The document provides information on pediatric hyperglycemia and diabetic ketoacidosis (DKA). It defines DKA as a life-threatening condition characterized by hyperglycemia, ketosis, and acidosis. Left untreated, DKA can lead to complications and death. The document outlines the pathophysiology, clinical presentation, assessment, and management of DKA to enhance the care of pediatric patients presenting with hyperglycemia or DKA.
This document defines diabetic ketoacidosis (DKA) and discusses its incidence, risk factors, signs, and treatment in children. DKA is characterized by hyperglycemia, acidosis, and ketosis. The risk of DKA is higher in children under 12, those with lower socioeconomic status or no family history of diabetes. Recurrent DKA occurs in 5% of children and accounts for 60% of DKA cases. Treatment involves fluid resuscitation, insulin therapy, electrolyte replacement, and close monitoring for cerebral edema, with consideration of ICU admission for severe cases. Successful management requires attention to detail, documentation, and repeated patient examination.
Diabetic Ketoacidosis in Children (DKA)Hardi Tahir
Diabetic ketoacidosis (DKA) is a life-threatening complication that occurs most often in patients with type 1 diabetes. It results from a lack of insulin and a buildup of ketones in the bloodstream, which leads to hyperglycemia and metabolic acidosis. Treatment involves insulin administration, intravenous fluids to correct dehydration and electrolyte imbalances, and monitoring for complications like cerebral edema. Careful rehydration and normalization of blood sugars and acid-base status are needed to resolve DKA.
The document discusses diabetic ketoacidosis (DKA), providing information on its pathophysiology, classification, epidemiology, clinical manifestations, diagnosis, and treatment in individuals with type 1 diabetes mellitus. DKA results from a lack of insulin leading to hyperglycemia and ketone production. Its presentation includes vomiting, Kussmaul breathing, and if severe, cerebral edema. Treatment involves fluid resuscitation, electrolyte replacement, low-dose insulin infusion to resolve acidosis without rapidly lowering blood glucose, and careful monitoring to prevent cerebral edema.
The document discusses diabetic ketoacidosis (DKA), a life-threatening complication that occurs most often in patients with type 1 diabetes. DKA is characterized by hyperglycemia, metabolic acidosis, and ketosis. It results from a lack of insulin and excess counterregulatory hormones that cause fat and protein breakdown. This leads to ketone accumulation and high blood glucose levels. Treatment involves insulin, intravenous fluids, electrolyte replacement, and monitoring for complications like cerebral edema.
This document discusses diabetic ketoacidosis (DKA), providing definitions, pathophysiology, diagnostic criteria, clinical features, and management approach. DKA is characterized by hyperglycemia, dehydration, and acidosis due to insulin deficiency. It is most commonly seen in type 1 diabetics and can be life-threatening. The document outlines treatment involving fluid replacement, insulin administration, electrolyte replacement, and addressing underlying causes such as infection. Complications discussed include cerebral edema, which has high mortality. Careful management is needed to safely resolve DKA and prevent complications.
Hypokalemia and hyperkalemia indore pedicon 2014 finalRajesh Kulkarni
This document discusses two case studies of pediatric patients presenting with electrolyte abnormalities. Case 1 involves a 2-year-old boy named Rahul who was brought to the emergency department with diarrhea and dehydration. His lab work showed sodium of 131 mEq/L and potassium of 2 mEq/L, indicating hypokalemia. Case 2 involves a 7-year-old girl named Vinita who was admitted to the PICU for severe diabetic ketoacidosis. Her initial potassium was 4.4 mEq/L but the resident was concerned about potential hyperkalemia with further potassium supplementation. The document then reviews the causes, clinical manifestations, diagnosis, and management of hypo- and hyperkalemia in
This document provides an overview of diabetic ketoacidosis (DKA), including its pathophysiology, diagnosis, treatment, and potential complications. It describes DKA as a serious complication of diabetes mellitus resulting from insulin deficiency and elevated counterregulatory hormones. The goals of treatment are fluid resuscitation, electrolyte replacement, and insulin therapy to reverse metabolic derangements while avoiding cerebral edema. Rapid treatment is important to reduce mortality, which can be up to 10% without treatment.
This document defines diabetic ketoacidosis (DKA) and discusses its incidence, risk factors, signs, and treatment in children. DKA is characterized by hyperglycemia, acidosis, and ketosis. The risk of DKA is higher in children under 12, those with lower socioeconomic status or no family history of diabetes. Recurrent DKA occurs in 5% of children and accounts for 60% of DKA cases. Treatment involves fluid resuscitation, insulin therapy, electrolyte replacement, and close monitoring for cerebral edema, with consideration of ICU admission for severe cases. Successful management requires attention to detail, documentation, and repeated patient examination.
Diabetic Ketoacidosis in Children (DKA)Hardi Tahir
Diabetic ketoacidosis (DKA) is a life-threatening complication that occurs most often in patients with type 1 diabetes. It results from a lack of insulin and a buildup of ketones in the bloodstream, which leads to hyperglycemia and metabolic acidosis. Treatment involves insulin administration, intravenous fluids to correct dehydration and electrolyte imbalances, and monitoring for complications like cerebral edema. Careful rehydration and normalization of blood sugars and acid-base status are needed to resolve DKA.
The document discusses diabetic ketoacidosis (DKA), providing information on its pathophysiology, classification, epidemiology, clinical manifestations, diagnosis, and treatment in individuals with type 1 diabetes mellitus. DKA results from a lack of insulin leading to hyperglycemia and ketone production. Its presentation includes vomiting, Kussmaul breathing, and if severe, cerebral edema. Treatment involves fluid resuscitation, electrolyte replacement, low-dose insulin infusion to resolve acidosis without rapidly lowering blood glucose, and careful monitoring to prevent cerebral edema.
The document discusses diabetic ketoacidosis (DKA), a life-threatening complication that occurs most often in patients with type 1 diabetes. DKA is characterized by hyperglycemia, metabolic acidosis, and ketosis. It results from a lack of insulin and excess counterregulatory hormones that cause fat and protein breakdown. This leads to ketone accumulation and high blood glucose levels. Treatment involves insulin, intravenous fluids, electrolyte replacement, and monitoring for complications like cerebral edema.
This document discusses diabetic ketoacidosis (DKA), providing definitions, pathophysiology, diagnostic criteria, clinical features, and management approach. DKA is characterized by hyperglycemia, dehydration, and acidosis due to insulin deficiency. It is most commonly seen in type 1 diabetics and can be life-threatening. The document outlines treatment involving fluid replacement, insulin administration, electrolyte replacement, and addressing underlying causes such as infection. Complications discussed include cerebral edema, which has high mortality. Careful management is needed to safely resolve DKA and prevent complications.
Hypokalemia and hyperkalemia indore pedicon 2014 finalRajesh Kulkarni
This document discusses two case studies of pediatric patients presenting with electrolyte abnormalities. Case 1 involves a 2-year-old boy named Rahul who was brought to the emergency department with diarrhea and dehydration. His lab work showed sodium of 131 mEq/L and potassium of 2 mEq/L, indicating hypokalemia. Case 2 involves a 7-year-old girl named Vinita who was admitted to the PICU for severe diabetic ketoacidosis. Her initial potassium was 4.4 mEq/L but the resident was concerned about potential hyperkalemia with further potassium supplementation. The document then reviews the causes, clinical manifestations, diagnosis, and management of hypo- and hyperkalemia in
This document provides an overview of diabetic ketoacidosis (DKA), including its pathophysiology, diagnosis, treatment, and potential complications. It describes DKA as a serious complication of diabetes mellitus resulting from insulin deficiency and elevated counterregulatory hormones. The goals of treatment are fluid resuscitation, electrolyte replacement, and insulin therapy to reverse metabolic derangements while avoiding cerebral edema. Rapid treatment is important to reduce mortality, which can be up to 10% without treatment.
Hypoglycemia is a potentially devastating metabolic emergency in children. It can cause cognitive impairment, seizures, cerebral palsy, and other neurological issues if severe and prolonged. The document discusses the various causes and classifications of hypoglycemia in infants and children, including transient neonatal hypoglycemia, persistent hypoglycemia due to conditions like hyperinsulinism, counterregulatory hormone deficiencies, and disorders of glycogenolysis and gluconeogenesis. Clinical features and key cases are also presented.
This document discusses the approach to hypoglycemia in childhood. It begins by defining hypoglycemia and describing the importance of glucose for brain development. It then discusses the pathophysiology of hypoglycemia, focusing on how the body maintains blood glucose levels through glycogenolysis, gluconeogenesis, and lipolysis. The clinical features of hypoglycemia are presented, distinguishing between sympathetic overactivity and neuroglycopenic symptoms. Common etiologies like hyperinsulinism, metabolic disorders, and systemic illnesses are outlined. The document concludes with recommendations for investigating hypoglycemia, managing acute episodes, and treating underlying causes to prevent long-term neurological consequences.
