This document discusses diabetic ketoacidosis (DKA) and other ketoacidotic syndromes. It defines DKA as an acute, life-threatening complication of diabetes characterized by hyperglycemia, ketoacidosis, and ketonuria. The document outlines the pathophysiology, clinical features, diagnostic testing, management, and complications of DKA. It also briefly discusses other ketoacidotic syndromes and their management.
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.
Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are two serious complications of diabetes that represent extremes of the hyperglycemia spectrum. DKA is characterized by hyperglycemia, metabolic acidosis, and ketonemia while HHS features very high blood glucose over 600 mg/dL without significant ketoacidosis. Both require intravenous fluid replacement and insulin therapy. Resolution of DKA requires normalization of acidosis markers and blood glucose under 200 mg/dL while HHS resolution involves blood glucose under 250-300 mg/dL and mental alertness with plasma osmolality under 315 mosmol/kg.
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 of diabetes caused by low insulin levels and high counterregulatory hormones. It is characterized by hyperglycemia, ketosis, and metabolic acidosis. Symptoms include thirst, frequent urination, nausea, vomiting, and altered mental status. Treatment involves insulin, intravenous fluids, electrolyte replacement, and treating any precipitating infections or stressors to stabilize the patient and resolve the acidosis. Careful monitoring of glucose, electrolytes, and acid-base status is required. Complications can include cerebral edema, thrombosis, arrhythmias, and pancreatitis if not properly managed.
Management of diabetic ketoacidosis (DKA) in children involves supportive measures, fluid replacement, correction of hyperglycemia with insulin, and electrolyte replacement. The goals are to rehydrate the patient, lower blood glucose levels safely, correct electrolyte imbalances, and treat any underlying precipitating causes or complications while educating families on preventing future episodes. Careful monitoring is needed to optimize fluids and insulin therapy while avoiding potential complications like cerebral edema.
acute complication of diabetes mellitus. cardinal biochemical features for DKA. pathophysiology of DKA. clinical assesment of DKA. investigation and management for DKA. complications of DKA.
This document provides information on causes, symptoms, pathophysiology, laboratory findings, management, and complications of diabetic ketoacidosis (DKA). It defines DKA as an acute complication of diabetes characterized by hyperglycemia, ketoacidosis, and ketonuria. The main causes are lack of insulin, infection, and non-compliance with treatment. Symptoms include nausea, vomiting, abdominal pain, fruity breath odor, and altered mental status. Laboratory findings include high blood glucose, low pH, high anion gap metabolic acidosis, and ketonemia. Management involves fluid resuscitation, insulin administration, electrolyte replacement, and treating any underlying infection. Complications can include hypokalemia, thrombosis
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.
Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are two serious complications of diabetes that represent extremes of the hyperglycemia spectrum. DKA is characterized by hyperglycemia, metabolic acidosis, and ketonemia while HHS features very high blood glucose over 600 mg/dL without significant ketoacidosis. Both require intravenous fluid replacement and insulin therapy. Resolution of DKA requires normalization of acidosis markers and blood glucose under 200 mg/dL while HHS resolution involves blood glucose under 250-300 mg/dL and mental alertness with plasma osmolality under 315 mosmol/kg.
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 of diabetes caused by low insulin levels and high counterregulatory hormones. It is characterized by hyperglycemia, ketosis, and metabolic acidosis. Symptoms include thirst, frequent urination, nausea, vomiting, and altered mental status. Treatment involves insulin, intravenous fluids, electrolyte replacement, and treating any precipitating infections or stressors to stabilize the patient and resolve the acidosis. Careful monitoring of glucose, electrolytes, and acid-base status is required. Complications can include cerebral edema, thrombosis, arrhythmias, and pancreatitis if not properly managed.
Management of diabetic ketoacidosis (DKA) in children involves supportive measures, fluid replacement, correction of hyperglycemia with insulin, and electrolyte replacement. The goals are to rehydrate the patient, lower blood glucose levels safely, correct electrolyte imbalances, and treat any underlying precipitating causes or complications while educating families on preventing future episodes. Careful monitoring is needed to optimize fluids and insulin therapy while avoiding potential complications like cerebral edema.
acute complication of diabetes mellitus. cardinal biochemical features for DKA. pathophysiology of DKA. clinical assesment of DKA. investigation and management for DKA. complications of DKA.
This document provides information on causes, symptoms, pathophysiology, laboratory findings, management, and complications of diabetic ketoacidosis (DKA). It defines DKA as an acute complication of diabetes characterized by hyperglycemia, ketoacidosis, and ketonuria. The main causes are lack of insulin, infection, and non-compliance with treatment. Symptoms include nausea, vomiting, abdominal pain, fruity breath odor, and altered mental status. Laboratory findings include high blood glucose, low pH, high anion gap metabolic acidosis, and ketonemia. Management involves fluid resuscitation, insulin administration, electrolyte replacement, and treating any underlying infection. Complications can include hypokalemia, thrombosis
This document provides guidelines for the first line management of adult patients with diabetic ketoacidosis (DKA). It discusses the causes and symptoms of DKA and outlines the key steps in treatment, which include fluid resuscitation, insulin therapy, monitoring of electrolytes and pH, and correcting dehydration and acidosis over 24 hours. The guidelines emphasize restoring circulating volume, reducing blood glucose, and correcting electrolyte imbalances to resolve DKA while avoiding potential complications.
Diabetic ketoacidosis (DKA) is a life-threatening complication of diabetes characterized by hyperglycemia, dehydration, and metabolic acidosis. It is diagnosed based on blood sugar over 14 mmol/L, presence of ketones, pH below 7.3, and bicarbonate below 18 mmol/L. Management involves rapid intravenous fluid resuscitation, gradual rehydration and electrolyte replacement, and insulin therapy to reverse hyperglycemia and ketosis while closely monitoring for complications. The goals are to correct estimated fluid deficits over 24 hours and lower blood glucose by 3-4 mmol/L per hour.
