontinue or reduce the dosage of any such agent. Other precipitating factors should also be addressed if they present. Withhold offending medications
Patient's drug history should be thoroughly reviewed. If he/she is using any precipitating/ aggravating drug, it is advisable to discontinue or reduce the dosage of any such agent. Other precipitating factors should also be addressed if they present.
Prevention of Deep vein thrombosis Recent studies show that the risk of venous thromboembolism, among diabetic patients, is greater than in the non-diabetic population. Dehydration associated with hyperglycemia may be a contributing factor for enhancing venous stasis. Central venous catheterization which is commonly used for rehydration processes is thought to increase the risk of venous thromboembolism. It should be removed as soon as possible after the initial treatment.
Prophylactic heparinization is not routinely recommended due to lack of evidence and risk of increased bleeding tendency.
Prevention of Deep vein thrombosis
Recent studies show that the risk of venous thromboembolism, among diabetic patients, is greater than in the non-diabetic population. Dehydration associated with hyperglycemia may be a contributing factor for enhancing venous stasis. Central venous catheterization which is commonly used for rehydration processes is thought to increase the risk of venous thromboembolism. It should be removed as soon as possible after the initial treatment.
Prophylactic heparinization is not routinely recommended due to lack of evidence and risk of increased bleeding tendency.
Prevention of further Hyperosmolar non ketotic episodes Patient and care givers should be educated regarding early identification and home management of emergencies related to diabetes mellitus such as hypoglycemic attacks, diabetic ketoacidosis and hyperosmolar non ketotic coma. Importance of adherence to blood glucose monitoring and compliance with prescribed medications should be emphasized. Patient should be kept well hydrated. Patient should be educated to drink more water and increase the frequency of blood glucose checking when they are ill. In addition advise to visit their health care provider in such instances. Prevention of further Hyperosmolar non ketotic episodes
Patient and care givers should be educated regarding early identification and home management of emergencies related to diabetes mellitus such as hypoglycemic attacks, diabetic ketoacidosis and hyperosmolar non ketotic coma. Importance of adherence to blood glucose monitoring and compliance with prescribed medications should be emphasized. Patient should be kept well hydrated. Patient should be educated to drink more water and increase the frequency of blood glucose checking when they are ill. In addition advise to visit their health care provider in such instances.

Management - Specific

Fact Explanation
Fluid therapy The first and most important step in the treatment of hyperosmolar hyperglycemic state is fluid replacement. Hyperosmolar non ketotic coma is a volume-depleted states with water deficit of approximately 9 liters.(or 100 to 200 mL per kg)
The initial fluid of choice is isotonic saline, which should be infused at the rate of 1-1.5 L during the first hour.
The choice of fluid for continued repletion depends on the hydration status, serum electrolyte levels, and urinary output.
In patients who are hypernatremic (> 150 mmol/L) or eunatremic, 0.45% NaCl infused at 4–14 ml/kg/hour is appropriate and in patients with hyponatremia 0.9% NaCl at a similar rate is preferred.
If the patient is in hypovolemic shock 0.9% sodium chloride 1 liter per hour should be administered along with a plasma expanders.
If the patient is in a cardiogenic shock, hemodynamic state should be monitored frequently.
After the initial rehydration, a liter of isotonic saline should be given each over 2 hours, 4 hours and 6 hours. The goal is to replace half of the estimated water deficit over a period of 12- 24 hours. In patients with hypotension, aggressive fluid therapy with isotonic saline should continue until blood pressure is stabilized. The administration of insulin without fluid replacement in such patients may further aggravate hypotension.
Early in fluid replacement, glucose level tends to decrease even before starting insulin. This acts as an index for the adequacy of fluid replacement whereas if the plasma glucose level fails to decline by 75 to 100 mg per dL (4.2 to 5.6 mmol per L) per hour, implies inadequate fluid volume or renal impairment.
The rate of fluid replacement in a child with hyperosmolar non ketotic coma should be less compared to an adult as the risk of cerebral edema is higher in the pediatric group.
Fluid therapy
The first and most important step in the treatment of hyperosmolar hyperglycemic state is fluid replacement. Hyperosmolar non ketotic coma is a volume-depleted states with water deficit of approximately 9 liters.(or 100 to 200 mL per kg)
The initial fluid of choice is isotonic saline, which should be infused at the rate of 1-1.5 L during the first hour.
The choice of fluid for continued repletion depends on the hydration status, serum electrolyte levels, and urinary output.
In patients who are hypernatremic (> 150 mmol/L) or eunatremic, 0.45% NaCl infused at 4–14 ml/kg/hour is appropriate and in patients with hyponatremia 0.9% NaCl at a similar rate is preferred.
If the patient is in hypovolemic shock 0.9% sodium chloride 1 liter per hour should be administered along with a plasma expanders.
If the patient is in a cardiogenic shock, hemodynamic state should be monitored frequently.
After the initial rehydration, a liter of isotonic saline should be given each over 2 hours, 4 hours and 6 hours. The goal is to replace half of the estimated water deficit over a period of 12- 24 hours. In patients with hypotension, aggressive fluid therapy with isotonic saline should continue until blood pressure is stabilized. The administration of insulin without fluid replacement in such patients may further aggravate hypotension.
Early in fluid replacement, glucose level tends to decrease even before starting insulin. This acts as an index for the adequacy of fluid replacement whereas if the plasma glucose level fails to decline by 75 to 100 mg per dL (4.2 to 5.6 mmol per L) per hour, implies inadequate fluid volume or renal impairment.
The rate of fluid replacement in a child with hyperosmolar non ketotic coma should be less compared to an adult as the risk of cerebral edema is higher in the pediatric group.
Potassium therapy If the serum potassium level is more than 5.5 mEq per liter or the patient is anuric. Once urine output is established, potassium replacement should be initiated with regular and frequent monitoring of serum electrolytes and continuous monitoring of cardiac rhythm.
If the serum potassium level is,
less than 3.3 mEq/L -administer potassium as potassium chloride alone or combined with potassium phosphate. Insulin should not be given until serum potassium level reaches 3.3 mEq per liter.
3.3 -5.0 - 20 to 30 mEq of potassium should be given in each liter of intravenous fluid to maintain the level between 4.0 - 5.0 mEq per liter.
More than 5.0 mEq/L - potassium should be held until the level is less than 5.0 mEq per liter.
Potassium therapy
If the serum potassium level is more than 5.5 mEq per liter or the patient is anuric. Once urine output is established, potassium replacement should be initiated with regular and frequent monitoring of serum electrolytes and continuous monitoring of cardiac rhythm.
If the serum potassium level is,
less than 3.3 mEq/L -administer potassium as potassium chloride alone or combined with potassium phosphate. Insulin should not be given until serum potassium level reaches 3.3 mEq per liter.
3.3 -5.0 - 20 to 30 mEq of potassium should be given in each liter of intravenous fluid to maintain the level between 4.0 - 5.0 mEq per liter.
More than 5.0 mEq/L - potassium should be held until the level is less than 5.0 mEq per liter.
Other electrolyte replacement (Phosphate, magnesium, and calcium) These ions are not corrected routinely due to lack of evidence. But if the patient become symptomatic, replacement of these electrolytes should be considered. Other electrolyte replacement (Phosphate, magnesium, and calcium)
These ions are not corrected routinely due to lack of evidence. But if the patient become symptomatic, replacement of these electrolytes should be considered.
Insulin therapy Adequate fluid replacement must be ensured before commencing insulin as insulin administration during dehydrate state can further shift water to the intracellular compartment worsening the hypotension in to a life threatening state.