Diabetic ketoacidosis (DKA) is a life-threatening complication of diabetes caused by low insulin levels and high levels of counter-regulatory hormones. This leads to hyperglycemia, lipolysis, ketogenesis, and metabolic acidosis. Common precipitants include infections, inadequate insulin treatment, and myocardial ischemia. Clinical features include nausea, vomiting, abdominal pain, dehydration, and Kussmaul breathing. Diagnosis involves measuring glucose, ketones, electrolytes, and acid-base status. Management consists of fluid resuscitation, insulin administration, electrolyte replacement, and treating any precipitating causes. Complications can include cerebral edema, cardiac dysrhythmias, and pulmonary edema. Pro
Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are two serious acute complications of diabetes characterized by high blood sugar levels. DKA involves ketones in the blood while HHS does not. Treatment for DKA involves rehydration with saline, potassium replacement, low-dose insulin therapy, monitoring blood sugars and electrolytes closely. The goals are to lower blood sugars and acid levels while replenishing fluids and salts. Complications can include low blood sugar, low potassium, or brain swelling.
1. Diabetes mellitus is a chronic metabolic disease characterized by hyperglycemia due to either lack of insulin production or insulin resistance. The two main types are type 1 DM caused by autoimmune destruction of insulin-producing beta cells, and type 2 DM caused by insulin resistance with relative insulin deficiency.
2. Symptoms of diabetes include increased thirst, frequent urination, and unexplained weight loss. Type 1 diabetes often presents with diabetic ketoacidosis, while type 2 diabetes is usually diagnosed through routine testing. Treatment involves lifestyle changes, oral medications, and sometimes insulin therapy to control blood glucose levels.
3. Strict control is important to prevent long-term complications affecting the eyes, kidneys, nerves, heart
Hypernatremia is defined as a serum sodium level above 145 mmol/L. It can be caused by excessive sodium intake, decreased water intake, or increased water loss through renal or non-renal routes. Signs and symptoms range from tremulousness and irritability to coma. Treatment involves slow correction of extracellular fluid volume and hypertonicity by oral or IV administration of water, with the rate of sodium level correction not exceeding 1 mmol/L per hour to avoid cerebral edema. The underlying cause, such as central diabetes insipidus, nephrogenic diabetes insipidus, or salt excess/gain must also be treated.
This document describes the case of an 8-year-old girl brought to the emergency department with vomiting, breathlessness, fever, and altered mental status due to diabetic ketoacidosis (DKA). Her history of type 1 diabetes and discontinuing insulin therapy for 2 days contributed to the development of DKA. On examination, she had a low blood pressure, tachycardia, and altered mental status. Laboratory findings showed high blood glucose, low bicarbonate, and ketones in the urine, consistent with DKA. She was treated according to the Milwaukee protocol for DKA, which involves slow correction of dehydration with intravenous fluids, administration of insulin, and monitoring of electrolytes and mental status. Her
Some additional things to ask in the history:
- Family history of similar episodes or endocrine disorders
- Dietary history, including any changes in appetite/food intake
- Growth pattern and any slowing of growth
- Pubertal development
Some additional things to examine:
- Vital signs - check for signs of dehydration, shock
- Detailed physical exam looking for signs of other endocrine abnormalities
- Developmental assessment
- Nutritional status
Investigations to consider:
- Electrolytes, liver/renal function tests
- Cortisol, ACTH to check for primary adrenal insufficiency
- Thyroid function tests
- Growth hormone stimulation test
- Blood glucose curve/
This document defines diabetic ketoacidosis (DKA) and describes its causes, pathophysiology, clinical manifestations, diagnostic criteria, and management. DKA is caused by low insulin levels and high counterregulatory hormones, resulting in hyperglycemia, dehydration, and metabolic acidosis. It is often triggered by missed insulin injections, illness, or stress in patients with type 1 diabetes. Treatment involves fluid resuscitation, insulin therapy, electrolyte replacement, and identifying/treating any precipitating causes to reverse the condition.
to download this presentation from this link
https://mohmmed-ink.blogspot.com/2020/11/diabetic-ketoacidosis.html
Diabetic Ketoacidosis, diabetus type 1 complection. diagnosisi and managment
DKA is a life-threatening complication that can occur in patients with type 1 or type 2 diabetes. It results from a lack of insulin and high levels of glucose and ketones in the blood. Symptoms may include nausea, vomiting, thirst, frequent urination, and abdominal pain. Treatment involves rapid fluid replacement, administration of insulin, and monitoring of electrolytes. Goals are to rehydrate the patient and lower glucose and ketone levels. Complications can include hypoglycemia, hypokalemia, and cerebral edema. With treatment, mortality rates for DKA are now below 5%. Prevention relies on patient education about sick day management of diabetes.
Dr. Amit Shekharay provides information on diabetic ketoacidosis (DKA) in children and its management. DKA results from severe insulin deficiency and can be life-threatening. Risk factors include poor metabolic control, previous DKA episodes, young age, psychiatric/eating disorders, and infection. DKA is diagnosed based on acidosis, ketone levels in blood or urine, and elevated blood glucose. Treatment involves fluid resuscitation, insulin therapy, electrolyte replacement, and monitoring for complications like cerebral edema. Recurrent DKA may indicate non-adherence to diabetes management, so education is important to prevent future episodes.
This case study describes a 47-year-old female patient presenting with diabetic ketoacidosis (DKA). She has a history of type 2 diabetes treated with metformin and insulin that she had defaulted from for 1 month. On presentation, she was dehydrated with a blood glucose of 19.3 mmol/L, high blood ketones, and venous pH of 7.19. She was diagnosed with DKA based on established criteria. Her management involved IV fluid resuscitation, insulin administration, monitoring, and treatment of an underlying infection. The goals of treatment were to lower ketones and raise bicarbonate levels while avoiding hypoglycemia and other complications.
This document summarizes neonatal hyperglycemia. It defines hyperglycemia in newborns as a blood glucose level >125 mg/dL or plasma glucose >150 mg/dL. The main causes of neonatal hyperglycemia are high rates of parenteral glucose infusion, prematurity, stress, sepsis, drugs like glucocorticoids and phenytoin, and rare cases of neonatal diabetes mellitus. Management involves monitoring blood glucose levels and administering insulin therapy if levels exceed 180-200 mg/dL to prevent risks like increased mortality and intraventricular hemorrhage in extremely premature infants.
Diabetic emergencies like diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are life-threatening complications of diabetes mellitus that require prompt recognition and treatment. Precipitating factors for DKA include infection, discontinuation or inadequate insulin therapy. The pathophysiology involves insulin deficiency leading to lipolysis and ketone body formation. Clinical features include hyperglycemia, dehydration, and metabolic acidosis. Treatment involves fluid resuscitation, electrolyte replacement, insulin therapy, and treating the underlying precipitant. While venous blood gases can provide adequate assessment of acid-base status, arterial samples are preferable in more severe cases. Initial electrolyte replacement is important
Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic syndrome (HHS) are acute complications of diabetes that result from insufficient insulin levels. DKA is characterized by high blood glucose, low pH and bicarbonate levels, and ketones in the blood or urine. HHS involves extremely high blood glucose without significant ketosis or acidosis. Treatment for DKA involves rehydration, insulin administration, and correcting electrolyte imbalances. Complications can include hypokalemia, hypoglycemia, and in rare cases cerebral edema in children. Proper patient education aims to prevent DKA episodes.
1. Diabetes mellitus is a chronic metabolic disorder characterized by hyperglycemia due to insulin deficiency or insulin resistance. Type 1 diabetes results from autoimmune destruction of pancreatic beta cells leading to absolute insulin deficiency. It commonly presents in children and requires lifelong insulin replacement therapy. Type 2 diabetes is characterized by insulin resistance with relative insulin deficiency and predominantly affects obese children. Proper diabetes education and management including insulin therapy, nutrition, monitoring and prevention of acute and chronic complications are essential in children with diabetes.
Management of diabetic ketoacidosis dkasahar Hamdy
This document discusses the management of diabetic ketoacidosis (DKA). It begins by explaining the pathophysiology of DKA involving hyperglycemia, ketonemia, and acidosis due to counterregulatory hormones and insulin deficiency. The diagnostic criteria for DKA are then provided. The document then outlines the initial evaluation and laboratory tests that should be performed. Finally, it details the five parts of treatment: 1) fluid replacement, 2) insulin administration, 3) potassium supplementation, 4) bicarbonate infusion if needed, and 5) phosphate/magnesium/calcium supplementation. Complications to watch out for during treatment are also listed.
The document discusses pediatric hyperglycemia and diabetic ketoacidosis (DKA). It notes that DKA is the most common cause of death in children with diabetes globally due to lack of access to insulin or improper insulin use. Risk factors for DKA include young age, poor diabetes control, missed insulin injections, and infection. The document outlines the pathophysiology of hyperglycemia and DKA and provides guidelines for assessment, management, complications, education, and resources regarding pediatric patients presenting with these conditions.
This document describes a study that evaluated the antidiabetic activity of extracts from four plants - Stevia raubdeana, Gymnema sylvestre, Withania somnifera, and Ocimum sanctum. Rats were induced with diabetes and divided into type 1 (severe), type 2 (sub and mild) models. The extracts were administered to normal, sub, and mild diabetic rats and their effects on blood glucose and lipid levels were measured. The most effective dose for sub and mild models was used to study the antidiabetic, hypolipidemic, and hepatoprotective effects in severe diabetic rats. Various parameters like blood glucose, lipids, liver and kidney function were tested to
Hypoglycemia is a potentially devastating metabolic emergency in children. It can cause cognitive impairment, seizures, cerebral palsy, and other neurological issues if severe and prolonged. The document discusses the various causes and classifications of hypoglycemia in infants and children, including transient neonatal hypoglycemia, persistent hypoglycemia due to conditions like hyperinsulinism, counterregulatory hormone deficiencies, and disorders of glycogenolysis and gluconeogenesis. Clinical features and key cases are also presented.