Diabetic ketoacidosis (DKA) is a life-threatening complication of type 1 diabetes caused by absolute insulin deficiency. It results in high blood sugar, ketone production, and severe metabolic acidosis. The document outlines the pathophysiology and clinical presentation of DKA and provides guidelines for management, including fluid resuscitation, insulin therapy, and potassium replacement to reverse the metabolic abnormalities while avoiding complications. Treatment aims to rehydrate the patient and lower blood sugar and ketone levels over 24 hours using intravenous fluids, insulin, and electrolyte supplementation.
Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are life-threatening emergencies caused by lack of insulin. DKA is characterized by ketosis and acidosis, while HHS involves extreme hyperglycemia and hyperosmolality without significant ketosis. Both require intravenous fluids and insulin to rehydrate the patient and lower blood glucose levels. Complications can include hypoglycemia, cerebral edema, electrolyte imbalances, and death if not properly treated.
Diabetes Ketoacidosis in Pediatrics discusses the diagnosis and treatment of diabetic ketoacidosis (DKA) in children. DKA results from insulin deficiency causing hyperglycemia and acidosis. Presentation may include vomiting, abdominal pain, and altered mental status. Treatment involves intravenous fluids, insulin therapy, and monitoring for complications like cerebral edema. Goals are to correct dehydration, electrolyte imbalances, and acidosis while slowly normalizing blood glucose and electrolyte levels to avoid cerebral edema, the leading cause of mortality in pediatric DKA.
- Diabetic ketoacidosis (DKA) is characterized by hyperglycemia, hyperketonemia, and metabolic acidosis due to insulin deficiency. It commonly occurs in type 1 diabetes and can be life-threatening if not treated.
- The pathophysiology involves insulin deficiency leading to hyperglycemia, lipolysis, and ketone body production. This causes dehydration, electrolyte imbalances, and metabolic acidosis. Treatment involves rapid volume expansion, insulin therapy to lower blood glucose levels slowly, and correcting electrolyte and acid-base abnormalities. Close monitoring is needed to prevent complications like cerebral edema.
- Diagnosis is based on hyperglycemia, ketonemia, and metabolic
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.
This document discusses glucose homeostasis and diabetic emergencies from an emergency perspective. It provides guidance on assessing altered mental status, including checking a blood sugar level. It describes insulin and its role in glucose metabolism. Diabetic ketoacidosis and hyperglycemic hyperosmolar state are life-threatening disorders that can result from lack of insulin or inability to use insulin properly. Proper treatment involves fluid resuscitation and insulin therapy while closely monitoring electrolytes. Hypoglycemia is also covered, noting it can result if insulin levels are too high.
Hyperglycemic crises like diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are life-threatening complications of diabetes that require prompt treatment. DKA occurs when there is uncontrolled hyperglycemia, ketosis, and acidosis due to insulin deficiency. It is more common in type 1 diabetes but can occur in type 2 diabetes during stress. HHS involves severe hyperglycemia without significant ketosis and mainly affects elderly patients with type 2 diabetes. Both conditions require fluid resuscitation, electrolyte replacement, insulin therapy, and treatment of any underlying causes to prevent complications like hypoglycemia, electrolyte imbalances, and cerebral edema.
The document provides information on the management of diabetic ketoacidosis (DKA). It discusses diagnosing DKA, including euglycemic DKA. Treatment involves three steps - correcting fluid deficits with isotonic saline, treating electrolyte abnormalities like potassium replacement, and administering insulin via continuous IV infusion. Monitoring of laboratory values is important to gauge resolution of ketoacidosis and switch to subcutaneous insulin when indicators are met. Complications can include hypoglycemia and hypokalemia.
DM medical emergencies 25-10-2023.pptxmanjujanhavi
This document discusses diabetic ketoacidosis (DKA) and its management. It notes that DKA is typically caused by insufficient insulin in type 1 diabetes patients, and can be precipitated by infection or errors in self-management. The key features of DKA include hyperglycemia, ketosis, and acidosis. Treatment aims to correct dehydration, lower blood glucose and ketone levels slowly and safely, and restore the usual insulin regimen. Fluid replacement, insulin therapy, potassium and bicarbonate management are discussed in detail. Risks like cerebral edema are also addressed. The document contrasts DKA with hyperosmolar hyperglycemic state, and provides guidelines for its specific management and monitoring.
This document discusses diabetic ketoacidosis (DKA) in children. It begins by defining DKA and noting it is the leading cause of morbidity and mortality in children with type 1 diabetes. The pathophysiology of DKA involves insulin deficiency leading to hyperglycemia and ketone production. Diagnosis criteria include hyperglycemia, dehydration, and metabolic acidosis. Management involves correcting dehydration, hyperglycemia, electrolyte imbalances, and the underlying precipitating cause, usually infection. Care must be taken to avoid rapid fluid administration and insulin doses to prevent cerebral edema, a potentially fatal complication of DKA treatment.
DKA diabetes ketoacidosis in children.pptssuser69abc5
This document provides information on diabetic ketoacidosis (DKA) in children and adolescents. It discusses the diagnosis of DKA which requires hyperglycemia, metabolic acidosis, and ketonemia. The severity of DKA is classified based on pH level. Precipitating factors include new onset type 1 diabetes, infections, and omission of insulin. Treatment involves fluid replacement, insulin therapy to lower blood glucose and correct acidosis, and correcting electrolyte imbalances. Complications can include cerebral edema, thrombosis, and hypokalemia. Careful monitoring during treatment is important to prevent complications and safely transition the patient to subcutaneous insulin.
Diabetic ketoacidosis is a medical emergency characterized by hyperglycemia, metabolic acidosis, and high levels of ketone bodies in the blood and urine. It occurs most often in patients with type 1 diabetes due to a lack of insulin but can also affect those with type 2 diabetes. Precipitating factors include infection, non-compliance with insulin therapy, and stress. Treatment involves rapid fluid resuscitation, administration of insulin, electrolyte replacement, and addressing the underlying cause. Management is conducted over three phases to stabilize the patient and transition them to subcutaneous insulin therapy. Complications can include cerebral edema, cardiac arrhythmias, hypoglycemia, and coma.
