Diabetic ketoacidosis (DKA) in children is defined by plasma glucose ≥ 11 mmol/L, venous pH ≤7.3 or serum bicarbonate ≤ 15 mEq/L with either ketonemia (Serum β-hydroxybutyrate > 3 mmol/L) or ketonuria. This condition, most especially, when combined with cerebral edema, is the leading cause of death and other severe complications of children with diabetes, especially in initial stages of the illness. Early recognition and proper management of this metabolic disturbance which occurs due to absolute or relative deficiency of insulin is necessary in order to avoid lethal consequences and other complications with chronic disability.
Epidemiology
The prevalence of DKA is not well defined because of the overall lack of precise epidemiologic studies. Among children with type 1 diabetes in high-income countries, the annual incidence of DKA varies between 1 and 10%.
Incidence in the United States
Newly presenting DKA is identified in thirty percent of children in whom type 1 diabetes is diagnosed. A cross-sectional study across the centers revealed that approximately one quarter of new type 1 diabetes identified have DKA which approximately equates to 4 per 100 000 children annually. Among all children who were presented with DKA, the youngest children, however, those under five years, had the highest risk with 37·3% of these children developing the condition.
Global incidence
Serum DKA rates rise with time in diabetic clients. Internationally, there is a lack of data; however, research reveals a large range of DKA rates, especially in socially deprived populations. Newly diagnosed children with diabetes are likely to present with DKA especially those under two years, children from ethnic minorities or low-income families. The cases involve greater risk for adolescent girls and children belonging to immigrant families in developed countries.
Anatomy
Pathophysiology
It helps in the uptake of glucose in tissues, the suppression of hepatic glucose output and increased fat synthesis. In insulin deficiency the body sets fasting like rate of glucose production and glycogen breakdown which raises the plasma glucose and counter regulatory hormones (glucagon cortisol among others) thus causing the metabolic derangements.
Hyperglycemia: Glucagon increases the liver glucose output which increases blood sugar concentrations beyond the ability of the kidney to reabsorb glucose and hence results in glucose loss in urine and water, (osmotic diuresis).
Fluid and Electrolyte Imbalance: Dehydration through diuresis, vomiting, and hyperventilation can be as much as 3-8% of body weight and involves major electrolyte depletion (potassium, sodium, phosphate, magnesium).
Ketoacidosis: Lack of insulin results in breakdown of fats resulting to production of ketones which causes acidosis. Poor circulation brings in lactic acidosis to the compounded list, and if not treated, can lead to renal failure and death.
Cerebral Edema: The cause of cerebral edema in DKA is unclear, which could be due of several reasons such as: Prolong untreated DKA, over aggressive fluid replenishment, and cerebral hypoxia. These are ischemia-reperfusion injury, osmolality variations during the treatment process, and sodium hydrogen transports respectively.
Etiology
Despite proper screening, newly diagnosed diabetes in children accounts for 25% of children with new cases of DKA, mainly because of missed diagnoses, especially in young children. In children with a previous diagnosis of diabetes, the precipitating factors of DKA are different according to age. Infections seems to be a more common cause in the younger children while missed insulin doses or emotional stress are causes prevalent in teenagers. CSII users are at a higher risk of DKA in case of malfunctions in insulin delivery because they do not have an insulin stock. DKA primarily occurs in the first year of CSII treatment. There are some children with type 1 diabetes who have recurrent DKA due to emotional stress even though they may never admit non-compliance, and they are referred to as ‘brittle diabetics.’ In developing countries, DKA is mostly associated with infection and insulin deficiency.
Genetics
Prognostic Factors
Morbidity and Mortality
DKA is the leading cause of diabetes-related deaths in children. The mortality rate if insulin is not administered is 100% while it has reduced to between 2-5% with the current treatments offered. Cerebral edema complicates DKA in approximately 1 % of patients and is the third most common cause of death in this population, the mortality rate being 20 – 25 % with substantial neurologic morbidity in up to 35 % of the survivors. However, few but severe adverse effects have been reported, including acute respiratory distress syndrome (ARDS), pulmonary oedema, pneumomediastinum, rhabdomyolysis and acute renal failure. Patients with significant acidosis or dehydration during DKA increases the risk of AKI or CNS dysfunction in children. Specifically for pregnant women, DKA doubles the risk of fetal mortality
Clinical History
Age group
Infants and Toddlers (0-4 years): Frequently, the problems are vague and include weakness, vomiting, and dehydration. It may cause Kussmaul breathing, and the patient may be confused or even act in a stupor. School-Aged Children (5-12 years): Present most of the times with features of classic DKA: abdominal pain, vomiting and Kussmaul respiration leading to hyponatremia and osmotic diuresis. These symptoms may resemble other more commonly presenting conditions such as gastroenteritis.
