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Diabetic Ketoacidosis - Coggle Diagram
Diabetic Ketoacidosis
Precipitating Factors
Omission or reduced daily insulin injections
Dislodgement or occlusion of insulin pump catheter
Infection
Pregnancy
Myocardial infarction
Cerebrovascular accident
Gastrointestinal hemorrhage
Pancreatitis
Pulmonary embolism
Major trauma
Surgery
Heat-related illness
Endocrinopathies
Hyperthyroidism
Pheochromocytoma
Cushing syndrome
Substance abuse
Cocaine
Medications
Steroids
Thiazides
Antipsychotics
Sympathomimetics
SGLT-2 inhibitors
Social and psychiatric factors
Poor economic background
Lack of insurance
Depression
Eating disorders
Emergency Department Management
Therapeutic Priorities
First priority is fluid volume resuscitation
Second priority is potassium replacement
Third priority is insulin therapy
Volume Repletion
Average deficits
Water deficit 100 mL per kg totaling 5 to 10 L
Sodium deficit 7 to 10 mEq per kg
Initial fluid choice
Normal saline or balanced crystalloid solution
Rate of 15 to 20 mL per kg per hour in first hour
Subsequent fluid therapy
Give 0.45% normal saline at 250 to 500 mL per hour if eunatremic or hypernatremic
Continue normal saline at 250 to 500 mL per hour if hyponatremic
Schedule replaces 50% deficit over first 12 hours and rest over next 12 hours
Transition at glucose 250 mg per dL
Add 5% dextrose in 0.45% normal saline
Prevents rapid decline in osmolality and hypoglycemia
Potassium Management
Total body deficit is 3 to 5 mEq per kg
Correction prediction
Serum potassium changes 0.5 mEq per L per 0.1 change in pH
Potassium level less than 3.3 mEq per L
Hold insulin therapy immediately
Administer IV potassium 20 to 30 mEq per hour
Resume insulin once potassium exceeds 3.3 to 3.5 mEq per L
Potassium level 3.3 to 5.2 mEq per L
Add 20 to 30 mEq potassium per liter of IV fluid
Maintain serum potassium between 4 and 5 mEq per L
Confirm urine output before initiation
Potassium level greater than 5.2 mEq per L
Withhold potassium replacement
Recheck serum potassium every 2 hours
Infusion safety limits
Maximum 10 mEq per hour via peripheral IV
Maximum 20 mEq per hour via central line
Total first 24 hours requirement usually 100 to 200 mEq
Insulin Therapy
IV Regular Insulin
Exposition with 0.14 unit per kg per hour continuous IV infusion without bolus
Alternative is 0.1 unit per kg bolus followed by 0.1 unit per kg per hour
IV bolus is not recommended in children and optional in adults
Target glucose drop rate
Expected decline 50 to 75 mg per dL per hour
If decline less than 10% in first hour give 0.14 unit per kg bolus
Dosing adjustment
When glucose reaches 200 to 250 mg per dL decrease drip to 0.02 to 0.05 unit per kg per hour
Maintain blood glucose between 150 and 200 mg per dL
Criteria for DKA resolution
Blood glucose less than 200 mg per dL
Serum bicarbonate greater than or equal to 18 mEq per L
Venous pH greater than 7.3
Calculated anion gap normal
Subcutaneous Insulin Regimen
Mild to moderate uncomplicated DKA alternative
Lispro 0.3 unit per kg initial then 0.1 unit per kg every hour
Or Lispro 0.3 unit per kg initial then 0.2 unit per kg every 2 hours
Transition to Subcutaneous Insulin
Patient must be able to eat
Overlap IV infusion and SC insulin for 2 to 4 hours
New-onset diabetics dose 0.5 to 0.8 unit per kg per day
Long-acting basal insulin given 2 hours before stopping IV drip
Bicarbonate Administration
pH greater than or equal to 6.9
Bicarbonate administration is not indicated
pH less than 6.9
Sodium bicarbonate 100 mmol in 400 mL water with 20 mEq KCl
Infuse at 200 mL per hour over 2 hours until venous pH exceeds 7.0