Diabetic ketoacidosis (DKA) is a state of absolute or relative insulin deficiency aggravated by ensuing hyperglycaemia, dehydration, and acidosis producing derangements in intermediary metabolism.
Diabetic ketoacidosis is a medical emergency caused by a lack of insulin and results in hyperglycemia, ketone production, and metabolic acidosis. It commonly occurs in people with type 1 diabetes but is increasingly seen in type 2 diabetes as well. Symptoms include thirst, frequent urination, nausea, vomiting, abdominal pain, and a fruity odor on the breath. Treatment involves intravenous fluids, insulin therapy, electrolyte replacement, and identifying and treating any underlying precipitating illnesses. Complications can include cerebral edema, hypoglycemia, and circulatory collapse if treatment is delayed.
A simple presentation on hypokalemia. The most common electrolyte disorder in the Critical Care practice.The presentation is based on a mortality and morbidity case report and discussion. It covers all the basic aspects of understanding the causes of hypokalemia in ICU and its management. Target audience are residents ICU and ER but all health care workers can benefit.
This document provides information on diabetic ketoacidosis (DKA) and hyperosmolar hyperglycaemic syndrome (HHS), two life-threatening emergencies that can occur in patients with diabetes. It defines DKA and HHS, describes their symptoms, causes, management including treatment goals, complications, and comparisons between the two conditions. The document emphasizes the importance of promptly diagnosing and treating these emergencies, closely monitoring patients, involving the diabetes care team, and considering all possible diagnoses including unusual presentations.
Diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS) are acute complications of diabetes that result from insufficient insulin. DKA is characterized by hyperglycemia, ketosis, and acidosis, while HHS features severe hyperglycemia without ketosis or acidosis. Both require intravenous fluid replacement and insulin therapy. Hypoglycemia is a potential complication of diabetes treatment caused by excessive insulin or insufficient food intake. It can cause neurological symptoms and be life-threatening. Careful glucose monitoring and management of medications and diet are important for preventing hypoglycemia.
This document provides an overview of stroke syndromes, including:
- Definitions of stroke and its mechanisms, and epidemiology statistics on stroke prevalence.
- Classification and descriptions of different types of ischemic and hemorrhagic stroke syndromes based on their locations and symptoms.
- Diagnostic evaluation process for acute stroke including imaging, vascular imaging, and diagnostic criteria.
- Guidelines for pre-hospital and emergency department management of acute stroke, including time goals, inclusion/exclusion criteria for thrombolysis, and scales to assess stroke severity.
This document provides an overview of upper gastrointestinal bleeding (UGIB). It begins with definitions and common presentations of UGIB. The initial approach involves rapid assessment and resuscitation of unstable patients. Diagnostic studies like endoscopy are important to identify the source of bleeding. Common causes of UGIB include peptic ulcers, esophageal/gastric varices, and angiodysplasia. Management depends on the cause and severity but typically involves hemostasis, preventing rebleeding, and treating the underlying condition.
This document provides guidelines for the first line management of adult patients with diabetic ketoacidosis (DKA). It discusses the causes and symptoms of DKA and outlines the key steps in treatment, which include fluid resuscitation, insulin therapy, monitoring of electrolytes and pH, and correcting dehydration and acidosis over 24 hours. The guidelines emphasize restoring circulating volume, reducing blood glucose, and correcting electrolyte imbalances to resolve DKA while avoiding potential complications.
Diabetic ketoacidosis (DKA) is a life-threatening complication of diabetes characterized by hyperglycemia, dehydration, and metabolic acidosis. It is diagnosed based on blood sugar over 14 mmol/L, presence of ketones, pH below 7.3, and bicarbonate below 18 mmol/L. Management involves rapid intravenous fluid resuscitation, gradual rehydration and electrolyte replacement, and insulin therapy to reverse hyperglycemia and ketosis while closely monitoring for complications. The goals are to correct estimated fluid deficits over 24 hours and lower blood glucose by 3-4 mmol/L per hour.
Diabetic ketoacidosis (DKA) is a life-threatening complication of type 1 diabetes caused by absolute insulin deficiency. It results in high blood sugar, ketone production, and severe metabolic acidosis. The document outlines the pathophysiology and clinical presentation of DKA and provides guidelines for management, including fluid resuscitation, insulin therapy, and potassium replacement to reverse the metabolic abnormalities while avoiding complications. Treatment aims to rehydrate the patient and lower blood sugar and ketone levels over 24 hours using intravenous fluids, insulin, and electrolyte supplementation.
Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are life-threatening emergencies caused by lack of insulin. DKA is characterized by ketosis and acidosis, while HHS involves extreme hyperglycemia and hyperosmolality without significant ketosis. Both require intravenous fluids and insulin to rehydrate the patient and lower blood glucose levels. Complications can include hypoglycemia, cerebral edema, electrolyte imbalances, and death if not properly treated.
Diabetes Ketoacidosis in Pediatrics discusses the diagnosis and treatment of diabetic ketoacidosis (DKA) in children. DKA results from insulin deficiency causing hyperglycemia and acidosis. Presentation may include vomiting, abdominal pain, and altered mental status. Treatment involves intravenous fluids, insulin therapy, and monitoring for complications like cerebral edema. Goals are to correct dehydration, electrolyte imbalances, and acidosis while slowly normalizing blood glucose and electrolyte levels to avoid cerebral edema, the leading cause of mortality in pediatric DKA.
- Diabetic ketoacidosis (DKA) is characterized by hyperglycemia, hyperketonemia, and metabolic acidosis due to insulin deficiency. It commonly occurs in type 1 diabetes and can be life-threatening if not treated.
- The pathophysiology involves insulin deficiency leading to hyperglycemia, lipolysis, and ketone body production. This causes dehydration, electrolyte imbalances, and metabolic acidosis. Treatment involves rapid volume expansion, insulin therapy to lower blood glucose levels slowly, and correcting electrolyte and acid-base abnormalities. Close monitoring is needed to prevent complications like cerebral edema.