Adolescents (13-19 years): More likely to present with various psychological stressors including emotional distress, and noncompliance with insulin therapy.
Physical Examination
The physical examination of a child with DKA will show such features as lethargy, irritability or apparent distress. Some of the clinical manifestation involve tachycardia and increased respiratory rate, especially Kussmaul respirations associated with metabolic acidosis. Epidermal turgidity is commonly impaired and mucous membranes can be dry due to the impaired water balance. Abdominal palpation may be painful, as if the child has gastroenteritis, and the child’s breath may smell fruity or like acetone because of the presence of ketones.
DKA can occur within hours to days and the acute presentation is more likely to be seen in the pediatric population. Symptoms maybe severe dehydration, confusion, lethargy, hypotension, and shock in severe cases.
Initial Assessment: Evaluating the nature and severity of signs and possible causes (infection, insulin omission): Tachycardia, hypertension, tachypnea, altered mental status.
Fluid Resuscitation: Give isotonic saline (0.9% NaCl) over the first hour starting at 10-20 mL/kg to replenish intravascular volume. Monitor the patient’s clinical status, serum electrolytes and urine output to balanced fluids. As soon as initial resuscitation becomes effective transition to hypotonic fluids (e.g. 0.45% NaCl).
Electrolyte Management: Monitor serum electrolytes at least daily with greater emphasis on potassium, sodium and chloride levels. Introduce potassium if its levels are low or if the patient has been vain and levels are low; high (above 5.5 mEq/L), normal levels (3.3 to 5.5). It is also advised that patients should not have frequent use of potassium-sparing agents with NSAIDs since this may lead to hyperkalemia.
Insulin Therapy: Im one of the earliest things stimulate a continuous IV insulin infusion (Usually at a rate of 0.1 unit of insulin per kilogram per hour) with the aim of lowering blood glucose concentration and inhibiting ketogenesis. Monitor blood glucose every 1-2 hours and vary insulin infusion rate only to allow glucose levels to decrease slowly (to 50-100 mg/dL/hour).
Acidosis Management Bicarbonate Therapy: It is generally advised not to use if pH is more than 6.9 because of adverse effects of the therapy. Continuous Monitoring: Monitor and screen every shift for changes in vital signs, neurological status and for the development of complications such as cerebral edema. Regular blood glucose and ketone measurements and serum electrolyte determination, blood pH and bicarbonate levels.
Identify and Treat Underlying Causes: Prescribe the right antibiotic if the doctor believes the patient has an infection or has a positive culture. Assess the patient’s diabetes care plan and along with that if required, educate and support will also be given.
Transition to Subcutaneous Insulin: It occurs after glucose levels are back to normal; acidosis is corrected (bicarbonate > 15 mEq/L); and the patient can take food by mouth. Stabilize the patient and initiate his/her regular routine with appropriate education on the control of the disease.
peNutritional support: After stabilisation, nutritional care according to protocols for hydration is essential for the affected individual to recover from a DKA while preventing further episodes.
Family support and psychosocial aspects: The family can be involved in the care, providing education to better manage the condition, help reduce anxiety and improve diabetes management as well.
Patient Education: One ongoing focus was educating children and families about diabetes management, including recognizing symptoms of DKA and administration of insulin to enable them to manage their condition effectively.
Interdisciplinary care: A multidisciplinary health care team of personnel with expertise provides comprehensive services addressing the medical, psychological component of recovery.
Role of Volume Expanders
Sodium chloride 0.9%: This solution is used for cardiopulmonary resuscitation and in cases of dehydration on diabetic ketoacidic pathology. To calculate the fluid deficit, evaluate the loss or gain in weight or else do a clinical assessment.
Role of Antidiabetics, Insulins
Regular Human Insulin: It is used as intravenous therapy for management of DKA, facilitate glucose uptake in cells and affect a mild decrease in blood glucose concentration. It is diluted to 1 U/mL, 50 units of insulin in 0.9% sodium chloride. Because of possible decrease in insulin available for injection from adsorption in the syringe and tubing, the amount should be regulated by the clinical response expected and obtained rather than the measured amount of insulin.
