Flashcards in Case 16 Deck (71):
What are key findings from the history of a child with DKA?
History of vomiting, polydipsia, altered mental status, abdominal pain.
What are key findings from the physical exam of a child with DKA?
Afebrile, Dehydration (tachycardic, dry oral mucosa, sunken eyes, skin tenting), Tachypneic
What is on the differential diagnosis for DKA?
Appendicitis, Increased ICP, Toxic ingestion, DKA, GI obstruction, Gastroenteritis, Pyelonephritis, Bacterial pneumonia
What are key findings from testing with DKA?
Hyperglycemia and Metabolic acidosis.
Glasgow coma scale (GCS):
-The most commonly accepted method for assessing patients with an altered level of consciousness
-The scale is used to assign a score in three categories (Best Eye Response, Best Verbal Response, and Best Motor Response)
-The three scores are added to result in a total score, with the highest possible score of 15.
-Patients with GCS of less than or equal to 8 may require aggressive intervention and management.
What is the eye-opening response scale of the GCS?
6 - N/A
5 - N/A
4 - Eyes open spontaneously
3 - Eyes open to verbal command
2 - Eyes open to pain
1 - No eye opening
What is the Verbal response scale of the GCS?
6 - N/A
5 - Oriented
4 - Confused, but able to answer questions
3 - Inappropriate words
2 - Incomprehensible sounds
1 - No verbal response
What is the Motor response scale or the GCS?
6 - Obeys commands
5 - Localizes pain
4 - Withdraws from pain
3 - Abnormal flexion, decorticate posture
2 - Extensor response, decerebrate posture
1 - No motor response, flaccid
What is the adjusted verbal response criteria for children under the age of five years?
5 - Smiles, oriented to sounds, follows objects, interacts
4 - Cries but consolable; inappropriate interactions
3 - Inconsistently inconsolable, moaning
2 - Inconsolable, agitated
1 - No verbal response
Type 1 diabetes:
Formerly called juvenile-onset or insulin dependent diabetes (IDDM).
Epidemiology of Type 1 diabetes:
Accounts for 5-10 percent of all people with diabetes.
What is the etiology of type 1 DM?
Either complete lack of, or too little, insulin. Thought to be caused by immune system-induced destruction of beta cells of the pancreas.
What is the presentation of type 1 DM?
Symptoms usually start in childhood or young adulthood. At presentation, patients are often seriously ill from sudden symptoms of high blood sugar at presentation.
What is the epidemiology of Type 2 DM?
Incidence of type 2 diabetes has recently increased (up to 10 fold) among pediatric population and accounts for up to half of all new cases of diabetes in certain populations.
What is the etiology of type 2 DM?
Inability of the body tissues to respond properly to insulin. Risk of resistance associated with genetics, obesity, increasing age, and duration of hyperglycemia.
What are risk factors for type 2 DM?
-Obesity: Mean body mass index (BMI) among children with type 2 DM is greater than 95th reference percentile for age
-Ethnicity: More prevalent in Native American, African American, Latino, Asian American, Pacific Islander populations.
-Age: peak age at diagnosis in youth is between 12 and 16 years (midpuberty)
-Sex (female, 3:1)
How does type 2 DM present?
May not have symptoms before diagnosis. Usually diagnosed in adulthood.
What screening is recommended for Type 2 DM?
ADA recommends checking fasting plasma glucose level every three years beginning at age 10 years (or onset of puberty if this is earlier) when:
-Child is overweight (BMI greater than 85th percentile for age and sex, weight for height greater than 85th percentile, or weight greater than 120 percent of ideal for height); plus has...
-Any two of the following risk factors:
--Maternal history of diabetes or gestational diabetes during the child's gestation
--Family history of type 2 DM in a first or second degree relative
--Race/ethnicity (Native American, AA, Latino, or Asian American, Pacific Islander)
--Signs of insulin resistance or conditions associated with insulin resistance (acanthosis nigricans, HTN, dyslipidemia, polycystic ovary syndrome)
What are four ways to diagnose diabetes according to the American Diabetes Association (ADA)?
1. Sx of diabetes (polyuria, polydipsia, and unexplained weight loss) plus random (any time of day without regard to time since last meal) plasma glucose concentration greater than or equal to 200 mg/dL (11.1 mmol/L)
2. Fasting (no caloric intake for at least 8 hours) blood glucose greater than or equal to 126 mg/dL (7.0 mmol/L)
3. Two-hour post-load glucose greater than or equal to 200 mg/dL (11.1 mmol/L) during an oral glucose tolerance test
4. Hemoglobin A1c (HbA1c) value greater than 6.5 percent in specifically certified laboratories
In the absence of unequivocal hyperglycemia or sx, results should be confirmed by repeating on a different day.