- Diagnosis is based on hyperglycemia, ketonemia, and metabolic
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.
This document discusses glucose homeostasis and diabetic emergencies from an emergency perspective. It provides guidance on assessing altered mental status, including checking a blood sugar level. It describes insulin and its role in glucose metabolism. Diabetic ketoacidosis and hyperglycemic hyperosmolar state are life-threatening disorders that can result from lack of insulin or inability to use insulin properly. Proper treatment involves fluid resuscitation and insulin therapy while closely monitoring electrolytes. Hypoglycemia is also covered, noting it can result if insulin levels are too high.
Hyperglycemic crises like diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are life-threatening complications of diabetes that require prompt treatment. DKA occurs when there is uncontrolled hyperglycemia, ketosis, and acidosis due to insulin deficiency. It is more common in type 1 diabetes but can occur in type 2 diabetes during stress. HHS involves severe hyperglycemia without significant ketosis and mainly affects elderly patients with type 2 diabetes. Both conditions require fluid resuscitation, electrolyte replacement, insulin therapy, and treatment of any underlying causes to prevent complications like hypoglycemia, electrolyte imbalances, and cerebral edema.
The document provides information on the management of diabetic ketoacidosis (DKA). It discusses diagnosing DKA, including euglycemic DKA. Treatment involves three steps - correcting fluid deficits with isotonic saline, treating electrolyte abnormalities like potassium replacement, and administering insulin via continuous IV infusion. Monitoring of laboratory values is important to gauge resolution of ketoacidosis and switch to subcutaneous insulin when indicators are met. Complications can include hypoglycemia and hypokalemia.
DM medical emergencies 25-10-2023.pptxmanjujanhavi
This document discusses diabetic ketoacidosis (DKA) and its management. It notes that DKA is typically caused by insufficient insulin in type 1 diabetes patients, and can be precipitated by infection or errors in self-management. The key features of DKA include hyperglycemia, ketosis, and acidosis. Treatment aims to correct dehydration, lower blood glucose and ketone levels slowly and safely, and restore the usual insulin regimen. Fluid replacement, insulin therapy, potassium and bicarbonate management are discussed in detail. Risks like cerebral edema are also addressed. The document contrasts DKA with hyperosmolar hyperglycemic state, and provides guidelines for its specific management and monitoring.
This document discusses diabetic ketoacidosis (DKA) in children. It begins by defining DKA and noting it is the leading cause of morbidity and mortality in children with type 1 diabetes. The pathophysiology of DKA involves insulin deficiency leading to hyperglycemia and ketone production. Diagnosis criteria include hyperglycemia, dehydration, and metabolic acidosis. Management involves correcting dehydration, hyperglycemia, electrolyte imbalances, and the underlying precipitating cause, usually infection. Care must be taken to avoid rapid fluid administration and insulin doses to prevent cerebral edema, a potentially fatal complication of DKA treatment.
DKA diabetes ketoacidosis in children.pptssuser69abc5
This document provides information on diabetic ketoacidosis (DKA) in children and adolescents. It discusses the diagnosis of DKA which requires hyperglycemia, metabolic acidosis, and ketonemia. The severity of DKA is classified based on pH level. Precipitating factors include new onset type 1 diabetes, infections, and omission of insulin. Treatment involves fluid replacement, insulin therapy to lower blood glucose and correct acidosis, and correcting electrolyte imbalances. Complications can include cerebral edema, thrombosis, and hypokalemia. Careful monitoring during treatment is important to prevent complications and safely transition the patient to subcutaneous insulin.
Diabetic ketoacidosis is a medical emergency characterized by hyperglycemia, metabolic acidosis, and high levels of ketone bodies in the blood and urine. It occurs most often in patients with type 1 diabetes due to a lack of insulin but can also affect those with type 2 diabetes. Precipitating factors include infection, non-compliance with insulin therapy, and stress. Treatment involves rapid fluid resuscitation, administration of insulin, electrolyte replacement, and addressing the underlying cause. Management is conducted over three phases to stabilize the patient and transition them to subcutaneous insulin therapy. Complications can include cerebral edema, cardiac arrhythmias, hypoglycemia, and coma.
Diabetic ketoacidosis (DKA) is a state of absolute or relative insulin deficiency aggravated by ensuing hyperglycaemia, dehydration, and acidosis producing derangements in intermediary metabolism.
Diabetic ketoacidosis is a medical emergency caused by a lack of insulin and results in hyperglycemia, ketone production, and metabolic acidosis. It commonly occurs in people with type 1 diabetes but is increasingly seen in type 2 diabetes as well. Symptoms include thirst, frequent urination, nausea, vomiting, abdominal pain, and a fruity odor on the breath. Treatment involves intravenous fluids, insulin therapy, electrolyte replacement, and identifying and treating any underlying precipitating illnesses. Complications can include cerebral edema, hypoglycemia, and circulatory collapse if treatment is delayed.
A simple presentation on hypokalemia. The most common electrolyte disorder in the Critical Care practice.The presentation is based on a mortality and morbidity case report and discussion. It covers all the basic aspects of understanding the causes of hypokalemia in ICU and its management. Target audience are residents ICU and ER but all health care workers can benefit.
This document provides information on diabetic ketoacidosis (DKA) and hyperosmolar hyperglycaemic syndrome (HHS), two life-threatening emergencies that can occur in patients with diabetes. It defines DKA and HHS, describes their symptoms, causes, management including treatment goals, complications, and comparisons between the two conditions. The document emphasizes the importance of promptly diagnosing and treating these emergencies, closely monitoring patients, involving the diabetes care team, and considering all possible diagnoses including unusual presentations.
Diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS) are acute complications of diabetes that result from insufficient insulin. DKA is characterized by hyperglycemia, ketosis, and acidosis, while HHS features severe hyperglycemia without ketosis or acidosis. Both require intravenous fluid replacement and insulin therapy. Hypoglycemia is a potential complication of diabetes treatment caused by excessive insulin or insufficient food intake. It can cause neurological symptoms and be life-threatening. Careful glucose monitoring and management of medications and diet are important for preventing hypoglycemia.