Insulin Lispro: This one is a short-acting insulin analogue that can also be given intravenously in a case of DKA only. Shorter acting insulin get into the bloodstream faster and lasts for a shorter period compared to common insulin which improves glucose usage. It is also prepared at 1U/mL of the solution, and dosage alterations should be made according to response due to adsorption problems.
Insulin Aspart: It is an analogue insulin recombinant which is differentiated with regular insulin through one amino acid difference. This product reduces the levels of blood glucose through stimulating increased glucose utilization in the tissues besides decreasing hepatic glucose output, decreasing lipolysis and increasing protein synthesis. Insulin aspart is an important component of metabolism process and helps in the proper use of the glucose.
Role of Electrolyte Supplements, Parenteral
Potassium Chloride: It is used in transmitting nerve impulses and in the contraction of cardiac muscles, in regulation of intracellular fluid, and in the functioning of skeletal and smooth muscles. It also contributes to the normal functioning of the kidneys.
Role of Diuretics, osmotic agents
Hypertonic Saline: It is sodium chloride solution which could be in place of mannitol to decrease the level of cerebral edema in patients with diabetic ketoacidosis.
Mannitol: It is an osmotic diuretic used in the management of cerebral edema. It is provided in 10% or 20% concentrations for infusion, although the 20% concentration is recommended for pediatric use.
Fluid Resuscitation: Giving fluids intravenously to replace lost fluids and potassium is another important step taken. This normally requires isotonic solutions (for example, normal saline) then hypotonic solutions to replace the lost fluids slowly.
Insulin Therapy: Intravenous insulin infusion is frequently administered as an IV insulin infusion to lower serum glucose concentrations and suppress ketone production. Blood glucose measurements are used to adjust the doses to the administration cautiously.
Electrolyte Management: Supplementation of electrolytes often and especially potassium should be done to avoid dangers like hypokalemia when using insulin since it moves potassium to the cellular fraction.
Monitoring and Supportive Care: Strict supervision of clinical indices such as pulse rate, blood pressure, level of consciousness and performing regular tests like blood glucose, ketones and electrolytes will help in the management and to detect any worsening of the condition.
The approach to managing pediatric diabetic ketoacidosis is divided into phases to avoid any default in managing this condition. The first phase is aimed at the initial assessment that involves fluid resuscitation, insulin therapy to lower blood glucose and ketone levels. During the intermediate phase, vital signs, serum electrolytes and neurological state should be frequently evaluated to identify potential complications, including hypokalemia and cerebral oedema. The resolution phase consists of a progressive withdrawal of insulin therapy, an assessment of fluid and electrolyte status, and defining a safe approach to transfer to subcutaneous insulin. Lastly, the rehabilitation or post-DKA phase focuses on teaching the patient more about diabetes care plans, a proper diet and ways of avoiding other cases of DKA in the future. All these phases are very vital in the management of DKA in children to provide adequate care.
Diabetic ketoacidosis (DKA) in children is defined by plasma glucose ≥ 11 mmol/L, venous pH ≤7.3 or serum bicarbonate ≤ 15 mEq/L with either ketonemia (Serum β-hydroxybutyrate > 3 mmol/L) or ketonuria. This condition, most especially, when combined with cerebral edema, is the leading cause of death and other severe complications of children with diabetes, especially in initial stages of the illness. Early recognition and proper management of this metabolic disturbance which occurs due to absolute or relative deficiency of insulin is necessary in order to avoid lethal consequences and other complications with chronic disability.
The prevalence of DKA is not well defined because of the overall lack of precise epidemiologic studies. Among children with type 1 diabetes in high-income countries, the annual incidence of DKA varies between 1 and 10%.
Incidence in the United States
Newly presenting DKA is identified in thirty percent of children in whom type 1 diabetes is diagnosed. A cross-sectional study across the centers revealed that approximately one quarter of new type 1 diabetes identified have DKA which approximately equates to 4 per 100 000 children annually. Among all children who were presented with DKA, the youngest children, however, those under five years, had the highest risk with 37·3% of these children developing the condition.
Global incidence
Serum DKA rates rise with time in diabetic clients. Internationally, there is a lack of data; however, research reveals a large range of DKA rates, especially in socially deprived populations. Newly diagnosed children with diabetes are likely to present with DKA especially those under two years, children from ethnic minorities or low-income families. The cases involve greater risk for adolescent girls and children belonging to immigrant families in developed countries.