Recheck potassium every 2 hours
Risks of bicarbonate
Paradoxical CNS acidosis
Hypokalemia
Impaired oxygen unloading via shift of oxygen dissociation curve
Delayed ketosis resolution
Potential worsening of cerebral edema
Phosphate Replacement
No routine role for IV phosphate in ED
Indications strictly reserved for severe hypophosphatemia less than 1.0 mg per dL
Replacement dose potassium phosphate 2.5 to 5 mg per kg IV
Risks include hypocalcemia and metastatic tissue calcification
Magnesium Replacement
Indications for serum magnesium less than 2.0 mEq per L
Dose magnesium sulfate 2 grams IV over 1 hour
Clinical Features
Evolution typically within 24 hours
Early symptoms
Polyuria
Polydipsia
Dehydration and hemodynamic signs
Tachycardia
Orthostasis or hypotension
Poor skin turgor
Dry mucous membranes
Hypothermia from peripheral vasodilation
Respiratory signs
Kussmaul respirations with increased rate and depth
Fruity breath odor from acetone
Gastrointestinal manifestations
Nausea and vomiting
Abdominal pain correlating with severity of acidosis
Attributed to gastric dilatation ileus or prostaglandin release
Mental status changes
Correlates closely with serum osmolality greater than 320 mOsm per L
Ranges from alert to drowsiness stupor or coma
Differential Diagnosis
Hyperosmolar Hyperglycemic State
Prominent mental status change
Blood glucose usually greater than 600 mg per dL
Absent or minimal anion gap acidosis
Alcoholic Ketoacidosis
Beta-hydroxybutyrate to acetoacetate ratio up to 10 to 1
Urine ketone may be trace or negative
Blood glucose normal or low
Starvation Ketoacidosis
Mild ketosis with bicarbonate greater than 18 mEq per L
Renal failure
Lactic acidosis
Metformin-associated type B lactic acidosis
Toxic ingestions
Salicylates
Methanol
Ethylene glycol
Acetaminophen
Epidemiology
Predominantly in Type 1 Diabetes Mellitus
Annual incidence in developed countries 13.4 to 14.9 per 1000 type 1 diabetics
Increasing incidence in newly diagnosed Type 2 Diabetes Mellitus
Especially in African Americans and Hispanics
Ketosis-prone type 2 diabetics recover insulin secretion after DKA resolution
Mortality rate less than 1% in experienced centers
Higher mortality in developing countries elderly and patients with comorbidities
Diagnosis and Laboratory Evaluation
Diagnostic Criteria
Blood glucose greater than 250 mg per dL
Anion gap greater than 10 to 12 mEq per L
Serum bicarbonate less than 15 mEq per L
Venous or arterial pH less than 7.3
Moderate ketonuria or ketonemia
Severity Classification
Mild DKA
Arterial pH 7.25 to 7.30
Serum bicarbonate 15 to 18 mEq per L
Anion gap greater than 10 mEq per L
Mental status alert
Moderate DKA
Arterial pH 7.00 to 7.24
Serum bicarbonate 10 to 15 mEq per L
Anion gap greater than 12 mEq per L
Mental status alert to drowsy
Severe DKA
Arterial pH less than 7.00
Serum bicarbonate less than 10 mEq per L
Anion gap greater than 12 mEq per L
Mental status stupor to coma
Euglycemic DKA
Blood glucose less than 250 mg per dL
Risk factors and conditions
SGLT-2 inhibitor therapy
Pregnancy
Young type 1 diabetics with vomiting
Impaired gluconeogenesis in alcohol abuse or liver failure
Starvation or low caloric intake
Patients presenting shortly after insulin administration
Key diagnostic test
Serum quantitative beta-hydroxybutyrate greater than 3 mEq per L
Laboratory Evaluation Nuances
Ketone detection
Nitroprusside reaction detects acetoacetate but not beta-hydroxybutyrate
Acetoacetate converts to beta-hydroxybutyrate in high NADH states
False positive urine ketone from sulfhydryl drugs like captopril