Insulin therapy should be commenced starting with an intravenous loading dose of 0.15 U/kg body weight (usually 10 U in adults). This is followed by a continuous infusion of insulin at a rate of 0.1 U/kg per hour (usually 5 to 7 U per hour in adults)
If the patient is in shock or the initial serum potassium level is less than 3.3 mEq/L, resuscitation with intravenous fluids or potassium replacement or both is instituted before commencing the insulin infusion . An insulin infusion of 5 to 7 U per hour should lower serum glucose concentrations by 50 to 75 mg/dL per hour. It this goal could not be acquired, intravenous insulin should be doubled with close monitoring of glucose.
When the patient can tolerate oral fluids, IV insulin can be replaced by subcutaneous insulin.
Insulin therapy
Adequate fluid replacement must be ensured before commencing insulin as insulin administration during dehydrate state can further shift water to the intracellular compartment worsening the hypotension in to a life threatening state.

Insulin therapy should be commenced starting with an intravenous loading dose of 0.15 U/kg body weight (usually 10 U in adults). This is followed by a continuous infusion of insulin at a rate of 0.1 U/kg per hour (usually 5 to 7 U per hour in adults)
If the patient is in shock or the initial serum potassium level is less than 3.3 mEq/L, resuscitation with intravenous fluids or potassium replacement or both is instituted before commencing the insulin infusion . An insulin infusion of 5 to 7 U per hour should lower serum glucose concentrations by 50 to 75 mg/dL per hour. It this goal could not be acquired, intravenous insulin should be doubled with close monitoring of glucose.
When the patient can tolerate oral fluids, IV insulin can be replaced by subcutaneous insulin.
Glucose When serum glucose reaches 300 mg per dL (16.7 mmol per L)
Change to 5% dextrose with 0.45% sodium chloride, and decrease insulin to 0.05 - 0.1 U per kg per hour to maintain serum glucose between 250 - 300 mg per dL until plasma osmolality is ≤ 315 mOsm per kg and the patient is mentally alert.
Glucose
When serum glucose reaches 300 mg per dL (16.7 mmol per L)
Change to 5% dextrose with 0.45% sodium chloride, and decrease insulin to 0.05 - 0.1 U per kg per hour to maintain serum glucose between 250 - 300 mg per dL until plasma osmolality is ≤ 315 mOsm per kg and the patient is mentally alert.