This document discusses the approach to hypoglycemia in childhood. It begins by defining hypoglycemia and describing the importance of glucose for brain development. It then discusses the pathophysiology of hypoglycemia, focusing on how the body maintains blood glucose levels through glycogenolysis, gluconeogenesis, and lipolysis. The clinical features of hypoglycemia are presented, distinguishing between sympathetic overactivity and neuroglycopenic symptoms. Common etiologies like hyperinsulinism, metabolic disorders, and systemic illnesses are outlined. The document concludes with recommendations for investigating hypoglycemia, managing acute episodes, and treating underlying causes to prevent long-term neurological consequences.
Diabetic ketoacidosis (DKA) is a life-threatening complication of diabetes caused by low insulin levels and high levels of counter-regulatory hormones. This leads to hyperglycemia, lipolysis, ketogenesis, and metabolic acidosis. Common precipitants include infections, inadequate insulin treatment, and myocardial ischemia. Clinical features include nausea, vomiting, abdominal pain, dehydration, and Kussmaul breathing. Diagnosis involves measuring glucose, ketones, electrolytes, and acid-base status. Management consists of fluid resuscitation, insulin administration, electrolyte replacement, and treating any precipitating causes. Complications can include cerebral edema, cardiac dysrhythmias, and pulmonary edema. Pro
Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are two serious acute complications of diabetes characterized by high blood sugar levels. DKA involves ketones in the blood while HHS does not. Treatment for DKA involves rehydration with saline, potassium replacement, low-dose insulin therapy, monitoring blood sugars and electrolytes closely. The goals are to lower blood sugars and acid levels while replenishing fluids and salts. Complications can include low blood sugar, low potassium, or brain swelling.
1. Diabetes mellitus is a chronic metabolic disease characterized by hyperglycemia due to either lack of insulin production or insulin resistance. The two main types are type 1 DM caused by autoimmune destruction of insulin-producing beta cells, and type 2 DM caused by insulin resistance with relative insulin deficiency.
2. Symptoms of diabetes include increased thirst, frequent urination, and unexplained weight loss. Type 1 diabetes often presents with diabetic ketoacidosis, while type 2 diabetes is usually diagnosed through routine testing. Treatment involves lifestyle changes, oral medications, and sometimes insulin therapy to control blood glucose levels.
3. Strict control is important to prevent long-term complications affecting the eyes, kidneys, nerves, heart
Hypernatremia is defined as a serum sodium level above 145 mmol/L. It can be caused by excessive sodium intake, decreased water intake, or increased water loss through renal or non-renal routes. Signs and symptoms range from tremulousness and irritability to coma. Treatment involves slow correction of extracellular fluid volume and hypertonicity by oral or IV administration of water, with the rate of sodium level correction not exceeding 1 mmol/L per hour to avoid cerebral edema. The underlying cause, such as central diabetes insipidus, nephrogenic diabetes insipidus, or salt excess/gain must also be treated.
This document describes the case of an 8-year-old girl brought to the emergency department with vomiting, breathlessness, fever, and altered mental status due to diabetic ketoacidosis (DKA). Her history of type 1 diabetes and discontinuing insulin therapy for 2 days contributed to the development of DKA. On examination, she had a low blood pressure, tachycardia, and altered mental status. Laboratory findings showed high blood glucose, low bicarbonate, and ketones in the urine, consistent with DKA. She was treated according to the Milwaukee protocol for DKA, which involves slow correction of dehydration with intravenous fluids, administration of insulin, and monitoring of electrolytes and mental status. Her
Some additional things to ask in the history:
- Family history of similar episodes or endocrine disorders
- Dietary history, including any changes in appetite/food intake
- Growth pattern and any slowing of growth
- Pubertal development
Some additional things to examine:
- Vital signs - check for signs of dehydration, shock
- Detailed physical exam looking for signs of other endocrine abnormalities
- Developmental assessment
- Nutritional status
Investigations to consider:
- Electrolytes, liver/renal function tests
- Cortisol, ACTH to check for primary adrenal insufficiency
- Thyroid function tests
- Growth hormone stimulation test
- Blood glucose curve/
This document defines diabetic ketoacidosis (DKA) and describes its causes, pathophysiology, clinical manifestations, diagnostic criteria, and management. DKA is caused by low insulin levels and high counterregulatory hormones, resulting in hyperglycemia, dehydration, and metabolic acidosis. It is often triggered by missed insulin injections, illness, or stress in patients with type 1 diabetes. Treatment involves fluid resuscitation, insulin therapy, electrolyte replacement, and identifying/treating any precipitating causes to reverse the condition.
to download this presentation from this link
https://mohmmed-ink.blogspot.com/2020/11/diabetic-ketoacidosis.html
Diabetic Ketoacidosis, diabetus type 1 complection. diagnosisi and managment
DKA is a life-threatening complication that can occur in patients with type 1 or type 2 diabetes. It results from a lack of insulin and high levels of glucose and ketones in the blood. Symptoms may include nausea, vomiting, thirst, frequent urination, and abdominal pain. Treatment involves rapid fluid replacement, administration of insulin, and monitoring of electrolytes. Goals are to rehydrate the patient and lower glucose and ketone levels. Complications can include hypoglycemia, hypokalemia, and cerebral edema. With treatment, mortality rates for DKA are now below 5%. Prevention relies on patient education about sick day management of diabetes.
Dr. Amit Shekharay provides information on diabetic ketoacidosis (DKA) in children and its management. DKA results from severe insulin deficiency and can be life-threatening. Risk factors include poor metabolic control, previous DKA episodes, young age, psychiatric/eating disorders, and infection. DKA is diagnosed based on acidosis, ketone levels in blood or urine, and elevated blood glucose. Treatment involves fluid resuscitation, insulin therapy, electrolyte replacement, and monitoring for complications like cerebral edema. Recurrent DKA may indicate non-adherence to diabetes management, so education is important to prevent future episodes.
This case study describes a 47-year-old female patient presenting with diabetic ketoacidosis (DKA). She has a history of type 2 diabetes treated with metformin and insulin that she had defaulted from for 1 month. On presentation, she was dehydrated with a blood glucose of 19.3 mmol/L, high blood ketones, and venous pH of 7.19. She was diagnosed with DKA based on established criteria. Her management involved IV fluid resuscitation, insulin administration, monitoring, and treatment of an underlying infection. The goals of treatment were to lower ketones and raise bicarbonate levels while avoiding hypoglycemia and other complications.
This document summarizes neonatal hyperglycemia. It defines hyperglycemia in newborns as a blood glucose level >125 mg/dL or plasma glucose >150 mg/dL. The main causes of neonatal hyperglycemia are high rates of parenteral glucose infusion, prematurity, stress, sepsis, drugs like glucocorticoids and phenytoin, and rare cases of neonatal diabetes mellitus. Management involves monitoring blood glucose levels and administering insulin therapy if levels exceed 180-200 mg/dL to prevent risks like increased mortality and intraventricular hemorrhage in extremely premature infants.
Diabetic emergencies like diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are life-threatening complications of diabetes mellitus that require prompt recognition and treatment. Precipitating factors for DKA include infection, discontinuation or inadequate insulin therapy. The pathophysiology involves insulin deficiency leading to lipolysis and ketone body formation. Clinical features include hyperglycemia, dehydration, and metabolic acidosis. Treatment involves fluid resuscitation, electrolyte replacement, insulin therapy, and treating the underlying precipitant. While venous blood gases can provide adequate assessment of acid-base status, arterial samples are preferable in more severe cases. Initial electrolyte replacement is important
Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic syndrome (HHS) are acute complications of diabetes that result from insufficient insulin levels. DKA is characterized by high blood glucose, low pH and bicarbonate levels, and ketones in the blood or urine. HHS involves extremely high blood glucose without significant ketosis or acidosis. Treatment for DKA involves rehydration, insulin administration, and correcting electrolyte imbalances. Complications can include hypokalemia, hypoglycemia, and in rare cases cerebral edema in children. Proper patient education aims to prevent DKA episodes.
1. Diabetes mellitus is a chronic metabolic disorder characterized by hyperglycemia due to insulin deficiency or insulin resistance. Type 1 diabetes results from autoimmune destruction of pancreatic beta cells leading to absolute insulin deficiency. It commonly presents in children and requires lifelong insulin replacement therapy. Type 2 diabetes is characterized by insulin resistance with relative insulin deficiency and predominantly affects obese children. Proper diabetes education and management including insulin therapy, nutrition, monitoring and prevention of acute and chronic complications are essential in children with diabetes.
Management of diabetic ketoacidosis dkasahar Hamdy
This document discusses the management of diabetic ketoacidosis (DKA). It begins by explaining the pathophysiology of DKA involving hyperglycemia, ketonemia, and acidosis due to counterregulatory hormones and insulin deficiency. The diagnostic criteria for DKA are then provided. The document then outlines the initial evaluation and laboratory tests that should be performed. Finally, it details the five parts of treatment: 1) fluid replacement, 2) insulin administration, 3) potassium supplementation, 4) bicarbonate infusion if needed, and 5) phosphate/magnesium/calcium supplementation. Complications to watch out for during treatment are also listed.