Diabetic ketoacidosis (DKA):
-A condition caused by relative or absolute deficit of insulin. Usually occurs in patients with type 1 diabetes, but can occasionally be found in patients with type 2 diabetes.
-Freq. of DKA at onset of diabetes inversely correlates with the regional incidence of type 1 diabetes in Europe and North America.
-Lack of insulin and excess glucagon and other coutnerregulatory hormones leads to a catabolic state resulting in hyperglycemia, excess ketones, and acidosis
-Increased lipolysis leads to increased mobilization of free fatty acids, which are then converted into ketones (acetoacetic and beta-hydroxybutyric acid); increased ketones lowers blood pH and leads to metabolic acidosis.
-When blood glucose levels reach about 180 mg/dL, osmotic diuresis occurs, leading to hypovolemia, dehydration, and a loss of sodium, potassium, and phosphate in the urine. Osmotic diuresis and hyperglycemia cause serum hyperosmolarity.
What is the diagnosis criteria for DKA?
-Random blood glucose greater than 200 mg/dL (greater than 11.1 mml/L)
-Venous pH less than 7.3 or serum bicarbonate less than 15 mEq/L (less than 15 mmol/L)
-Moderate or large ketonuria or ketonemia
What are there three main types of dehydration?
(Sodium = 130-150 mEq/L or mmol/L) Sodium and water losses are balanced. This is the most common type of dehydration in children, including children presenting with acute gastroenteritis.
(sodium less than 130 mEq/L or mmol/L) Sodium losses exceed water losses. Mild forms can be seen in viral gastroenteritis. More severe forms (less than 120 mEq/L) can be seen in free water or diluted formula replacement, or in adrenal insufficiency.
(sodium greater than 150 mEq/L or mmol/L) Water losses exceed sodium losses. This is seen most commonly in breastfeeding failure, use of inappropriate rehydration solutions, and diabetes insidious. Associated with highest mortality.
Using foreign language interpreters:
Failure to appreciate the important of culture and language in pediatric emergencies may result in multiple adverse consequences, including:
-Difficulties obtaining informed consent
-Dissatisfaction with care
-Lower quality of care
Why do children have a higher risk of dehydration than adults?
-Higher surface area-to-body mass ratio
-Higher basal metabolic rate
-Higher percent body water
What does the physical exam look like in MILD dehydration?
Neurological status - alert, consolable or irritable.
Pulse - age-appropriate or slightly increased.
Buccal mucosa/lips - Moist or tacky.
Eyes - Moist, not sunken.
Tears, if crying - present.
Urine output - Diminished.
Fontanel (if patent) - flat.
Skin (touch) - Unremarkable.
Skin (turgor) - good.
Capillary refill - less than 2 seconds.
What does the physical exam look like in MODERATE dehydration?
Neurological status - Alert, irritable.
Pulse - slightly increased.
Buccal mucosa/lips - Dry.
Eyes - Slightly dry/deep-set.
Tears, if crying - present, reduced.
Urine output - significantly diminished.
Fontanel (if patent) - Soft, slightly depressed.
Skin (touch) - Dry
Skin (turgor) - Mild tenting.
Capillary refill - 2-3 seconds.
What does the physical exam look like in SEVERE dehydration?
Neurologic status - Lethargic, obtunded.
Pulse - increased.
Buccal mucosa/lips - parched/cracked.
Eyes - dry/sunken.
Tears, if crying - Absent.
Urine output - Oliguric.
Fontanel (if patent) - Sunken.
Skin (touch) - Clammy.
Skin (turgor) - Significant tenting or no turgor.
Capillary refill - greater than 3 seconds.
A helpful Mnemonic for Writing admission orders:
A- Admit (floor, room, service, attending, resident)
D- Diagnosis (list in order of priority)
C- Condition (good, fair, guarded, critical)
A- Activity (ad lib, bed rest)
N- Nursing (ins and outs, wound care)
I- IV fluids (type and rate)
What is on the differential diagnosis for DKA?
Appendicitis, Toxic ingestion, Gastroenteritis, Gastrointestinal obstruction, Increased ICP, Bacterial pneumonia, pyelonephritis.
Common dx in pediatrics. Causes vomiting, but abdominal pain - typically migrating to the RLQ is a more prominent feature than in DKA. Patients often febrile.
History is key in this diagnosis. Vomiting and altered mental status or obtundation without a fever would be expected. Dehydration is possible depending on the extent of vomiting and the degree to which any change in mental status impairs oral intake. Tachypnea can be seen in aspirin overdose. Abdominal pain seen with iron ingestion.
Most common cause of vomiting. May be viral or bacterial. Abdominal pain - often colicky - would be expected, but also would likely have a fever, perhaps diarrhea.