This document provides an overview of stroke syndromes, including:
- Definitions of stroke and its mechanisms, and epidemiology statistics on stroke prevalence.
- Classification and descriptions of different types of ischemic and hemorrhagic stroke syndromes based on their locations and symptoms.
- Diagnostic evaluation process for acute stroke including imaging, vascular imaging, and diagnostic criteria.
- Guidelines for pre-hospital and emergency department management of acute stroke, including time goals, inclusion/exclusion criteria for thrombolysis, and scales to assess stroke severity.
This document provides an overview of upper gastrointestinal bleeding (UGIB). It begins with definitions and common presentations of UGIB. The initial approach involves rapid assessment and resuscitation of unstable patients. Diagnostic studies like endoscopy are important to identify the source of bleeding. Common causes of UGIB include peptic ulcers, esophageal/gastric varices, and angiodysplasia. Management depends on the cause and severity but typically involves hemostasis, preventing rebleeding, and treating the underlying condition.
- Dr. Tamagnsew presented a seminar on the management of digitalis toxicity. The presentation covered the mechanism of action, pharmacokinetics, signs and symptoms, and management of digitalis toxicity.
- Digitalis toxicity can cause a variety of cardiac arrhythmias and other symptoms. Diagnosis involves physical exam, ECG, lab tests including serum digoxin level.
- Treatment focuses on preventing further absorption, enhancing elimination, and administering digoxin antibody fragments (digibind) based on ingested dose or serum level to neutralize digoxin effects for life-threatening arrhythmias or end-organ toxicity.
This document summarizes a seminar on discontinuing mechanical ventilation. It discusses weaning parameters like the ratio of respiratory rate to tidal volume. Common weaning methods include spontaneous breathing trials, gradually reducing support on modes like SIMV and PSV. Prerequisites for extubation include ensuring airway protection and patency. Factors that can lead to weaning or extubation failure are also reviewed. The objective is for residents to understand weaning and extubation processes and techniques.
Oxygen therapy is the administration of oxygen to treat hypoxemia. It has been used in modern medicine for almost 100 years and is a cost-effective way to reduce mortality from several illnesses. Hypoxemia can be detected clinically, through pulse oximetry, or blood gas analysis. Oxygen is administered through various devices like nasal cannulas, face masks, bag valve masks, CPAP, or intubation and mechanical ventilation depending on the severity of hypoxemia. Proper administration and monitoring of oxygen therapy is important.
A 74-year-old woman presented to the emergency department with fever, flank pain, dysuria, and altered mental status for 3 days. Her vital signs and physical exam were notable for a temperature of 38.1°C, heart rate of 120, blood pressure of 120/70, tenderness on exam of the costovertebral angle, and a Glasgow Coma Scale of 14/15. Laboratory tests showed a white blood cell count of 8,000 with 65% neutrophils and leukocytes and bacteria found on urinalysis. The document defines sepsis and septic shock, reviews screening tools like SIRS, qSOFA, NEWS, and lactate levels. It also outlines the management of sepsis,
1) This document discusses acute pain management and provides guidelines for assessment and treatment.
2) Proper pain assessment involves using scales like numerical rating, visual analog, or FLACC for pediatrics to determine severity and guide treatment. Factors like location, intensity, and aggravating factors should be considered.
3) Treatment follows a tiered approach based on pain severity and can include non-pharmacological methods as well as pharmacological options like paracetamol, NSAIDs, opioids, and ketamine. Proper pain management in the ED is important to prevent chronic pain.
This document discusses bradyarrhythmias, which are heart rhythms that are slower than normal. It defines key measurements in electrocardiograms including the P wave, PR interval, QRS complex, and QT interval. Common types of bradyarrhythmias include sinus bradycardia, junctional rhythm, and atrioventricular blocks. Treatment depends on whether the patient is stable or unstable and may involve medications to increase heart rate like atropine or transcutaneous pacing. The document provides details on evaluating and treating different types of bradycardic rhythms and their underlying causes.
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
Clinic ^%[+27633867063*Abortion Pills For Sale In Tembisa Central19various
Clinic ^%[+27633867063*Abortion Pills For Sale In Tembisa Central Clinic ^%[+27633867063*Abortion Pills For Sale In Tembisa CentralClinic ^%[+27633867063*Abortion Pills For Sale In Tembisa CentralClinic ^%[+27633867063*Abortion Pills For Sale In Tembisa CentralClinic ^%[+27633867063*Abortion Pills For Sale In Tembisa Central
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
2. OUT LINE
• Objectives
• Diabetic Ketoacidosis
• Epidemiology
• Pathophysiology
• Clinical features
• Diagnostic testing
• Management
• Complications
• Disposition and follow-up
• Ketoacidotic syndromes
8/30/2022 Kibrom Tsegay, EMCC R1 2
3. Objectives
• Understanding the definition and pathophysiology of
DKA and other ketoacidotic syndromes
• Understanding Clinical features and Diagnostic testing in
DKA
• Understand Management of DKA and its complications
• Understanding the disposition and follow-up of DKA
patient
• Understanding Ketoacidotic syndromes and their
management
8/30/2022 Kibrom Tsegay, EMCC R1 3
4. Diabetic Ketoacidosis
• Acute, life-threatening complication of
diabetes mellitus.