The document discusses pediatric hyperglycemia and diabetic ketoacidosis (DKA). It notes that DKA is the most common cause of death in children with diabetes globally due to lack of access to insulin or improper insulin use. Risk factors for DKA include young age, poor diabetes control, missed insulin injections, and infection. The document outlines the pathophysiology of hyperglycemia and DKA and provides guidelines for assessment, management, complications, education, and resources regarding pediatric patients presenting with these conditions.
This document describes a study that evaluated the antidiabetic activity of extracts from four plants - Stevia raubdeana, Gymnema sylvestre, Withania somnifera, and Ocimum sanctum. Rats were induced with diabetes and divided into type 1 (severe), type 2 (sub and mild) models. The extracts were administered to normal, sub, and mild diabetic rats and their effects on blood glucose and lipid levels were measured. The most effective dose for sub and mild models was used to study the antidiabetic, hypolipidemic, and hepatoprotective effects in severe diabetic rats. Various parameters like blood glucose, lipids, liver and kidney function were tested to
Nursing 5263 Hypoglycemia And Hyperglyemia[1]Kelly Miller
This document discusses hypoglycemia and hyperglycemia in adolescents and young adults with type 1 diabetes. It defines normal and abnormal blood glucose levels and the common causes and management of hypoglycemia and hyperglycemia in this patient population. The document also outlines the potential complications of uncontrolled blood sugar levels, both short term like diabetic ketoacidosis, and long term like damage to organs and body systems. Prevention strategies like blood glucose monitoring, meal planning, exercise and medication adherence are also discussed.
A 33-year-old man presented with diabetic ketoacidosis (DKA) characterized by generalized weakness, excessive urination, thirst, and abdominal pain. DKA results from insulin deficiency and hyperglycemia, causing metabolic acidosis. The patient had type 2 diabetes and was non-compliant with medication. Initial labs showed hyperglycemia, ketonemia, and signs of dehydration and infection. He was treated with IV fluids, insulin, antibiotics, and close monitoring. Nursing care focused on correcting dehydration and electrolyte imbalances, stabilizing blood glucose, and educating on diet and medication compliance to prevent future DKA episodes.
This document provides information about diabetes, including:
- Types of diabetes such as type 1, type 2, prediabetes, and gestational diabetes.
- Symptoms of diabetes like increased urination, thirst, hunger, weight loss and blurred vision.
- Causes of diabetes which vary depending on genetics, family history, ethnicity and lifestyle factors.
- Risk factors for diabetes including nutrition, physical activity, weight, and lifestyle habits.
- Treatment options like diet, exercise, oral medications, insulin and prevention through healthy behaviors.
- Nursing process details for a case study patient with increased urination and weight loss, including assessments, diagnoses, goals, interventions and evaluations.
This document discusses diabetes mellitus (DM) in children, specifically type 1 DM. It defines DM as a metabolic disorder characterized by hyperglycemia resulting from defects in insulin secretion or action. Type 1 DM is an autoimmune disease leading to beta cell destruction in the pancreas and absolute insulin deficiency. Clinical presentation of type 1 DM includes symptoms of hyperglycemia like polyuria and polydipsia, and in severe cases diabetic ketoacidosis. Management involves insulin administration, medical nutrition therapy, exercise and education to maintain blood glucose control and prevent complications.
Diabetic ketoacidosis (DKA) results from insulin deficiency and increased counterregulatory hormones, which causes metabolic changes including hyperglycemia, ketonemia, and metabolic acidosis. DKA is most commonly caused by new onset type 1 diabetes, omission of insulin injections, or inadequate management of infection. Treatment of DKA involves intravenous fluids to restore circulating volume and replace electrolyte deficits, insulin therapy to lower glucose and ketone levels, and management of complications. Recent evidence suggests a range of fluid protocols can be safely used without increasing risks of cerebral edema.
1) Juvenile diabetes is caused by insulin deficiency resulting from the destruction of insulin-producing pancreatic beta cells. It is the most common chronic disease in childhood.
2) Symptoms include excessive thirst, hunger, fatigue, and frequent urination. Diagnosis is confirmed through blood tests showing high blood sugar and ketone levels.
3) Treatment involves managing blood sugar levels through diet, exercise, and insulin therapy tailored to the child's age. The goal is to prevent complications like hypoglycemia, diabetic ketoacidosis, and long-term effects on organs. Strict management is needed from infancy through adolescence.
Risk factors for diabetes during childhoodPratyush1693
Diabetes is a chronic metabolic disorder characterized by high blood glucose levels due to defects in insulin production or insulin resistance. The number of people with diabetes has risen dramatically worldwide from 108 million in 1980 to 422 million in 2014. India has a high prevalence of diabetes, with urban areas having higher rates than rural areas. Diabetes can be classified into type 1, type 2, gestational diabetes and other types. Risk factors include family history, age, ethnicity and obesity. Preventing and managing diabetes through lifestyle changes, medication and routine screening can reduce complications like kidney disease, eye problems and heart disease. Recent research focuses on vaccines to prevent type 1 diabetes and restoring insulin production through treatments like the BCG vaccine.
Diabetes as presented by cheruiyot sambu in kapkatet county hospital. cheruiyot sambu
Diabetes is a group of metabolic diseases where a person has high blood glucose due to either inadequate insulin production or cells not responding properly to insulin. Type 1 diabetes occurs when the pancreas does not produce insulin, while type 2 occurs when the body does not produce enough insulin or cells do not respond properly to insulin. Symptoms of diabetes include increased urination, thirst, hunger, weight loss, fatigue, and changes in mood or vision. Treatment involves physical activity, healthy diet, and potentially insulin injections or tablets. Uncontrolled diabetes can lead to complications affecting the eyes, feet, heart, kidneys and other organs.
Type 1 diabetes is characterized by little or no insulin production due to destruction of pancreatic beta cells. It commonly develops in childhood or adolescence and requires lifelong insulin treatment. Symptoms include increased thirst, urination, hunger, and weight loss. Complications can include retinopathy, neuropathy, kidney disease and cardiovascular disease if not properly managed. Treatment involves frequent blood glucose monitoring, insulin administration, following a balanced diet, and regular exercise.
This document discusses diabetes mellitus and related conditions. It begins by defining diabetes mellitus as a metabolic disorder characterized by high blood glucose levels due to defects in insulin production or insulin action. The document then discusses the signs and symptoms of diabetes, including increased urination, thirst, weight loss, and high blood sugar. It describes the causes of diabetes, types of diabetes (type 1 and type 2), and related conditions like hyperinsulinism and hypoglycemia. Treatment options are provided for managing blood sugar levels and symptoms.
Type1 diabetes mellitus Final yr MBBS LectureSajjad Sabir
This document provides information on pediatric diabetes mellitus (DM). It discusses that juvenile DM results from absolute lack of insulin and most pediatric patients have type 1 DM requiring lifelong insulin. The causes include progressive loss of islet cell function and insulin resistance. Type 1 DM is insulin dependent and most common in childhood while type 2 DM usually occurs in older children. The management of pediatric DM involves insulin therapy, diet, exercise, blood glucose monitoring, patient education and managing complications like hypoglycemia, diabetic ketoacidosis, and long-term effects.
This document provides information on diabetes mellitus including:
- It defines diabetes as a metabolic disorder causing high blood sugar levels over time due to the body's inability to respond to or produce insulin.
- There are two main types of diabetes - type 1 usually occurs at a young age and type 2 which is more common in obese adults over 30.
- Symptoms include frequent urination, thirst, and hunger as the body turns to other energy sources without enough insulin.
- Treatment involves nutritional therapy, insulin administration, oral medications, education, and managing acute complications like hypoglycemia and ketoacidosis.
- Long term complications can impact the cardiovascular, ocular, renal, and neurological systems if blood sugar
Diabetes is a disease where blood glucose levels are too high due to the body not producing enough insulin or not properly using the insulin it does produce. There are three main types of diabetes: type 1 where the body does not produce insulin; type 2 where the body does not properly use insulin; and gestational diabetes which occurs during pregnancy. Diabetes is diagnosed through blood tests and managed through lifestyle changes like diet and exercise as well as medication like insulin. Treatment aims to control blood sugar levels to prevent complications.
This document provides information on diabetes mellitus (DM), including definitions, types, pathophysiology, clinical manifestations, diagnosis, and management. It begins by defining the objectives of the session and introducing the pancreas and pancreatic hormones like insulin, glucagon, and somatostatin. It then defines DM, describes the two main types (type 1 and type 2), and other less common types. Risk factors, clinical features, diagnostic criteria involving blood tests, and potential complications of both short-term and long-term hyperglycemia are outlined. Management of DM focuses on diet, exercise, and medication like insulin or oral hypoglycemic agents.
The document provides an overview of diabetes, including:
- The history and prevalence of diabetes globally and in Iran.
- The main types of diabetes - type 1, type 2, and gestational diabetes - and their pathophysiology.
- Risk factors, symptoms, diagnostic tests and treatment guidelines for diabetes.
- The goals of diabetes management including controlling blood sugar, blood pressure, and cholesterol levels.
The document discusses non-drug management of diabetes mellitus through lifestyle changes including diet and exercise. It covers definitions of diabetes, types of diabetes, principles of diabetes care like learning about diabetes and monitoring health indicators. It provides details on healthy diet, types of exercise, testing before exercise and sample exercise programs. The non-drug management aims to control blood sugar levels through patient education, monitoring and encouraging lifestyle modifications.