The causes of obstruction, not a common diagnosis, include volvulus, intussusception, adhesions from previous surgeries, and cancer. It often causes vomiting (sometimes bilious) and abdominal pain without fever.
Vomiting and diffuse abdominal pain - both as a consequence of acidosis - are often presenting symptoms. (A patient with known diabetes who has been vomiting should be assumed to be in DKA until proven otherwise.) A history of polydipsia, polyuria, and weight loss is highly suggestive. Severe dehydration from osmotic diuresis is a prominent feature. Change in level of consciousness may occur depending on the level of dehydration and electrolyte abnormalities; its presence is also concerning for cerebral edema.
Increased intracranial pressure (ICP):
Signs and symptoms of increased ICP include vomiting and papilledema. Patient may exhibit an altered level of consciousness, often accompanied by headache.
Fairly common febrile illness which rarely causes vomiting, although pleural inflammation may result in abdominal pain. Change in mental status may be observed if patient is septic.
Presents with fever, urinary frequency, abdominal pain, and/or costovertebral angle tenderness. Dehydration is often seen due to vomiting and increased temperature.
Anti-endomysial and tissue transglutaminase antibodies with serum IgA level:
Due to increased risk of other autoimmune diseases, the ADA recommends that every child with new-onset type 1 diabetes be screened for celiac disease at diagnosis.
Anti-pancreatic antibodies (including insulin, GAD, and IA2):
Will confirm whether diabetes type 1 or 2. (There is an increasing incidence of type 2 diabetes among even very young children.)
Blood urea nitrogen (BUN) and creatinine:
Renal function should be normal, although creatinine may be elevated in cases of severe dehydration.
This test may be done quickly at the bedside via capillary glucose measurement (fingerstick). By definition, result will be elevated in diabetes and DKA.
Serum ketones or a serum beta-hydroxybutyrate level:
Serial levels are useful to monitor response to therapy.
Can be low, normal, or elevated even though total body potassium is low. Acidosis drives potassium out of the cells and into the blood. As the acidosis is corrected, the potassium will drop.
Hyponatremia results from the osmotic movement of water into the extracellular space in response to the hyperglycemia and hyperosmolarity (dilution hyponatremia), as well as from increased renal sodium losses. Remember to calculate a sodium corrected for the hyperosmolarity.
Increased risk for other autoimmune disease in patients with type 1 diabetes mellitus.
Helpful to quickly identify glycosuria and ketonuria. In DKA, urinary ketones are elevated from serum ketones spilling over into urine. Urine ketones should be monitored with every void until they clear. This helps in determining when it is appropriate to change from IV insulin therapy to subQ insulin.
Venous pH and bicarbonate:
Will confirm level of metabolic acidosis caused by elevated ketoacids in the blood.
What are the goals of rehydration therapy in DKA?
-Determine fluid deficit (percent dehydration)
--Determine type of dehydration
--Maintain daily needs
--Replace ongoing losses
-Manage acid-base and electrolyte imbalances
-Diagnose and treat primary condition
-Obtain access: Intravenous vs. nasogastric tube. Consider intraosseous line in case of emergency
What are the four basic steps of fluid management?
1. Provide bolus fluids to restore intravascular volume
2. Correct dehydration
3. Provide maintenance fluids
4. Replace ongoing losses
Provide bolus fluids to restore intravascular volume:
Administer serial 10-20 mL/kg boluses of 0.9% saline until patient urinates and vital signs and mental status have normalized.
-Amount of fluid required depends upon degree of dehydration
-Fluid deficit is difference between pre-illness weight and current weight. May calculate as follows:
--Pre-illness weight = current weight/(100- percent dehydrated) x 0.01
--1 kg = 1 liter of water
-Fluid composition (0.3 percent saline, 0.45 saline, 0.9 saline, etc.) and rate of infusion are dictated by the serum sodium concentration/osmolarity. In hyponatremic dehydration a sodium deficit is calculated, and in hypernatremic dehydration a free water deficit is calculated.
-Patients with hypernatremic dehydration and those in DKA must be corrected evenly over 48 hours to prevent cerebral edema due to rapid shifts in intracellular fluid volume.
Provide maintenance fluids:
-Maintenance fluids replace daily insensible losses (perspiration and respiration) and normal urine output (approx. 2 cc/kg/hr for children less than 15 kg and 1 cc/kg/hr for children greater than 15 kg and adults).
-In general, 0.45 percent saline (1/2 normal saline) and 5 percent dextrose is used to provide maintenance fluids.
-Three commonly used methods of calculating maintenance fluids: caloric expenditure, body surface, and Holliday-Segar.