• Characterized by hyperglycemia, ketoacidosis
and ketonuria
8/30/2022 Kibrom Tsegay, EMCC R1 4
5. Epidemiology
• Predominant in type 1 diabetes mellitus
• Increasing in non insulin dependent diabetics
• Incidence of ~ 10,000 cases/year in US
• Mortality decreased to <1% (prior to insulin
was 100%)
• Mortality is up to 5%, in patients with
significant comorbidity & advanced age
8/30/2022 Kibrom Tsegay, EMCC R1 5
9. Pathophysiology …
–Lipolysis
• Serum FFA
– Acetone, hydroxybutyrate,acetoacetic
acid
–Increased ketone production with
decreased ketone use leads to
ketoacidosis
–Vomiting ,anion gap metabolic
acidosis
8/30/2022 Kibrom Tsegay, EMCC R1 9
10. • Dehydration and electrolyte loss
–Increased glucose load in kidney leads
to increased glucose in urine and
osmotic diuresis
• Osmotic diuresis + poor intake and vomiting,
produces profound dehydration and
electrolyte imbalance
• Volume depletion leads to impaired GFR
• RAAS activation
8/30/2022 Kibrom Tsegay, EMCC R1 10
11. Causes
• An acute insult leads to decompensation of a
chronic disease
• Inadequate insulin therapy and infection are
the most common precipitants
• New onset diabetes (particularly in children)
• Myocardial ischemia or infarction
• Alcohol or drug related problem
8/30/2022 Kibrom Tsegay, EMCC R1 11
12. CLINICAL FEATURES
• Clinical manifestations of DKA are related
directly to hyperglycemia, volume depletion,
and acidosis.
• Polyuria and polydipsia are usually the only
symptoms until ketonemia and acidosis
develop
8/30/2022 Kibrom Tsegay, EMCC R1 12
15. Diagnosis
• Traditionally, DKA is divided into mild,
moderate, and severe states based on total-
body deficits of water and electrolytes.
8/30/2022 Kibrom Tsegay, EMCC R1 15
16. Diagnosis….
• Definitive diagnosis is established by
laboratory criteria (hyperglycemia, ketosis and
acidosis
• Blood glucose level >250 milligrams/dL
• Anion gap >10 to 12 mEq/L
• Bicarbonate level <15 mEq/L and a pH <7.3
with moderate ketonuria or ketonemia
• Urine ketone >=+2
8/30/2022 Kibrom Tsegay, EMCC R1 16
17. • EUGLYCEMIC DKA
– glucose <250mg/dl
• Patients presenting shortly after receiving insulin
• Type1diabetics who are young and vomiting
• Patients with impaired gluconeogenesis (alcohol abuse
or liver failure)
• Low caloric intake/starvation
• Pregnancy
• SGLT2inhibitors
8/30/2022 Kibrom Tsegay, EMCC R1 17
18. Diagnostic Testing
• Essential Diagnostic Tests
– Serum glucose
• Typically > 250 mg/dL
• Euglycemic DKA (< 250 mg/dL)
– Blood gas
• Patients will exhibit an anion gap metabolic
• Electrolytes: hypo/hyper/normokalemia,hyponatremia
• Arterial or venous blood gas can be used
8/30/2022 Kibrom Tsegay, EMCC R1 18
19. – Urinalysis
• Glucosuria
• Ketonuria
– Electrocardiogram (EKG)
• Typically will exhibit non-specific changes including
sinus tachycardia
• Can see changes associated with hyperkalemia or
hypokalemia
8/30/2022 Kibrom Tsegay, EMCC R1 19
20. Diagnostic Testing…cont.
• Serum potassium
– Patients with DKA are total body K+ depleted
• Osmotic diuresis + vomiting lead to potassium loss
• Often depleted by 100’s of mEq
– Initial serum K+ can be elevated, normal or low
• Potassium elevation 2ry to acidemia + hyperglycemia
• 4-6% of patients will present with hypokalemia
• Serum K+ correction: subtract 0.6 mEq/L from the
laboratory K+ value for every 0.1 decrease in pH
8/30/2022 Kibrom Tsegay, EMCC R1 20
21. • Sodium and Other Electrolytes
– Osmotic diuresis leads -> excessive renal losses of
NaCl
– Hyperglycemia artificially lowers serum sodium l
– Correction factor: Add 1.6 mEq Na for every 100
mg/dL the glucose is >100mg/dl
– Osmotic diuresis -> urinary losses and total-body
depletion of phosphorous, calcium, and magnesium
– Hemoconcentration ->
8/30/2022 Kibrom Tsegay, EMCC R1 21
22. ?
• If the potassium is reported as 5 mEq/L and
the pH is 6.94, the corrected potassium value
would be ?
• IF RBS is 400mg/dl , and measured Na is 130
what is the corrected Na measurenment?
8/30/2022 Kibrom Tsegay, EMCC R1 22
23. Diagnostic Testing…cont.
• BUN/Cr
– Patients will often exhibit prerenal acute kidney
injury
– BUN/Cr ratio will be elevated reflecting
intravascular volume depletion
• Serum ketones are typically unnecessary in the
Emergency Department
• Blood cultures and other laboratory tests should be
done as clinically indicated
8/30/2022 Kibrom Tsegay, EMCC R1 23
24. Management
• Basics:
• ABCs, IV, Cardiac Monitor and 12-lead EKG
• Establish at least 2 peripheral IVs as patients typically
require multiple medication and infusions
• Diagnosis should be suspected at triage
• Begin aggressive fluid therapy before receiving
laboratory results
• Diligently search for the underlying cause
8/30/2022 Kibrom Tsegay, EMCC R1 24
25. Management…
• The goals of therapy are
– volume repletion
– reversal of the metabolic consequences of insulin
insufficiency
– correction of electrolyte and acid-base imbalances
– recognition and treatment of precipitating causes
– avoidance of complications
8/30/2022 Kibrom Tsegay, EMCC R1 25
26. Management…
• VOLUME REPLETION
– Role
• Replenish intravascular depletion resulting from
osmotic diuresis
• Correct decreased GFR
• The average adult patient has a water deficit of 100
mL/ kg (5 to 10 L)
• sodium deficit of 7 to 10 mEq/kg
•
8/30/2022 Kibrom Tsegay, EMCC R1 26
27. Management…
• VOLUME REPLETION
– ADA: 1000-1500 mL of 0.9% NS during the first hour
– After the 1st hr: maintain between 250 and 500mL/h
• Adjust to hemodynamic and electrolyte status
• ADA:Patients with eu or hypernatremia
0.45%NS
• UK: 9% NS continued throughout the
management
– Blood glucose <250 mg/dL -> add 5% dextrose
– Patient in hypovolemic shock ?