The document summarizes non-drug management of diabetes mellitus. It discusses lifestyle changes like following a healthy diet, regular exercise, and weight control as important non-drug approaches. Monitoring health indicators like blood glucose, blood pressure, cholesterol and attending regular medical checkups are also emphasized to manage diabetes and prevent complications long-term without relying solely on medication.
The document summarizes non-drug management of diabetes mellitus. It discusses lifestyle changes like following a healthy diet, regular exercise, and weight control as important non-drug approaches. Monitoring health indicators like blood glucose, blood pressure, cholesterol and attending regular medical checkups are also emphasized to manage diabetes and prevent complications long-term without relying solely on medication.
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Healthy Eating Habits:
Understanding Nutrition Labels: Teaches how to read and interpret food labels, focusing on serving sizes, calorie intake, and nutrients to limit or include.
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Physical Benefits: Discusses how exercise aids in weight management, muscle and bone health, cardiovascular health, and flexibility.
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Encourages consistency, variety in exercises, setting realistic goals, and finding enjoyable activities to maintain motivation.
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2. Today, almost a century after the discovery of insulin,
the most common cause of death in a child with
diabetes, from a global perspective, is lack of access
to insulin or improper use of insulin.
Many children die even before their diabetes is
diagnosed. Around the world, forces have united to
make it come true that no child should die from
diabetes or its complications.
2
3. Define and explain pediatric hyperglycemia and DKA
Highlight current standards of care regarding pediatric
hyperglycemia and DKA management
Provide educational resources to health care
professionals to share with pediatric patients and
families dealing with issues related to pediatric
hyperglycemia and DKA
Goals
3
5. Purpose
The purpose of this educational module is to enhance the care
of pediatric patients who present with hyperglycemia and
diabetic ketoacidosis (DKA) through appropriate:
ASSESSMENT
MANAGEMENT
PREVENTION OF COMPLICATIONS
DISPOSITION
PATIENT & PARENT/CAREGIVER EDUCATION
5
6. Objectives
At the end of this module you will be able to:
Describe the mechanisms of hyperglycemia and DKA
Perform an initial assessment on a child who is experiencing
hyperglycemia and DKA
Describe the clinical presentation of a pediatric patient with DKA
Understand the physiologic changes taking place in a pediatric
patient with DKA
Develop an effective management plan
Discuss cerebral edema as a complication of pediatric DKA
Develop a plan for appropriate admission, transfer or referral
Formulate appropriate discharge instructions
6
7. The following publications were the primary sources of
information for this module, and will be referenced throughout:
American Diabetes Association (ADA)1
Standards of Medical Care in Diabetes – 2017. Diabetes Care.
American Diabetes Association (ADA)2
Diabetic Ketoacidosis in Infants, Children, and Adolescents
A consensus statement from the American Diabetes Association
European Society for Paediatric Endocrinology (ESPE)3
Lawson Wilkins Pediatric Endocrine Society (LWPES)3
European Society for Paediatric Endocrinology / Lawson Wilkins Pediatric
Endocrine Society Consensus Statement on Diabetic Ketoacidosis in Children
and Adolescents
International Society for Pediatric and Adolescent Diabetes (ISPAD)4
Diabetic Ketoacidosis in Children and Adolescents with Diabetes
ISPAD Clinical Practice Consensus Guidelines 2009 Compendium
Main Resources
7
8. Frequency of DKA
DKA occurs in children with:
New-onset of type 1 diabetes mellitus
Established type 1 diabetes mellitus during risk episodes
May occur in children with type 2 diabetes mellitus
8
9. DKA Risk Factors
Young children
Poor diabetes control
Previous episodes of DKA
Missed insulin injections
Insulin pump failure
Infection or other illnesses
Low socioeconomic status
Lack of adequate health insurance
Psychiatric disorders (i.e., eating disorders)
9
10. Illinois EMSC Statewide DKA QI
DKA record review (532 records total) - high percentage of cases
reported documentation of: full set of vital signs, blood glucose level,
and neurological status during initial assessment
However, documentation of ongoing/hourly ED monitoring for same
indicators was much less consistent
Percentage of documentation even lower for hospitals that (on survey)
reported ED ongoing monitoring was “not defined in policy” or performed “per
physician decision”
93%
70%
93%
58%
52%
37%
0%
20%
40%
60%
80%
100%
Vital Signs Blood Glucose Neurological Assessment
ED Monitoring of Pediatric DKA Patients (532 records)
Initial Hourly
10
11. Practice Deviations
(within 1st hour of treatment)
Guideline Recommendations
Administer an IV fluid bolus 15-20
mL/kg 0.45% NaCl over the first
hour
The recommended fluid course is 10-20
mL/kg 0.9% NaCl over the first hour
Administer an IV insulin drip of
0.1 units/kg/hour
Current guidelines recommend administering
insulin after the initial fluid resuscitation, not
concurrently
Administer an IV insulin bolus of
0.1 units/kg
Current guidelines suggest IV insulin bolus
may increase the risk of cerebral edema, and
should not be used at the start of therapy
Wait for more laboratory results
before giving any fluids
Current guidelines recommend initial IV fluid
administration should begin immediately
Illinois EMSC Statewide DKA QI
** Additional findings from the statewide QI project (responses to survey and case
scenarios) seem to indicate concerning deviations from the current treatment
guidelines for pediatric DKA patients within the first hour of treatment**
11
12. Understanding Diabetes
Diabetes mellitus, often referred to simply as diabetes.
Diabetes is a condition in which the body:
Does not produce enough insulin, and/or
Does not properly respond to insulin
Insulin is a hormone produced in the pancreas. Insulin enables
cells to absorb glucose in order to turn it into energy.
12
13. The cause of diabetes in children continues to be a mystery.
Genetics
Environmental factors
Obesity
Lack of exercise
Diabetes: An Epidemic
13
14. Type 1 vs. Type 2
Type 1 diabetes Type 2 diabetes
Diagnosed in children
and young adults
Typically diagnosed in
adulthood
Previously known as
Juvenile Diabetes
Also found in overweight
children
Insulin-dependent Non-insulin-dependent
Body does not produce
insulin
Body fails to produce
and properly use insulin
14
17. Hypoglycemia
Low blood glucose: treated when less than 60 mg/dL
Develops because the body doesn’t have enough glucose to
burn energy
Can happen suddenly
Can be treated quickly and easily by eating or drinking a small
amount of glucose rich food
The signs and symptoms include:
Low blood glucose
Hunger
Headache
Confusion, shakiness, dizziness
Sweating
If hypoglycemia is suspected, check the blood glucose concentration
17
18. Hyperglycemia
High blood glucose: treated when greater than 200 mg/dL
Develops when the body has too much glucose in the blood
Serious problem if not treated
A major cause of many of the complications in children with
diabetes
The signs and symptoms include:
High blood glucose
High levels of glucose in the urine
Frequent urination
Increased thirst
If hyperglycemia is suspected, check the blood glucose concentration
18
19. Hypoglycemia vs. Hyperglycemia
Low blood glucose
(less than 60 mg/dL)
Signs and symptoms include:
Shakiness
Dizziness
Sweating
Hunger
Headache
Pale skin color
Mental or behavior changes
Lethargy
Clumsy or jerky movements
Seizure
Difficulty concentrating
Tingling sensations around the
mouth
Signs and symptoms include:
Classic symptoms:
Polyphagia (excessive hunger)
Polyuria (excessive urine/urination)
Polydipsia (excessive thirst)
Other symptoms might include:
Blurred vision
Fatigue
Weight loss
Slow-healing cuts and sores
Headaches
Difficulty concentrating
Vaginal and skin infections
High blood glucose
(greater than 200 mg/dL)
19
20. Ketosis
Ketones
Acidic substances that are made when the body breaks down
fat for energy
Ketosis
Presence of excess ketones in the body
Blood ketone concentration between 0.3 and 7.0 mmol/L
Ketoacidosis
Severe form of ketosis
Reflects levels of 7.0 mmol/L or higher
Lowers the pH to 7.3 or lower
20
21. Acidosis
Increased acidity of the blood
Acidemia is a pH below 7.35
Signs & Symptoms
Deep, rapid breathing (known as Kussmaul’s respirations)
confusion or lethargy
abdominal pain
Blood tests to diagnose metabolic acidosis may include:
Arterial or venous blood gas
Electrolytes: Na+ (sodium), K+ (potassium), Cl- (chloride) and
HCO3
- (bicarbonate) (total CO2 content)
21
22. DKA is a complex metabolic state of:
hyperglycemia, ketosis, and acidosis
Symptoms include:
Deep, rapid breathing
Fruity breath odor
Very dry mouth
Nausea and vomiting
Lethargy/drowsiness
DKA is life-threatening and needs immediate treatment
22
23. The biochemical criteria for the diagnosis of DKA3,4
Hyperglycemia - blood glucose greater than 200 mg/dL
Ketosis - ketones present in blood and/or urine
Acidosis - pH less than 7.3 and/or
bicarbonate less than 15 mmol/L
Classic Triad of DKA
23
24. DKA is generally categorized by the severity of the acidosis.
MILD – Venous pH less than 7.3 and/or
bicarbonate concentration less than 15 mmol/L
MODERATE – Venous pH less than 7.2 and/or
bicarbonate concentration less than 10 mmol/L
SEVERE – Venous pH less than 7.1 and/or
bicarbonate concentration less than 5 mmol/L
Classification of DKA
24
25. Two Emergencies of Diabetes
Hypoglycemia
Low blood glucose
Fast – within seconds
Too much insulin
Too little food
Too much exercise
without food
Missing or delayed
meals/snacks
Stress/overexcitement in
young children
Low (less than 60 mg/dL)
None in urine or blood
Hyperglycemia
Ketoacidosis/DKA
Presence of ketones
Slow - within hours or days
Insufficient insulin
Missed insulin dose(s)
Infections/illness
Stress response
High (greater than 200 mg/dL)
Moderate/large in urine or
blood
Due to:
Time of onset:
Causes:
Blood glucose:
Ketones:
25
26. New Emerging Third Emergency:
Hyperglycemic Hyperosmolar Syndrome (HHS)
Similar symptoms to DKA
Elevated blood glucose
Dehydration
Altered mental status
HHS5,6
Severe dehydration
Little or no ketone accumulation
Elevated blood glucose levels greater than 600 mg/dL,
frequently exceeds 1000 mg/dL
Elevated serum osmolality (over 320 mOsm/kg H2O)
Children with type 2 diabetes may be at greatest risk
Occurs infrequently in children, so data regarding the optimal
approach to treatment are lacking
26
27. Mild DKA Moderate DKA Severe DKA HHS
Blood glucose >200 mg/dL >200 mg/dL >200 mg/dL >600 mg/dL
Venous pH < 7.3 < 7.2 < 7.1 > 7.3
Serum
bicarbonate
< 15 mEq/L < 10 mEq/L < 5 mEq/L > 15 mEq/L
Urine ketones Positive Positive Positive Small or none
Blood ketones Positive Positive Positive Small or none
Beta-
hydroxybutyrate
High High High
Normal or
elevated
Serum osmolality Variable Variable Variable
> 320
mOsm/kg
H2O
Alteration in
mental status
Alert Alert/drowsy Stupor/coma Stupor/coma
Classifications of DKA
Diagnostic Criteria for Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic State
27
28. Pathophysiology of DKA
Wolfsdorf J, Glaser N, Sperling MA; American Diabetes Association. Diabetic ketoacidosis in infants, children, and
adolescents: A consensus statement from the American Diabetes Association. Diabetes Care. 2006;29(5):1150-1159.
Reprinted with permission from The American Diabetes Association. 28
33. Thorough History is Imperative!
Preexisting diabetes
History of diabetes and duration
Last meal/carbohydrate intake
Current and routine blood glucose levels
Standard insulin regimen
Last insulin dose
Type of insulin and route
Past hospitalization history
Duration of symptoms
Nausea/vomiting/abdominal pain
Precipitating factors
Physical exertion
Change in eating habits/diets
Stress
Missed insulin dose
Illness
New onset diabetes
Recent history of
Polyuria
Polydipsia
Polyphagia
Weight loss
Past medical history
Family history of diabetes
History/duration of symptoms
Headache
Blurry vision
Nausea/vomiting/ abdominal pain
Difficulty in breathing
Changes in behavior
Precipitating factors
Concurrent illness or infection
33
34. Physical Assessment
Assess for dehydration
Vital signs, mucous membranes, capillary refill, skin (color,
temperature and turgor)
Assess for acidosis
Fruity breath odor
Deep, rapid breathing → Kussmaul’s respirations
Assess mental status → watch for cerebral edema!
AVPU
PGCS
Assess for signs/symptoms of possible infection
34
35. Assessment Resources
Systematic Assessment
Pediatric Assessment Triangle (PAT)
Primary Assessment (ABCDE)
Secondary Assessment (FGHI)
Triage (E-U-N)
Emergency Severity Index (ESI)
AVPU Scale
Pediatric Glasgow Coma Scale (PGCS)
For more information, click on these links or proceed to Appendix A
35
39. Blood Glucose Testing
A blood glucose test measures
the amount of glucose in the
blood
Blood glucose tests are done to
screen and monitor treatment
Normal glucose range is between
80 and 120 mg/dL
39
40. Ketone Testing
Below 0.6 mmol/L
Readings below 0.6 mmol/L are in the normal range.
Above 1.5 mmol/L
Readings above 1.5 mmol/L in the presence of hyperglycemia indicate the
child may be at risk for developing diabetic ketoacidosis (DKA).
0.6 to 1.5 mmol/L
Readings between 0.6 and 1.5 mmol/L may indicate the development of a
problem that may require medical assistance.
Blood Ketone Reading Indications
Urine Ketone Testing
Out-dated or expired test strips may cause a false-positive reading.
40
41. Blood Gases
ABG arterial blood sample or VBG venous blood sample are both
adequate to determine blood pH.
VBG is sufficient unless altered level of consciousness
Remember: arterial puncture is a painful procedure; consider using topical
anesthetic as a pain reducing therapy
An ABG provides a snapshot of the blood’s pH + PO2 + PCO2 = HCO3
pH – indicates if acidotic or alkalemic
PO2 – the amount of oxygen dissolved in the blood
PCO2 – the amount of carbon dioxide dissolved in the blood
HCO3 – the amount of bicarbonate in the blood
Metabolic acidosis is defined as a low pH
and decreased HCO3
Metabolic alkalosis is defined as a high pH
and increased HCO3 41
43. Be prepared to
make adjustments
frequently!
Goals Of Therapy
• Correct dehydration
• Correct acidosis and reverse ketosis
• Restore normal blood glucose levels
• Avoid complications of therapy
Not All Children Are The Same!
43
44. Treatment Overview
Follow established guidelines
Consider need for consultation and transfer to higher level of care
Recognize and prevent serious complications such as cerebral
edema
Maintain strict NPO
IV fluids
Phase I
Initial volume expansion
Phase II
Replacement of fluid deficit
Maintenance fluids
Insulin administration (begins after the initial fluid resuscitation)
Continuous IV insulin infusion
Subcutaneous/Intramuscular
Electrolyte replacement
Reassessment and ongoing monitoring
44
45. Management of Pediatric Patients with DKA
Initial hour - start IV fluids
IV Fluids Insulin Potassium Dextrose
Adapted from:
Kitabchi AE, Umpierrez GE, Murphy MB, et al; American Diabetes Association. Hyperglycemic crises in diabetes. Diabetes Care.
2004;27(Suppl. 1):S94-S102
Complete initial evaluation
Advance to slide 49 Advance to slide 51 Advance to slide 54 Advance to slide 61
45
46. IV Fluid Administration
The goal of the first hour of treatment
fluid resuscitation
confirmation of DKA by
laboratory studies
The goals of the second and succeeding
hours
slow correction of
hyperglycemia, metabolic
acidosis and ketosis
continued volume
replacement
This usually requires several
hours and meticulous attention
to the patient's response to
therapy
IV Fluids
Determine hydration status
Mild to moderate dehydration Hypovolemic shock
Administer
0.9% NS 10 mL/kg/hr
over initial hour
Administer
0.9% NS 20 mL/kg
bolus infused as
quickly as possible
Replace fluid deficit evenly over 48hr with 0.45 – 0.9% NS
Adapted from:
Kitabchi AE, Umpierrez GE, Murphy MB, et al; American Diabetes Association. Hyperglycemic crises in diabetes. Diabetes Care.
2004;27(Suppl. 1):S94-S102 46
47. IV Fluid Key Points
Start IV fluids: 10-20 mL/kg of 0.9%NS over the first hour
In a severely dehydrated patient, this may need to be repeated
Fluids should not exceed 50 mL/kg over first 4 hours of therapy
Clinical assessment of dehydration to determine fluid volume
Children with DKA have a fluid deficit in the range of 5-10%
Mild DKA 3-4% dehydration
Moderate DKA 5-7% dehydration
Severe DKA 10% dehydration
Shock is rare in pediatric DKA
Replace fluid deficit evenly over 48 hours
REMINDER: Serum sodium decreases by 1.6mEq/L for every
100-mg/dl increase in serum glucose concentration above 100mg/dl,
therefore no electrolyte correction is needed
ALL PATIENTS WITH DKA REQUIRE SUPPLEMENTAL FLUIDS
47
48. Insulin Administration
Insulin therapy
Turns off the production of ketones
Decreases blood glucose
Low-dose insulin infusion
Decreases risk of hypoglycemia or
hypokalemia
Goal is to decrease blood glucose by
100mg/dL/hour
Do not reduce or discontinue the insulin infusion
based solely upon the blood glucose
The insulin infusion should be continued until
the ph >7.30 and/or the HCO3 >15 mEq/L and the
serum ketones have cleared
Insulin treatment is begun after the initial fluid resuscitation
INSULIN
IV insulin infusion
regular insulin
0.1 units/kg/hr
Continue until acidosis
clears
(pH >7.30, HC03 >15 mEq/L)
Decrease to
0.05 units/kg/hr
until SQ insulin
initiated
Adapted from:
Kitabchi AE, Umpierrez GE, Murphy MB, et al; American Diabetes Association. Hyperglycemic crises in
diabetes. Diabetes Care. 2004;27(Suppl. 1):S94-S102 48
49. Insulin Key Points
Prior to insulin administration, reassess vital signs, blood glucose level
and neurological status
Insulin is administered as a continuous intravenous infusion of
regular insulin at a rate of 0.1 units/kg per hour (prepared by
pharmacy)
Insulin is a “High-Alert” medication, therefore two nurses should
verify the insulin order, dose, and volume prior to administration
IV tubing should be primed with the insulin solution before
administration
Do not give insulin as a bolus
At the time of insulin infusion, make sure any indwelling
insulin pump has been disconnected and/or stopped
49
50. Insulin Key Points (cont.)
The dose of insulin should remain at 0.1 units/kg/hour until
the acidosis resolves (pH 7.3 and/or bicarbonate >15 mEq/L)
Do not decrease rate or stop the insulin administration based
solely on glucose values
Once blood glucose reaches 250 mg/dL, maintain insulin and
begin dextrose infusion
If the acidosis is not improving, consult with a Pediatric
Endocrinologist or Intensivist since the insulin dose may need
to be increased to 0.15 or 0.20 units/kg/hour
If IV infusion is not possible, insulin injected intramuscularly
or subcutaneously every 1 or 2 hours can be effective
50
51. Potassium Administration:
General Guidelines
Start replacing potassium after initial fluid resuscitation
and concurrent with starting insulin therapy
MONITOR CLOSELY!!!