It helps in the uptake of glucose in tissues, the suppression of hepatic glucose output and increased fat synthesis. In insulin deficiency the body sets fasting like rate of glucose production and glycogen breakdown which raises the plasma glucose and counter regulatory hormones (glucagon cortisol among others) thus causing the metabolic derangements.
Hyperglycemia: Glucagon increases the liver glucose output which increases blood sugar concentrations beyond the ability of the kidney to reabsorb glucose and hence results in glucose loss in urine and water, (osmotic diuresis).
Fluid and Electrolyte Imbalance: Dehydration through diuresis, vomiting, and hyperventilation can be as much as 3-8% of body weight and involves major electrolyte depletion (potassium, sodium, phosphate, magnesium).
Ketoacidosis: Lack of insulin results in breakdown of fats resulting to production of ketones which causes acidosis. Poor circulation brings in lactic acidosis to the compounded list, and if not treated, can lead to renal failure and death.
Cerebral Edema: The cause of cerebral edema in DKA is unclear, which could be due of several reasons such as: Prolong untreated DKA, over aggressive fluid replenishment, and cerebral hypoxia. These are ischemia-reperfusion injury, osmolality variations during the treatment process, and sodium hydrogen transports respectively.
Despite proper screening, newly diagnosed diabetes in children accounts for 25% of children with new cases of DKA, mainly because of missed diagnoses, especially in young children. In children with a previous diagnosis of diabetes, the precipitating factors of DKA are different according to age. Infections seems to be a more common cause in the younger children while missed insulin doses or emotional stress are causes prevalent in teenagers. CSII users are at a higher risk of DKA in case of malfunctions in insulin delivery because they do not have an insulin stock. DKA primarily occurs in the first year of CSII treatment. There are some children with type 1 diabetes who have recurrent DKA due to emotional stress even though they may never admit non-compliance, and they are referred to as ‘brittle diabetics.’ In developing countries, DKA is mostly associated with infection and insulin deficiency.
Morbidity and Mortality
DKA is the leading cause of diabetes-related deaths in children. The mortality rate if insulin is not administered is 100% while it has reduced to between 2-5% with the current treatments offered. Cerebral edema complicates DKA in approximately 1 % of patients and is the third most common cause of death in this population, the mortality rate being 20 – 25 % with substantial neurologic morbidity in up to 35 % of the survivors. However, few but severe adverse effects have been reported, including acute respiratory distress syndrome (ARDS), pulmonary oedema, pneumomediastinum, rhabdomyolysis and acute renal failure. Patients with significant acidosis or dehydration during DKA increases the risk of AKI or CNS dysfunction in children. Specifically for pregnant women, DKA doubles the risk of fetal mortality
Age group
Infants and Toddlers (0-4 years): Frequently, the problems are vague and include weakness, vomiting, and dehydration. It may cause Kussmaul breathing, and the patient may be confused or even act in a stupor. School-Aged Children (5-12 years): Present most of the times with features of classic DKA: abdominal pain, vomiting and Kussmaul respiration leading to hyponatremia and osmotic diuresis. These symptoms may resemble other more commonly presenting conditions such as gastroenteritis.
Adolescents (13-19 years): More likely to present with various psychological stressors including emotional distress, and noncompliance with insulin therapy.
The physical examination of a child with DKA will show such features as lethargy, irritability or apparent distress. Some of the clinical manifestation involve tachycardia and increased respiratory rate, especially Kussmaul respirations associated with metabolic acidosis. Epidermal turgidity is commonly impaired and mucous membranes can be dry due to the impaired water balance. Abdominal palpation may be painful, as if the child has gastroenteritis, and the child’s breath may smell fruity or like acetone because of the presence of ketones.
DKA can occur within hours to days and the acute presentation is more likely to be seen in the pediatric population. Symptoms maybe severe dehydration, confusion, lethargy, hypotension, and shock in severe cases.
Initial Assessment: Evaluating the nature and severity of signs and possible causes (infection, insulin omission): Tachycardia, hypertension, tachypnea, altered mental status.
Fluid Resuscitation: Give isotonic saline (0.9% NaCl) over the first hour starting at 10-20 mL/kg to replenish intravascular volume. Monitor the patient’s clinical status, serum electrolytes and urine output to balanced fluids. As soon as initial resuscitation becomes effective transition to hypotonic fluids (e.g. 0.45% NaCl).