8/30/2022 Kibrom Tsegay, EMCC R1 27
28. Management…
• 9% NaCl (Normal Saline)
• Large volume infusions can cause hyperchloremic
metabolic acidosis (unclear impact on patient)
• In profoundly acidemic patients, avoidance of NS may be
beneficial
• Lactated Ringers
– Closer to physiologic solution
– Does not cause hyperchloremic metabolic acidosis
– Other options: balanced solutions (i.e. Plasma-Lyte)
8/30/2022 Kibrom Tsegay, EMCC R1 28
29. Management…
• Electrolyte Disorder Correction
–Potassium – most important lab value in DKA
–Aggressive repletion frequently necessary
–Patients often 100s of mEq depleted
–DKA treatments (i.e. fluids, insulin) will
decrease serum potassium level
–Insulin infusion shifts potassium intracellularly
8/30/2022 Kibrom Tsegay, EMCC R1 29
30. Management…
• •
POTASSIUM REPLACEMENT
– Replace after adequate renal function (urine
output) is assessed
– K+ >5.2 initiate regular insulin & check K+ in 2 hrs
– K+ >3.3 <5.2 add 20-30 meq of K+ to each L of
fluid and continue insulin drip
– K+ <3.3 hold insulin drip and give K+ @20-30
meq/hr until K+ is >3.3 then initiate insulin drip
8/30/2022 Kibrom Tsegay, EMCC R1 30
31. Management…
• Bicarbonate for acidosis
– Hypothetically prevent cardiorespiratory compromise
– Potential deleterious effects
• Worsening hypokalemia and intracellular acidosis
• Inhibition of RBC oxygen release at tissue level
• Delay in improvement of ketosis
– If pH <6.9 give 100 mmol NaHCO3 in 400ml of water with
20 meq KCL at 200 ml/hr
– Repeat q 2 hours until pH >7 + Check K+ q 2 hrs
8/30/2022 Kibrom Tsegay, EMCC R1 31
32. Management…
• Sodium
– Typically dilutional hyponatremia
– Will correct without specific treatment
• Magnesium
– Hypokalemia = Hypomagnesaemia
• Both electrolytes lost during osmotic diuresis
• Cannot replete intracellular K+ without Mg
• Serum Mg level may not correlate with total body stores
• Add 0.35 mEq/kg of Mg in the fluids of the first 3 to 4 hrs
8/30/2022 Kibrom Tsegay, EMCC R1 32
33. Management…
• Insulin therapy
–Ultimately, patients will require insulin
repletion in order to reverse pathophysiology
in DKA and stop ketosis
–Don’t give insulin if K+ is <3.3, replace K+ and
fluid deficit first
8/30/2022 Kibrom Tsegay, EMCC R1 33
34. Management…
• Dose
– Continuous Regular infusion 0.14 units/kg
– Bolus 0.1units/kg then 0.1/kg/hr continuous infusion
– If serum glucose doesn’t fall by 50-70mg/dl in the first
hour double rate of infusion
– When serum glucose reaches 200 mg/dl decrease
infusion rate by 0.02-0.05 units/kg/hr
– Continue insulin infusion until ketoacidosis is resolved,
blood glucose <200, subcutaneous insulin is begun
8/30/2022 Kibrom Tsegay, EMCC R1 34
35. Management…
• Transition from IV Insulin After DKA Correction
– It is important to overlap the IV and SC insulin for
2 to 4 hours to avoid potential relapse to
hyperglycemia or DKA
– New-onset diabetics can be started on a total daily
dose of 0.5 to 0.8 unit/kg/dL,
– previously treated diabetic patients can be
restarted on their previous insulin dosage.
8/30/2022 Kibrom Tsegay, EMCC R1 35
36. Continued Management
• Continuous Monitoring
– Vital Signs
– Urine output
– Serum glucose, K+, Cl–, HCO3
–, pH q1 hour until
stable
• Insulin Infusion
– Continue until anion gap normalizes
– When serum glucose < 250 mg/dL add
D5W/0.45%NS solution to avoid hypoglycemia
8/30/2022 Kibrom Tsegay, EMCC R1 36
38. Complications…
• COMPLICATIONS RELATED TO THERAPY
– Hypokalemia from inadequate K+ replacement
– Hypoglycemia
– Alkalosis from overaggressive bicarbonate
replacement
– pulmonary edema from overaggressive hydration
– Cerebral edema
8/30/2022 Kibrom Tsegay, EMCC R1 38
39. Complications…
• Cerebral Edema
• Excess accumulation of intracellular and extracellular
fluid in the brain
• Rare (< 1%) complication but high mortality (> 30%)
• More common in patients with newly diagnosed
diabetes presenting with DKA
• Cause: it is unclear what causes patients to develop
cerebral edema
• usually develops within 4 to 12 hours but can present
up to 24 to 48 hours after starting treatment
8/30/2022 Kibrom Tsegay, EMCC R1 39
40. Complications…
• Signs + Symptoms
– potential neurologic deterioration
• New onset or intensifying headache
• Decline in level of consciousness, Lethargy
• Focal neurologic deficits (CN III, IV or VI palsy common)
– recurrent vomiting, incontinence, irritability,
– abnormal respirations,
– delayed rise in serum sodium with treatment,
8/30/2022 Kibrom Tsegay, EMCC R1 40
41. Complications…
• Management
– Prompt administration of mannitol help to abort
further neurologic deterioration
– Elevate head of bed to 30 degrees
– Decrease IV fluid infusion
– Mannitol: 1 gm/kg over 20 minutes
– 3% Hypertonic saline: 5-10 ml/kg
8/30/2022 Kibrom Tsegay, EMCC R1 41
42. Complications…
• Best Practice to Prevent Cerebral Edema
– Slow reduction of osmolality during treatment
– Avoid large volumes of hypotonic fluid
– Drop blood glucose slowly during treatment
– Do not allow plasma Na+ to fall during treatment
– Avoid unnecessary bicarbonate during treatment
– Avoid hypoxia, hypo-K+,PO4, Mg
8/30/2022 Kibrom Tsegay, EMCC R1 42