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  1. BURKE BJ. Hyperglycaemic hyperosmolar non-ketotic diabetic coma presenting as severe dysphagia. Br Med J [online] 1980 Jun 14, 280(6229):1421-1422 [viewed 01 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1601723
  2. CHAMBERS T. Letter: Possible aetiology of hyperglycaemia in hyperosmolar dehydration. Arch Dis Child [online] 1975 Mar, 50(3):250 [viewed 02 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/1173748
  3. CHIASSON JL, ARIS-JILWAN N, BéLANGER R, BERTRAND S, BEAUREGARD H, ÉKOé JM, FOURNIER H, HAVRANKOVA J. Diagnosis and treatment of diabetic ketoacidosis and the hyperglycemic hyperosmolar state CMAJ [online] 2003 Apr 1, 168(7):859-866 [viewed 01 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC151994
  4. FONSECA V, PHEAR DN. Hyperosmolar non-ketotic diabetic syndrome precipitated by treatment with diuretics. Br Med J (Clin Res Ed) [online] 1982 Jan 2, 284(6308):36-37 [viewed 01 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1495393
  5. GOTO H, KUMAGAI T, MOMOZAKI N. MRI findings of occipital seizures in non-ketotic hyperglycemia. Intern Med [online] 2011, 50(4):367-8 [viewed 02 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/21325774
  6. HEGGARTY H, TRINDADE P, BRYAN EM. Hyperglycaemia in hyperosmolar dehydration. Arch Dis Child [online] 1973 Sep, 48(9):740-1 [viewed 02 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/4733644
  7. KITABCHI AE, UMPIERREZ GE, MILES JM, FISHER JN. Hyperglycemic Crises in Adult Patients With Diabetes Diabetes Care [online] 2009 Jul, 32(7):1335-1343 [viewed 01 June 2014] Available from: doi:10.2337/dc09-9032
  8. LIN JJ, CHANG MK. Hemiballism-hemichorea and non-ketotic hyperglycaemia. J Neurol Neurosurg Psychiatry [online] 1994 Jun, 57(6):748-50 [viewed 02 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/8006661
  9. MAHON WA, HOLLAND J, UROWITZ MB. Hyperosmolar, non-ketotic diabetic coma. Can Med Assoc J [online] 1968 Dec 7, 99(22):1090-1092 [viewed 01 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1945472
  10. MATZ R. Management of the Hyperosmolar Hyperglycemic Syndrome, Am Fam Physician. [online] 1999 Oct,1,60(5),1468-1476 [viewed 01 June 2014] Available from: http://www.aafp.org/afp/1999/1001/p1468.html
  11. MATZ R. Management of the Hyperosmolar Hyperglycemic Syndrome, Am Fam Physician. [online] 1999 Oct,1,60(5),1468-1476 [viewed 01 June 2014] Available from: http://www.aafp.org/afp/1999/1001/p1468.html
  12. NG CL. Diagnostic challenge--is this really a stroke? Aust Fam Physician [online] 2006 Oct, 35(10):805-8 [viewed 02 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/17019457
  13. PARK J, KIM DJ, KIM HY, SEO JA, KIM SG, BAIK SH, CHOI DS. Extensive venous thrombosis of the upper extremity in a diabetic patient with a hyperosmolar hyperglycemic state. Korean J Intern Med [online] 2006 Dec, 21(4):244-7 [viewed 02 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/17249507
  14. PHILIP C, JACOB J, GUPTA S. Hyperosmolar Hyperglycemic Non Ketotic Coma and Rhabdomyolysis- An Uncommon Clinical Encounter. Libyan J Med [online] 2009 December [viewed 01 June 2014] Available from: doi:10.4176/090708
  15. SHIMIZU M, KINOSHITA K, HATTORI K, OTA Y, KANAI T, KOBAYASHI H, TOKUDA Y. Physical signs of dehydration in the elderly. Intern Med [online] 2012, 51(10):1207-10 [viewed 02 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/22687791
  16. STONER GD, Hyperosmolar Hyperglycemic State, Am Fam Physician[online]. 2005,71,1723-30. [viewed 01 June 2014] Available from: http://www.aafp.org/afp/2005/0501/p1723.html
  17. STONER GD, Hyperosmolar Hyperglycemic State, Am Fam Physician[online]. 2005,71,1723-30. [viewed 01 June 2014] Available from: http://www.aafp.org/afp/2005/0501/p1723.html
  18. THIM T, KRARUP NH, GROVE EL, ROHDE CV, LøFGREN B. Initial assessment and treatment with the Airway, Breathing, Circulation, Disability, Exposure (ABCDE) approach. Int J Gen Med [online] 2012:117-21 [viewed 02 June 2014] Available from: doi:10.2147/IJGM.S28478
  19. VIDYARTHI M., CHOWDHURY T. A.. Diagnosis and early management of hyperglycaemic emergencies in the emergency department. QJM [online] December, 105(3):296-297 [viewed 01 June 2014] Available from: doi:10.1093/qjmed/hcr252
  20. WEBB AK, PHILLIPS MJ, HANSON GC. Iatrogenic nondiabetic hyperosmolar states J R Soc Med [online] 1979 Aug, 72(8):578-586 [viewed 01 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1436911