Electrolyte Management: Monitor serum electrolytes at least daily with greater emphasis on potassium, sodium and chloride levels. Introduce potassium if its levels are low or if the patient has been vain and levels are low; high (above 5.5 mEq/L), normal levels (3.3 to 5.5). It is also advised that patients should not have frequent use of potassium-sparing agents with NSAIDs since this may lead to hyperkalemia.
Insulin Therapy: Im one of the earliest things stimulate a continuous IV insulin infusion (Usually at a rate of 0.1 unit of insulin per kilogram per hour) with the aim of lowering blood glucose concentration and inhibiting ketogenesis. Monitor blood glucose every 1-2 hours and vary insulin infusion rate only to allow glucose levels to decrease slowly (to 50-100 mg/dL/hour).
Acidosis Management Bicarbonate Therapy: It is generally advised not to use if pH is more than 6.9 because of adverse effects of the therapy. Continuous Monitoring: Monitor and screen every shift for changes in vital signs, neurological status and for the development of complications such as cerebral edema. Regular blood glucose and ketone measurements and serum electrolyte determination, blood pH and bicarbonate levels.
Identify and Treat Underlying Causes: Prescribe the right antibiotic if the doctor believes the patient has an infection or has a positive culture. Assess the patient’s diabetes care plan and along with that if required, educate and support will also be given.
Transition to Subcutaneous Insulin: It occurs after glucose levels are back to normal; acidosis is corrected (bicarbonate > 15 mEq/L); and the patient can take food by mouth. Stabilize the patient and initiate his/her regular routine with appropriate education on the control of the disease.
Critical Care/Intensive Care
Pediatrics, Cardiology
peNutritional support: After stabilisation, nutritional care according to protocols for hydration is essential for the affected individual to recover from a DKA while preventing further episodes.
Family support and psychosocial aspects: The family can be involved in the care, providing education to better manage the condition, help reduce anxiety and improve diabetes management as well.
Patient Education: One ongoing focus was educating children and families about diabetes management, including recognizing symptoms of DKA and administration of insulin to enable them to manage their condition effectively.
Interdisciplinary care: A multidisciplinary health care team of personnel with expertise provides comprehensive services addressing the medical, psychological component of recovery.
Critical Care/Intensive Care
Pediatrics, Cardiology
Sodium chloride 0.9%: This solution is used for cardiopulmonary resuscitation and in cases of dehydration on diabetic ketoacidic pathology. To calculate the fluid deficit, evaluate the loss or gain in weight or else do a clinical assessment.
Critical Care/Intensive Care
Pediatrics, Cardiology
Regular Human Insulin: It is used as intravenous therapy for management of DKA, facilitate glucose uptake in cells and affect a mild decrease in blood glucose concentration. It is diluted to 1 U/mL, 50 units of insulin in 0.9% sodium chloride. Because of possible decrease in insulin available for injection from adsorption in the syringe and tubing, the amount should be regulated by the clinical response expected and obtained rather than the measured amount of insulin.
Insulin Lispro: This one is a short-acting insulin analogue that can also be given intravenously in a case of DKA only. Shorter acting insulin get into the bloodstream faster and lasts for a shorter period compared to common insulin which improves glucose usage. It is also prepared at 1U/mL of the solution, and dosage alterations should be made according to response due to adsorption problems.
Insulin Aspart: It is an analogue insulin recombinant which is differentiated with regular insulin through one amino acid difference. This product reduces the levels of blood glucose through stimulating increased glucose utilization in the tissues besides decreasing hepatic glucose output, decreasing lipolysis and increasing protein synthesis. Insulin aspart is an important component of metabolism process and helps in the proper use of the glucose.
Critical Care/Intensive Care
Pediatrics, Cardiology
Potassium Chloride: It is used in transmitting nerve impulses and in the contraction of cardiac muscles, in regulation of intracellular fluid, and in the functioning of skeletal and smooth muscles. It also contributes to the normal functioning of the kidneys.
Critical Care/Intensive Care
Pediatrics, Cardiology
Hypertonic Saline: It is sodium chloride solution which could be in place of mannitol to decrease the level of cerebral edema in patients with diabetic ketoacidosis.
Mannitol: It is an osmotic diuretic used in the management of cerebral edema. It is provided in 10% or 20% concentrations for infusion, although the 20% concentration is recommended for pediatric use.
Critical Care/Intensive Care
Pediatrics, Cardiology
Fluid Resuscitation: Giving fluids intravenously to replace lost fluids and potassium is another important step taken. This normally requires isotonic solutions (for example, normal saline) then hypotonic solutions to replace the lost fluids slowly.