What is the Holliday-Segar method of calculating maintenance fluids?
-First 10 kg body weight: 100 cc/kg/day
-Second 10 kg (10-20 kg): 50 cc/kg/day
-Each additional kg body weight over 20 kg: 20 cc/kg/day
Replace ongoing losses:
-In many patients with dehydration, losses may continue, even after replacement therapy has begun.
-The amount and type of replacement fluid is determined by the source of the losses (Eg, ongoing diarrhea, excessive emesis or nasogastric tube output, increased insensible losses due to fever or tachypnea. Ongoing urinary losses in DKA are not typically replaced.)
Treatment of diabetic ketoacidosis (DKA):
-Assessment and stabilization of airway, breathing, circulation (ABCs)
-Admit to hospital unit with staff trained in management of children in DKA (often intensive care unit)
-Obtain pediatric endocrinology consultation
-Correction of patient's fluid status and acidosis:
--Resuscitation with an intravenous fluid bolus is crucial to restore intravascular volume
---Administer bolus of 0.9 percent saline at 20 mL/kg over 60 min.
-Attach CV monitor to assess response to therapy and identify potentially lethal cardiac rhythm disturbances
-Monitor vital signs frequently
-Recheck fingerstick glucose every 30-60 min.
-After pt. has received initial volume expansion, may start insulin drip and being maintenance and replacement fluids (potassium should not be added until serum potassium level is known).
-In DKA, replacement fluids are administered evenly over 48 hours.
-Continue insulin drip until no ketones in serum and pH greater than 7.3 and/or the bicarb. greater than 15 and/or anion gap is closed.
-If ketones are still present or acidosis still exists, continue to give insulin and add dextrose to the fluids if the blood glucose drops below 300 mg/dL.
What is the goal of treating hyperglycemia in DKA?
Goal is to decrease blood glucose by 80-100 mg/dL per hour.
What are hypoglycemic symptoms?
Tremulousness, Diaphoresis, Confusion, Irritability, Hunger, Lethargy, Slurred speech, Loss of consciousness, Seizures
How do you prevent hypoglycemia when treating DKA?
To preven hypoglycemia, have blood glucose goal of no lower than 120 mg/dL, but no higher than 200 to 250 mg/dL. Glucose may be added to the IV fluids if the glucose falls too quickly. For example:
-Add 5 percent dextrose when blood glucose is 250-300 mg/dL (about two to three hours after giving insulin)
-Add 10 percent dextrose when blood glucose is 180-200 mg/dL
-Occurs in 0.5-1 percent of pediatric DKA cases
-Leading cause of diabetes-related death in children
-May occur at any point in management of DKA, even before treatment is initiated
What are risk factors for cerebral edema?
-High BUN concentration at presentation
-Profound acidosis with hypocapnia
-Attenuated rise in measured serum sodium with treatment
-Administration of bicarbonate
What are signs of cerebral edema?
Severe headaches, restlessness, irritability, inappropriate slowing of heart rate and rise in blood pressure, hypoxia, sudden deterioration of mental status, signs of increasing intracranial pressure and brainstem dysfunction
Cerebral edema must be treated as soon as it is suspected! Treatment includes:
-Slowed rate of fluid administration
-Transfer to intensive care unit
-Many categories of human insulin preparations
-Differ in onset of action, peak, and duration times
-Longer onset of action and time to peak action = longer duration of action
-Both rapid-acting and basal insulin are bioengineered
Initial total daily dose of subQ insulin:
-Varies with weight, age, pubertal status, and presence or absence of DKA.
-Children recovering from DKA may require up to 1 unit/kg per day of insulin.
-Children w/o DKA at presentation may be treated with 0.25 to 0.75 unit/kg per day, depending on age and pubertal status.
-In period of weeks after diagnosis, insulin dosages may need to be adjusted multiple times as patients enter the "honeymoon phase" (temporary appearance of remission).
SubQ insulin regimens:
Many options; all have these two components:
1. Basal insulin: An intermediate to long acting preparation to suppress hepatic glucose production and maintain normoglycemia in the fasting state
2. Prandial insulin: Doses of short-acting insulin taken before meals and/or snacks to cover expected carbohydrate load.
Traditional insulin regimen:
Divide total daily dose into three insulin injections per day administered as follows:
-2/3 of the total dose in the morning (1/3 rapid or short acting, 2/3 intermediate acting like NPH)
-1/6 of the total at dinner as rapid or short acting insulin
-1/6 of the total before bed as intermediate acting insulin
What is the "basal-bolus" regimen?
-Half the total daily dose in form of an "ultra-long-acting" basal insulin given at bedtime (such as insulin glargine, which lasts greater than 24 hours)
-Remaining half split evenly among all three meals