Serum beta-hydroxybutyrate is the preferred quantitative test
Acid-base assessment
Venous pH is approximately 0.03 lower than arterial pH
Venous blood gas replaces arterial blood gas routinely
PCO2 lower than expected indicates coexisting primary respiratory alkalosis
Sodium correction
Standard formula adds 1.6 mEq per L per 100 mg per dL glucose above 100
Factor 2.4 preferred especially when blood glucose exceeds 400 mg per dL
Creatinine
Factitious elevation due to acetoacetate interference with assay
Leukocyte count
Stress leukocytosis is common
WBC greater than 25000 or band count greater than 10000 suggests infection
Pathophysiology
Core mechanism
Relative insulin deficiency
Counterregulatory hormone excess
Glucagon as primary counterregulatory hormone
Catecholamines
Cortisol
Growth hormone
Response to cellular starvation
Insulin physiological actions
Liver
Facilitates glucose uptake and conversion to glycogen
Inhibits glycogenolysis
Suppresses gluconeogenesis
Increases lipogenesis
Adipose tissue
Forms triglycerides from free fatty acids and glycerol
Inhibits breakdown of triglycerides
Skeletal muscle
Stimulates amino acid uptake and muscle protein synthesis
Inhibits release of amino acids from muscle and liver
Metabolic cascade
Hyperglycemia from excess production and underutilization
Glucosuria when exceeding glomerular maximal threshold
Osmotic diuresis causing marked water and electrolyte loss
Prerenal azotemia and dehydration
Renin-angiotensin-aldosterone system activation
Exacerbates renal potassium loss
Ketoacidosis pathogenesis
Lipolysis delivers free fatty acids bound to albumin to liver
Hepatic mitochondrial beta-oxidation generates ketone bodies
Ketone body equilibrium
Acetoacetic acid and beta-hydroxybutyrate
Acetoacetic acid metabolizes to acetone
Depletion of hepatic glycogen favors ketogenesis
Decreased peripheral utilization of ketones
Acid-base derangements
High anion gap metabolic acidosis from ketoacids
Hyperchloremic acidosis from ketoanion excretion exchanging for chloride
Paradoxical vasodilation from prostaglandin I2 and E2 release
Special Clinical Populations
Recurrent DKA
Address insulin noncompliance
Screen for cocaine and substance abuse
Involve social services and diabetes education teams
Patients with Insulin Pumps
Immediately disconnect and turn off insulin pump
Treat with standard IV fluid and insulin infusion protocols
Pregnancy
Fetal mortality reaches approximately 30%
Triggered at lower blood glucose levels
Baseline lower fasting glucose and higher counterregulatory hormones
Compensated chronic respiratory alkalosis reduces bicarbonate buffer capacity
Maternal acidosis leads to decreased uterine perfusion and fetal hypoxemia
Priority is rapid maternal resuscitation and electrolyte normalization
Complications
Therapy-related Complications
Hypoglycemia
Severe hypokalemia
Hypophosphatemia
Acute respiratory distress syndrome
Cerebral Edema
Most common cause of mortality in children and adolescents
Typically develops within 4 to 12 hours of therapy
Warning signs
Severe headache
Lethargy or mental status change
Incontinence
Bradycardia
Pupillary changes
Seizures
Immediate treatment
IV Mannitol 1 to 2 grams per kg
Alternative is 3% hypertonic saline 5 to 10 mL per kg over 30 minutes
Fluid restriction and intubation
Avoid glucocorticoids
Prevention strategy
Slow reduction of osmolality
Gradual glucose reduction
Avoid excessive hypotonic fluids
Maintain serum sodium
Later Disease Complications
Non-anion gap hyperchloremic metabolic acidosis
Vascular thrombosis in cerebral or muscular arteries
Refractory acidosis from occult sepsis
Mucormycosis