Insulin Therapy: Intravenous insulin infusion is frequently administered as an IV insulin infusion to lower serum glucose concentrations and suppress ketone production. Blood glucose measurements are used to adjust the doses to the administration cautiously.
Electrolyte Management: Supplementation of electrolytes often and especially potassium should be done to avoid dangers like hypokalemia when using insulin since it moves potassium to the cellular fraction.
Monitoring and Supportive Care: Strict supervision of clinical indices such as pulse rate, blood pressure, level of consciousness and performing regular tests like blood glucose, ketones and electrolytes will help in the management and to detect any worsening of the condition.
Critical Care/Intensive Care
Pediatrics, Cardiology
The approach to managing pediatric diabetic ketoacidosis is divided into phases to avoid any default in managing this condition. The first phase is aimed at the initial assessment that involves fluid resuscitation, insulin therapy to lower blood glucose and ketone levels. During the intermediate phase, vital signs, serum electrolytes and neurological state should be frequently evaluated to identify potential complications, including hypokalemia and cerebral oedema. The resolution phase consists of a progressive withdrawal of insulin therapy, an assessment of fluid and electrolyte status, and defining a safe approach to transfer to subcutaneous insulin. Lastly, the rehabilitation or post-DKA phase focuses on teaching the patient more about diabetes care plans, a proper diet and ways of avoiding other cases of DKA in the future. All these phases are very vital in the management of DKA in children to provide adequate care.
Diabetic ketoacidosis (DKA) in children is defined by plasma glucose ≥ 11 mmol/L, venous pH ≤7.3 or serum bicarbonate ≤ 15 mEq/L with either ketonemia (Serum β-hydroxybutyrate > 3 mmol/L) or ketonuria. This condition, most especially, when combined with cerebral edema, is the leading cause of death and other severe complications of children with diabetes, especially in initial stages of the illness. Early recognition and proper management of this metabolic disturbance which occurs due to absolute or relative deficiency of insulin is necessary in order to avoid lethal consequences and other complications with chronic disability.
The prevalence of DKA is not well defined because of the overall lack of precise epidemiologic studies. Among children with type 1 diabetes in high-income countries, the annual incidence of DKA varies between 1 and 10%.
Incidence in the United States
Newly presenting DKA is identified in thirty percent of children in whom type 1 diabetes is diagnosed. A cross-sectional study across the centers revealed that approximately one quarter of new type 1 diabetes identified have DKA which approximately equates to 4 per 100 000 children annually. Among all children who were presented with DKA, the youngest children, however, those under five years, had the highest risk with 37·3% of these children developing the condition.
Global incidence
Serum DKA rates rise with time in diabetic clients. Internationally, there is a lack of data; however, research reveals a large range of DKA rates, especially in socially deprived populations. Newly diagnosed children with diabetes are likely to present with DKA especially those under two years, children from ethnic minorities or low-income families. The cases involve greater risk for adolescent girls and children belonging to immigrant families in developed countries.
It helps in the uptake of glucose in tissues, the suppression of hepatic glucose output and increased fat synthesis. In insulin deficiency the body sets fasting like rate of glucose production and glycogen breakdown which raises the plasma glucose and counter regulatory hormones (glucagon cortisol among others) thus causing the metabolic derangements.
Hyperglycemia: Glucagon increases the liver glucose output which increases blood sugar concentrations beyond the ability of the kidney to reabsorb glucose and hence results in glucose loss in urine and water, (osmotic diuresis).
Fluid and Electrolyte Imbalance: Dehydration through diuresis, vomiting, and hyperventilation can be as much as 3-8% of body weight and involves major electrolyte depletion (potassium, sodium, phosphate, magnesium).
Ketoacidosis: Lack of insulin results in breakdown of fats resulting to production of ketones which causes acidosis. Poor circulation brings in lactic acidosis to the compounded list, and if not treated, can lead to renal failure and death.
Cerebral Edema: The cause of cerebral edema in DKA is unclear, which could be due of several reasons such as: Prolong untreated DKA, over aggressive fluid replenishment, and cerebral hypoxia. These are ischemia-reperfusion injury, osmolality variations during the treatment process, and sodium hydrogen transports respectively.