In general, in patients with DKA, there is a significant
potassium deficit that must be replaced
Potassium replacement should continue throughout IV
fluid therapy
The maximum recommended rate of IV potassium
replacement is institution specific
51
Consult with your Pharmacist before administering potassium
52. Potassium Administration (cont.)
When initial serum potassium
is <2.5 mmol/L (hypokalemia)
Administer 0.5-1 mEq/kg of potassium
chloride in IV
Administer at rates specified by your
institutional protocol or utilize a
standard pediatric reference
Start potassium replacement early,
even before starting insulin therapy
52
53. Potassium Administration (cont.)
When initial serum potassium is
2.5 - 3.5 mmol/L
Administer potassium 40 mEq/L in
IV solution until serum potassium > 3.5
mmol/L
Monitor serum potassium hourly
Administer potassium 30 – 40 mEq/L in
IV solution to maintain serum potassium
at 3.5 – 5.0 mmol/L
53
54. Potassium Administration (cont.)
When initial serum potassium is
3.5 - 5.0 mmol/L
• Administer potassium 30 – 40 mEq/L in
IV solution to maintain serum
potassium at 3.5 – 5.0 mmol/L
• Monitor serum potassium hourly
Normal serum potassium level ranges between 3.5 to 5.0 mmol/L
54
55. Potassium Administration (cont.)
When initial serum potassium is
> 5.0 mmol/L (hyperkalemia)
Do not give IV potassium in initial fluids
Monitor serum potassium hourly until
< 5.0 mmol/L
Then begin IV fluids with potassium to
maintain serum potassium at 3.5 – 5.0
mmol/L
Defer potassium replacement therapy
until child has voided
55
56. EKG
Hypokalemia
Flattening T wave, widening of the QT
interval, and appearance of U waves
Hyperkalemia
Tall, peaked symmetrical, T waves
and shortening of QT intervals
Normal serum potassium level ranges between 3.5 to 5.0 mmol/L
56
57. Potassium Key Points
Potassium loss in DKA due to:
vomiting
osmotic diuresis
Potassium levels should be maintained at 3.5 – 5.0 mmol/L
Abnormal or critical values require hourly potassium checks
Consult with a Pediatric Endocrinologist or Intensivist about
abnormal values
Suggested potassium replacement can be administered as
follows:
Potassium phosphate with potassium chloride
Potassium phosphate with potassium acetate
Suggested administration:
Potassium Phosphate 20mEq + Potassium Acetate 20mEq
(unless hypophosphatemia develops)
57
58. Dextrose Administration
Maintain glucose between
150 to 250 mg/dL to
prevent hypoglycemia
Check glucose hourly until
stable
Check electrolytes every
2-4 hrs until stable
Dextrose
Add to IV fluids when the blood glucose
concentration reaches 250 mg/dL
Change to 5% dextrose with 0.45 NaCl at a
rate to complete rehydration in 48 hr
Check glucose hourly and electrolytes every
2-4 hr until stable
After resolution of DKA, initiate SQ insulin
0.5 – 1.0 units/kg/day (or according to insulin
dosing guidelines per institution or physician
policy)
Adapted from:
Kitabchi AE, Umpierrez GE, Murphy MB, et al; American
Diabetes Association. Hyperglycemic crises in diabetes.
Diabetes Care. 2004;27(Suppl. 1):S94-S102
58
59. Bicarbonate
Bicarbonate therapy should only be considered in cases of:
Severe acidemia
Life-threatening hyperkalemia11
Bicarbonate therapy is generally contraindicated in Pediatric
DKA due to increased risk of cerebral edema.7,8,9,10
Consult with a Pediatric Endocrinologist and/or
Intensivist prior to initiating bicarbonate!
59
60. Monitoring
Hourly assessments:
Vital signs
pulse, respiratory rate, B/P, oxygen saturation, temperature, and
pain level (as applicable)
Neurological status
Accurate fluid intake/output
Point-of-care-testing blood glucose level
Potassium level
A flow sheet is invaluable for monitoring and documentation
Children presenting with DKA must be monitored closely
Notify the treating physician immediately with any critical lab values or
change in mental status.
60
61. Monitoring (cont.)
Every 2 hours:
Urine ketones
Serum β-OH
Labs (repeated every 2– 4 hours or more frequently, as indicated in more
severe cases)
serum glucose, electrolytes, BUN, calcium, magnesium,
phosphorus, hematocrit, and blood gases
Continuous cardiac monitoring
Amount of administered insulin
All insulin rate/dose changes should be doubled checked by two nurses
and documented on the flow sheet.
61
62. Additional Measures
Administer oxygen
Insert additional peripheral intravenous
catheter
for repetitive blood sampling, and/or
if insulin drip is initiated
Children with altered mental status or consciousness,
consider:
Secure the airway
Nasogastric suction
Bladder catheterization
62
63. Introduction of Oral Fluids
Oral fluids should be introduced:
only when substantial clinical improvement has occurred –
note that mild acidosis/ketosis may still be present
When oral fluid is tolerated, IV fluid should be reduced
Ketoacidosis is resolved when:
• blood glucose is < 200 mg/dL
• serum bicarbonate is ≥ 15 mEq/L and/or venous pH > 7.3
• oral intake is tolerated
If continuing fluids for hydration,
remove dextrose from the IV.
63
64. Transition to Subcutaneous Insulin Injections
Typically occurs in the inpatient setting
Transition to subcutaneous insulin when:
Ketoacidosis has resolved, and
Oral intake is tolerated
Initiate subcutaneous insulin 0.5-1.0 unit/kg/day
Before a mealtime
Before stopping the insulin infusion
After transitioning to subcutaneous insulin, frequent blood glucose monitoring
is required to avoid marked hyperglycemia and hypoglycemia
Do not stop the insulin infusion before the first injection
The dose and type of subcutaneous insulin given should be based on
hospital or physician guidelines
64
65. High-Risk Patients
New-onset diabetes
Severe DKA (including long duration of symptoms)
Compromised circulation
Depressed level of consciousness
Increased risk for cerebral edema
children less than 5 years of age
Any child who might benefit from consultation with pediatric
critical care specialists and transfer to specialized pediatric
critical care centers
Consult with a Pediatric Endocrinologist/Intensivist as soon as DKA is suspected
65
66. Inter-facility Pediatric Transfer Guideline
Inter-facility transfer guideline is defined as:12
hospital-to-hospital (including out of State/Territory) procedural and administrative
policies for transferring critically ill children to facilities that provide specialized
pediatric care, or pediatric services not available at the referring facility
Components of a Pediatric Inter-facility transfer guidelines
should include:
Process for initiating a transfer
the roles and responsibilities of the referring facility
the roles and responsibilities of the referral center
responsibilities for requesting transfer and communication
Process for selecting an appropriate facility
Process for selecting an appropriately staffed transport service
Process for patient transfer
66
67. Transport: Selecting a Facility
Factors to consider when selecting the appropriate facility:
PICU or pediatric unit specializing in diabetes care with:
Written guidelines for DKA management in children
A specialist with training and expertise in the management of DKA
Experienced nursing staff trained in monitoring and management of
DKA
Access to laboratories for frequent and timely evaluation of critical labs
Timely transfer to a specialty care center is essential
67
68. Transport: Mode of Transport
Process for selecting appropriate method of transport:
The referring physician, in consultation with the receiving
center, should:
Determine the method of transport
Use appropriate personnel to accompany the child
Critical care transport team
Transport staff matches child’s acuity
Utilize appropriate sized equipment and medication
Use a specialized transport team for any child already started
on an insulin infusion
68
69. Transport: Patient Transfer
Process for patient transfer:
Obtain informed consent
Plan transfer of:
Medical record
Copy of signed transport consent
Personal belongings
Provide family with receiving institution information
and directions
The overall goal is to expedite safe transport of the
child using trained staff with appropriate equipment
and medications
69
72. DKA Management: Serious Complications
Cerebral Edema
Pulmonary Edema
CNS Hemorrhage or Thrombosis
Cardiac Arrhythmias
Pancreatitis
Renal Failure
Cerebral edema due to DKA is almost exclusively a pediatric condition
72
73. Unclear Pathogenesis
DKA-related cerebral edema remains poorly understood
Many theories proposed13,14,15,16
Data from literature has not clearly supported any particular
theory
Treatment causing or exacerbating cerebral edema has been
particularly controversial
Continues to be a topic of current review19,20
73
74. Cerebral Edema: Facts
Occurs in less than 1% of
Pediatric DKA episodes
Accounts for 60% to 90% of all
DKA deaths
10% to 25% of survivors have
permanent neurological injury
74
75. Cerebral Edema: Presentation
May develop without warning
symptoms
Asymptomatic cerebral swelling
is believed to occur more
frequently
Occurs most frequently 4-12
hours after therapy initiation
May occur before treatment is
initiated.