43. Complications…
• LATER COMPLICATIONS
– Metabolic acidosis refractory to routine therapy
• Unrecognized infection (lactic acidosis)
• Rarely insulin antibodies
• Improper preparation or administration of the insulin
drip
– Shock that is unresponsive to aggressive fluid
therapy
– Hyperchloremic non–anion gap metabolic acidosis
8/30/2022 Kibrom Tsegay, EMCC R1 43
44. Complications…
• Late vascular thrombosis
– Cerebral vessels appear to be most susceptible
– Volume depletion, low CO, increased blood
viscosity, and underlying atherosclerosis may
predispose the elderly to this complication
– Thrombosis may occur
• Several hrs or days after institution of therapy
• After resolution of ketoacidosis
– No studies support prophylactic anticoagulant use
8/30/2022 Kibrom Tsegay, EMCC R1 44
45. DISPOSITION AND FOLLOW-UP
• Experienced nursing staff trained in
monitoring and management of DKA
• Written guidelines for DKA management
• Access to a laboratory
• presenting early in the course of their illness
who can tolerate oral liquids may be managed
safely in the ED or observation unit and
discharged after 6 to 12 hours of therapy
8/30/2022 Kibrom Tsegay, EMCC R1 45
47. SPECIAL POPULATIONS
• RECURRENT DKA PATIENTS
• PATIENTS WITH INSULIN PUMPS
• DKA IN PREGNANCY
8/30/2022 Kibrom Tsegay, EMCC R1 47
48. • DKA IN PREGNANCY
– fetal mortality rate of approximately 30%
– Lower maternal fasting glucose relative insulin
deficiency
– increased levels of counter regulatory hormones
– vomiting and urinary tract infections are increased
– Maternal hyperglycemia, acidosis, hypokalemia
also happen in the fetus
8/30/2022 Kibrom Tsegay, EMCC R1 48
49. Ketoacidotic Syndromes
• Several conditions result in excessive
production of ketoacids
• The challenge is to differentiate excessive,
uncontrolled ketoacidosis from
• Physiologic ketonemia
• States where excessive ketones may be
produced
• Toxin altering normal metabolism
8/30/2022 Kibrom Tsegay, EMCC R1 49
51. PATHOPHYSIOLOGY
• Ketones are produced through metabolism of
long-chain fatty acids
• Serum ketones are also used as an energy
source for the brain
• The normal blood ketone level is about 1
milligram/dL
8/30/2022 Kibrom Tsegay, EMCC R1 51
52. PATHOPHYSIOLOGY
• Ketone production is typically tightly regulated
– prevent excessive ketoacid production and
metabolic acidosis
– Ketones are metabolized as rapidly as they are
formed
• low levels of insulin are not found in
ketoacidotic syndromes except DKA
8/30/2022 Kibrom Tsegay, EMCC R1 52
53. PATHOPHYSIOLOGY
• Pathologic states arise when production
exceeds metabolism or consumption, resulting
in metabolic acidosis.
• Acetyl coenzyme A, an energy source that can
enter the citric acid cycle for metabolism, is
produced in the liver and then converted to
the ketones β-hydroxybutyrate and
acetoacetate.
8/30/2022 Kibrom Tsegay, EMCC R1 53
54. COMMON KETOACIDOTIC
SYNDROMES
• •
ALCOHOLIC KETOACIDOSIS
– Occur in alcoholic patients who enter a period of
fasting after a dramatic period of ethanol binging
– results in metabolic acidosis and dehydration,
with variable levels of serum glucose
– Nausea, vomiting, abdominal pain
– Elevated ratio of β-hydroxybutyrate to
acetoacetate(10:1)
8/30/2022 Kibrom Tsegay, EMCC R1 54
55. • •
STARVATION KETOSIS
– During periods of fasting (overnight) or increased
energy demands (exercise), local ketone
production increases
– As the duration of carbohydrate fasting increases
• hepatic ketone production and Intracerebral ketone
utilization increase
8/30/2022 Kibrom Tsegay, EMCC R1 55
56. • STARVATION KETOSIS
– Fasts of 14 days are well tolerated in those with
• Adequate endogenous insulin and no other
• No coexisting condition that alters the serum
hormonal milieu
– Pregnancy induced 24 to 48 hours of vomiting
and inadequate oral intake can lead to
• ketone production with metabolic acidosis, ketonuria,
and dehydration
8/30/2022 Kibrom Tsegay, EMCC R1 56
57. • NUTRITIONAL KETOSIS
– athletic performance enhancement
• KETOGENIC DIET
– weight control and seizures
• TOXIC INGESTIONS
– primary result of the toxin
– acetone, aspirin, isoniazid, isopropanol ,methanol,
and propylene glycol
• INBORN ERRORS OF METABOLISM
8/30/2022 Kibrom Tsegay, EMCC R1 57
58. TREATMENT
• Treatment of ketoacidosis is supportive
• Reestablish intravascular volume
• Monitor and correct electrolyte abnormalities
• Administer supplemental dextrose
• Acidosis should clear within 12 to 24 hours
8/30/2022 Kibrom Tsegay, EMCC R1 58
59. DISPOSITION AND FOLLOW-UP
• Adults with an uncomplicated ED course can
be discharged home
– resolution of acidosis
– the patient is able to tolerate oral fluids
• When caring for complicated conditions
coordinate care with the primary team
treating the underlying disorder
8/30/2022 Kibrom Tsegay, EMCC R1 59
60. Reference
• ROSEN’S EMERGENCY MEDICINE:CONCEPTS
AND CLINICAL PRACTICE, 8th edition
• Tintinalli’s Emergency Medicine A
Comprehensive Study Guide, 9th edition
• Uptodate
• DKA protocol for Emergency and critical unit
of Tikur Anbessa Specialized Hospital
• ADA/UK guidelines
8/30/2022 Kibrom Tsegay, EMCC R1 60