Despite proper screening, newly diagnosed diabetes in children accounts for 25% of children with new cases of DKA, mainly because of missed diagnoses, especially in young children. In children with a previous diagnosis of diabetes, the precipitating factors of DKA are different according to age. Infections seems to be a more common cause in the younger children while missed insulin doses or emotional stress are causes prevalent in teenagers. CSII users are at a higher risk of DKA in case of malfunctions in insulin delivery because they do not have an insulin stock. DKA primarily occurs in the first year of CSII treatment. There are some children with type 1 diabetes who have recurrent DKA due to emotional stress even though they may never admit non-compliance, and they are referred to as ‘brittle diabetics.’ In developing countries, DKA is mostly associated with infection and insulin deficiency.
Morbidity and Mortality
DKA is the leading cause of diabetes-related deaths in children. The mortality rate if insulin is not administered is 100% while it has reduced to between 2-5% with the current treatments offered. Cerebral edema complicates DKA in approximately 1 % of patients and is the third most common cause of death in this population, the mortality rate being 20 – 25 % with substantial neurologic morbidity in up to 35 % of the survivors. However, few but severe adverse effects have been reported, including acute respiratory distress syndrome (ARDS), pulmonary oedema, pneumomediastinum, rhabdomyolysis and acute renal failure. Patients with significant acidosis or dehydration during DKA increases the risk of AKI or CNS dysfunction in children. Specifically for pregnant women, DKA doubles the risk of fetal mortality
Age group
Infants and Toddlers (0-4 years): Frequently, the problems are vague and include weakness, vomiting, and dehydration. It may cause Kussmaul breathing, and the patient may be confused or even act in a stupor. School-Aged Children (5-12 years): Present most of the times with features of classic DKA: abdominal pain, vomiting and Kussmaul respiration leading to hyponatremia and osmotic diuresis. These symptoms may resemble other more commonly presenting conditions such as gastroenteritis.
Adolescents (13-19 years): More likely to present with various psychological stressors including emotional distress, and noncompliance with insulin therapy.
The physical examination of a child with DKA will show such features as lethargy, irritability or apparent distress. Some of the clinical manifestation involve tachycardia and increased respiratory rate, especially Kussmaul respirations associated with metabolic acidosis. Epidermal turgidity is commonly impaired and mucous membranes can be dry due to the impaired water balance. Abdominal palpation may be painful, as if the child has gastroenteritis, and the child’s breath may smell fruity or like acetone because of the presence of ketones.
DKA can occur within hours to days and the acute presentation is more likely to be seen in the pediatric population. Symptoms maybe severe dehydration, confusion, lethargy, hypotension, and shock in severe cases.
Initial Assessment: Evaluating the nature and severity of signs and possible causes (infection, insulin omission): Tachycardia, hypertension, tachypnea, altered mental status.
Fluid Resuscitation: Give isotonic saline (0.9% NaCl) over the first hour starting at 10-20 mL/kg to replenish intravascular volume. Monitor the patient’s clinical status, serum electrolytes and urine output to balanced fluids. As soon as initial resuscitation becomes effective transition to hypotonic fluids (e.g. 0.45% NaCl).
Electrolyte Management: Monitor serum electrolytes at least daily with greater emphasis on potassium, sodium and chloride levels. Introduce potassium if its levels are low or if the patient has been vain and levels are low; high (above 5.5 mEq/L), normal levels (3.3 to 5.5). It is also advised that patients should not have frequent use of potassium-sparing agents with NSAIDs since this may lead to hyperkalemia.
Insulin Therapy: Im one of the earliest things stimulate a continuous IV insulin infusion (Usually at a rate of 0.1 unit of insulin per kilogram per hour) with the aim of lowering blood glucose concentration and inhibiting ketogenesis. Monitor blood glucose every 1-2 hours and vary insulin infusion rate only to allow glucose levels to decrease slowly (to 50-100 mg/dL/hour).
Acidosis Management Bicarbonate Therapy: It is generally advised not to use if pH is more than 6.9 because of adverse effects of the therapy. Continuous Monitoring: Monitor and screen every shift for changes in vital signs, neurological status and for the development of complications such as cerebral edema. Regular blood glucose and ketone measurements and serum electrolyte determination, blood pH and bicarbonate levels.
Identify and Treat Underlying Causes: Prescribe the right antibiotic if the doctor believes the patient has an infection or has a positive culture. Assess the patient’s diabetes care plan and along with that if required, educate and support will also be given.
Transition to Subcutaneous Insulin: It occurs after glucose levels are back to normal; acidosis is corrected (bicarbonate > 15 mEq/L); and the patient can take food by mouth. Stabilize the patient and initiate his/her regular routine with appropriate education on the control of the disease.