75
76. Cerebral Edema: Risk Factors
Younger age (e.g., infants and children < 5 yrs)
New-onset diabetes
High glucose levels
Severe dehydration (elevated BUN/creatinine)
Severe acidosis (lower pH, HCO3, pCO2)
Treatment with bicarbonate
76
77. Cerebral Edema: Rate of Fluid Rehydration?
Controversial Issue
Does a faster rate of rehydration increase risk of cerebral
edema? 19,20
Should there be gradual, even fluid replacement during
treatment?
77
19,20
78. Cerebral Edema: Warning Signs & Symptoms
Major criteria:14
Altered mental status/fluctuating LOC
Sustained HR deceleration (not due to sleep or improved
intravascular volume)
Age-inappropriate incontinence
Minor criteria:
Vomiting
Headache
Lethargy
Diastolic B/P 90 bpm
Age 5 years
78
79. Cerebral Edema: Treatment
Reduce rate of intravenous fluids
Elevate head of bed to at least a 30° angle
Give mannitol 0.25 - 1 gram/kg IV over 20 minutes
May repeat if no initial response in 30 minutes to 2 hours
Have mannitol ready at bedside and calculate dose beforehand
Initiate treatment as soon as
cerebral edema is suspected
79
80. Intubation for impending respiratory failure
avoid aggressive hyperventilation
CNS imaging studies (non-contrast CT scan)
treatment should not be delayed while waiting results.
Transfer and or admit to PICU.
These measures may be life-saving when initiated promptly
(before coma) and may prevent neurologic sequelae.
Cerebral Edema: Treatment (cont.)
80
81. Key Points of Cerebral Edema
Cerebral edema as a complication of DKA is almost exclusively a
condition of childhood
The pathophysiology is still not completely understood
Occurs most frequently 4-12 hours after therapy initiation
Clinical diagnosis is based on major and minor criteria
The clinical course is variable
81
82. Requires urgent recognition and intervention
Treatment of choice is mannitol (0.25 - 1 gram/kg)
Requires admission to a PICU
Intubation may be required, but hyperventilation should be avoided
A non-contrast CT scan is needed to confirm the diagnosis of cerebral
edema and to rule out other causes
Key Points of Cerebral Edema (cont.)
82
84. Management of an episode of DKA is not
complete until the cause has been identified and
an attempt made to prevent it.
Better access to medical care
Proper education
Effective communication with health care provider
DKA Can Be Prevented!
84
85. How To Reduce Episodes Of DKA
All children and families with diabetes should receive
comprehensive diabetes health care and education.
Recognize the early warning signs and symptoms
of ketoacidosis
Take home measurements of blood ketone levels for earlier diagnosis
Frequent insulin pump checks for blockages, kinks,
or disconnections
Have access to a 24-hour diabetes telephone help-line
85
86. Diabetic Education
How to use a glucose monitoring device
to check glucose levels
How to draw up insulin and give
injections
How to recognize and treat
hypoglycemia, including administration
of glucagon
Understand the basic principles of diet
in terms of both content and timing of
meals and snacks
86
87. Discharge Instructions
Before discharge:
Meet with diabetes provider/educator and arrange follow-up
Ensure child and family know when and where they are to return for
follow-up care
87
88. Sick Day Management: Overview
When to contact PCP/Endocrinolgist/Diabetic Educator
Blood glucose goals
Use of supplemental insulin during illness
Medications to suppress fever and treat infections
Initiation of an easily digestible liquid diet containing
carbohydrates and salt
MOST IMPORTANT
Never discontinue or withhold insulin
Seek professional advice early in the course of illness
88
89. Sick Day Management: Basics
Successful sick day management must include:
Involvement of the child
Involvement of parent and family members
The ability to measure blood glucose
The ability to measure urine and/or blood ketones
Knowledge of insulin administration
Know how to take a temperature, respirations and pulse
Know current weight
Able to communicate signs and symptoms to health care
professionals
89
90. Effective School-based Diabetes
Management
Basic diabetes training for all staff
Shared responsibilities for care, with leadership by school
nurse
Self management is allowed in all school settings for students
with capacity
These principles have been endorsed by the American Academy of Pediatrics, American Association of Clinical
Endocrinologists, American Association of Diabetes Educators, American Dietetic Association, Children with Diabetes
Disability Rights Education Defense Fund, Juvenile Diabetes Research Foundation, Lawson Wilkins Pediatric Endocrine
Society, and Pediatric Endocrine Nursing Society.
90
93. Resources
Children with Diabetes Foundation
www.childrensdiabetesfoundation.org
European Society for Pediatric Endocrinology
www.eurospe.org
Lawson Wilkins Pediatric Endocrine Society
www.lwpes.org
93
94. Juvenile Diabetes Research Foundation
www.jdrf.org
International Diabetes Federation
www.idf.org
International Society for Pediatric and Adolescent Diabetes
www.ispad.org
Resources
94
96. References
1. American Diabetes Association. Standards of Medical Care in
Diabetes – 2017. Diabetes Care. 2017;Volume 40, Supplement 1.
2. Wolfsdorf J, Glaser N, Sperling MA; American Diabetes Association.
Diabetic ketoacidosis in infants, children, and adolescents: A
consensus statement from the American Diabetes Association.
Diabetes Care. 2006;29(5):1150-1159.
3. Dunger DB, Sperling MA, Acerini CL, et al. European Society for
Paediatric Endocrinology/Lawson Wilkins Pediatric Endocrine Society
consensus statement on diabetic ketoacidosis in children and
adolescents. Pediatrics. 2004;113(2):e133–e140.
4. Wolfsdorf J, Craig ME, Daneman D, et al. ISPAD Clinical Practice
Consensus Guidelines 2009 Compendium. Diabetic ketoacidosis in
children and adolescents with diabetes. Pediatric Diabetes.
2009;10(Suppl. 12):118–133.
5. Kitabchi AE, Umpierrez GE, Murphy MB, et al. American Diabetes
Association. Hyperglycemic crises in diabetes. Diabetes Care.
2004;27(Suppl. 1):S94-S102.
96
97. References
6. Dean H, Sellers E, Kesselman M. Acute hyperglycemic emergencies
in children with type 2 diabetes. Paediatr Child Health.
2007;12(1):43-44.
7. Glaser NS, Barnett P, McCaslin I, et al. Risk factors for cerebral
edema in children with diabetic ketoacidosis. N Engl J Med.
2001;344(4):264-269.
8. Assal JP, Aoki TT, Manzano FM, Kozak GP. Metabolic effects of
sodium bicarbonate in management of diabetic ketoacidosis.
Diabetes. 1974;23:405– 411.
9. Ohman JL Jr, Marliss EB, Aoki TT, et al. The cerebrospinal fluid in
diabetic ketoacidosis. N Engl J Med. 1971;284:283–290.
10. Edge J, Jakes R, Roy Y, et al. The UK prospective study ofcerebral
oedema complicating diabeticketoacidosis. Arch Dis Child. 2005;90
(Suppl. 11):A2–A3.
11. Narins RG, Cohen JJ. Bicarbonate therapy for organic acidosis: the
case for its continued use. Ann Intern Med. 1987;106:615–618.
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98. References
12. EMS for Children Performance Measures. Implementation Manual
for State Partnership Grantees, 2017 Edition (pg 57 - 63). Retrieved
April 19, 2017 from
http://www.nedarc.org/performanceMeasures/documents/EMS%20
Perf%20Measures%20Manual%20Web_0217.pdf.
13. Glaser NS, Cerebral injury and cerebral edema in children with
diabetic ketoacidosis: could cerebral ischemia and reperfusion injury
be involved? Pediatr Diabetes. 2009;10:534-541.
14. Muir AB, Quisling RG, Yang MCK, Rosenbloom AL. Cerebral edema in
childhood diabetic ketoacidosis: Natural history, radiographic
findings and early identification. Diabetes Care. 2004;27(7):1541-
1546.
15. Bohn D. Understanding the pathophysiology of cerebral edema in
diabetic ketoacidosis: Another brick in the wall? Pediatr Crit Care
Med. 2010;11(3):421-423.
16. Levin DL. Cerebral edema in diabetic ketoacidosis. Pediatr Crit Care
Med. 2008;9(3):320-329.
17. Poirier MP, Greer D, Satin-Smith M. A prospective study of the “two-
bag system” in diabetic ketoacidosis management. Clin Pediatr.
2004;43:809-813. 98
99. References
18. Grimberg A, Cerri RW, Satin-Smith M, Cohen P. The "two bag
system" for variable intravenous dextrose and fluid administration:
Benefits in diabetic ketoacidosis management. J Pediatr.
1999;134:376-378.
19. Glaser NS, Wooton-Gorges SL, Buonocore MH, et al. Subclinical
Cerebral Edema in Children with diabetic ketoacidosis randomized to
2 different rehydration protocols. Pediatrics. 2013;131(1):e73-e80.
20. Glaser NS, Ghetti S, Casper TC, et al. Pediatric diabetic
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99