Critical Care/Intensive Care
Pediatrics, Cardiology
peNutritional support: After stabilisation, nutritional care according to protocols for hydration is essential for the affected individual to recover from a DKA while preventing further episodes.
Family support and psychosocial aspects: The family can be involved in the care, providing education to better manage the condition, help reduce anxiety and improve diabetes management as well.
Patient Education: One ongoing focus was educating children and families about diabetes management, including recognizing symptoms of DKA and administration of insulin to enable them to manage their condition effectively.
Interdisciplinary care: A multidisciplinary health care team of personnel with expertise provides comprehensive services addressing the medical, psychological component of recovery.
Critical Care/Intensive Care
Pediatrics, Cardiology
Sodium chloride 0.9%: This solution is used for cardiopulmonary resuscitation and in cases of dehydration on diabetic ketoacidic pathology. To calculate the fluid deficit, evaluate the loss or gain in weight or else do a clinical assessment.
Critical Care/Intensive Care
Pediatrics, Cardiology
Regular Human Insulin: It is used as intravenous therapy for management of DKA, facilitate glucose uptake in cells and affect a mild decrease in blood glucose concentration. It is diluted to 1 U/mL, 50 units of insulin in 0.9% sodium chloride. Because of possible decrease in insulin available for injection from adsorption in the syringe and tubing, the amount should be regulated by the clinical response expected and obtained rather than the measured amount of insulin.
Insulin Lispro: This one is a short-acting insulin analogue that can also be given intravenously in a case of DKA only. Shorter acting insulin get into the bloodstream faster and lasts for a shorter period compared to common insulin which improves glucose usage. It is also prepared at 1U/mL of the solution, and dosage alterations should be made according to response due to adsorption problems.
Insulin Aspart: It is an analogue insulin recombinant which is differentiated with regular insulin through one amino acid difference. This product reduces the levels of blood glucose through stimulating increased glucose utilization in the tissues besides decreasing hepatic glucose output, decreasing lipolysis and increasing protein synthesis. Insulin aspart is an important component of metabolism process and helps in the proper use of the glucose.
Critical Care/Intensive Care
Pediatrics, Cardiology
Potassium Chloride: It is used in transmitting nerve impulses and in the contraction of cardiac muscles, in regulation of intracellular fluid, and in the functioning of skeletal and smooth muscles. It also contributes to the normal functioning of the kidneys.
Critical Care/Intensive Care
Pediatrics, Cardiology
Hypertonic Saline: It is sodium chloride solution which could be in place of mannitol to decrease the level of cerebral edema in patients with diabetic ketoacidosis.
Mannitol: It is an osmotic diuretic used in the management of cerebral edema. It is provided in 10% or 20% concentrations for infusion, although the 20% concentration is recommended for pediatric use.
Critical Care/Intensive Care
Pediatrics, Cardiology
Fluid Resuscitation: Giving fluids intravenously to replace lost fluids and potassium is another important step taken. This normally requires isotonic solutions (for example, normal saline) then hypotonic solutions to replace the lost fluids slowly.
Insulin Therapy: Intravenous insulin infusion is frequently administered as an IV insulin infusion to lower serum glucose concentrations and suppress ketone production. Blood glucose measurements are used to adjust the doses to the administration cautiously.
Electrolyte Management: Supplementation of electrolytes often and especially potassium should be done to avoid dangers like hypokalemia when using insulin since it moves potassium to the cellular fraction.
Monitoring and Supportive Care: Strict supervision of clinical indices such as pulse rate, blood pressure, level of consciousness and performing regular tests like blood glucose, ketones and electrolytes will help in the management and to detect any worsening of the condition.
Critical Care/Intensive Care
Pediatrics, Cardiology
The approach to managing pediatric diabetic ketoacidosis is divided into phases to avoid any default in managing this condition. The first phase is aimed at the initial assessment that involves fluid resuscitation, insulin therapy to lower blood glucose and ketone levels. During the intermediate phase, vital signs, serum electrolytes and neurological state should be frequently evaluated to identify potential complications, including hypokalemia and cerebral oedema. The resolution phase consists of a progressive withdrawal of insulin therapy, an assessment of fluid and electrolyte status, and defining a safe approach to transfer to subcutaneous insulin. Lastly, the rehabilitation or post-DKA phase focuses on teaching the patient more about diabetes care plans, a proper diet and ways of avoiding other cases of DKA in the future. All these phases are very vital in the management of DKA in children to provide adequate care.
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