Peds Case 16- 7Y/o W Abd Pain And Vomiting

Front 1

omiting is seen more commonly in children less than 3 years, where viral gastroenteritis and dehydration are more common. Significant vomiting in a 7-year-old child is less common

Back 1

not be allowed to take anything by mouth. Depending on the diagnosis, Isabella may need surgery, in which case she'll need to have an empty stomach. Additional vomiting might also worsen existing metabolic derangements and, given her altered mental status, may increase her risk of aspiration

Front 2

total possible score of 15, patients with a GCS of 8 or less may require aggressive intervention and management. For children under the age of 5 years, there are adjusted verbal response criteria.

Back 2

Eye Opening Response
4 - Eyes open spontaneously
3 - Eyes open to verbal command
2 - Eyes open to pain
1 - No eye opening

Verbal Response
5 - Oriented (smiles, orients to sounds, follows objects interacts)
4 - Confused, but able to answer questions (cries but is consolable w inapp interactions)
3 - Inappropriate words (inconsistently inconsolable)
2 - Incomprehensible sounds (inconsolable, agitated)
1 - No verbal response

Motor Response
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

Front 3

children have a higher risk of dehydration than adults because:

Back 3

1. Children have a higher surface area to body mass ratio, hence a greater relative area for evaporation to occur.

2. Children have higher basal metabolic rates than adults, which generates heat and expends water.

3. Children have a higher percentage of body weight that is water. In infants, 70% of body weight is water; 65% in children; and 60% in adults. Because of this, children under 4 years of age have a particularly increased risk of dehydration.

Front 4

Not pyloric stenosis and inborn errors of metabolism b/c she is 7y/o

Back 4

inborn error of metabolism can certainly present with Isabella's findings, the fact that she has been otherwise healthy for her first seven years of life makes a congenital metabolic disorder unlikely. Similarly, pyloric stenosis usually presents between 3-12 weeks of age

Front 5

Toxic ingestion

Back 5

vomiting, altered mental status, and obtundation.

Dehydration is possible depending on the extent of vomiting and the degree to which any change in mental status impairs oral intake.

The degree of dehydration in our patient seems out of proportion to the amount of vomiting

Front 6

GI obstruction

Back 6

Vomiting, abdominal pain and absence of fever
lack of bilious vomiting and abdominal distention argue against this diagnosis.

Front 7

Gastroenteritis

Back 7

most common cause of vomiting, but gastroenteritis usually presents with fever, colicky abdominal pain and diarrhea. Again, the degree of dehydration seems out of proportion to the amount of vomiting.

Front 8

appendicitis

Back 8

abd pain more than vomiting
altered level of consciousness, this degree of dehydration, and lack of fever argue against

Front 9

ICP

Back 9

Vomiting, altered mental status and lack of fever
abdominal pain and tachypnea would not be not expected

lack of cushings triad

Front 10

bacterial pneumonia

Back 10

pneumonia should always be considered in the evaluation of a child with abdominal pain
tachypnea

pain more than vomiting

Pleural inflammation often results in abdominal pain and, less often, vomiting. Lack of fever argues strongly against this diagnosis and altered mental status does not fit

Front 11

pyelonephritis

Back 11

vomiting and abdominal pain, but CVA tenderness is more likely. Lack of fever and this degree of dehydration also speak against this diagnosis

Front 12

DKA

Back 12

Vomiting is often a presenting symptom, as are increased respiratory rate and vague abdominal pain.

Dehydration of this degree is a prominent feature of DKA due to a combination of vomiting and osmotic diuresis, and it often leads to altered mental status

usually T1D
misdiagnosed as flu
vomiting, weight loss, dehydration, shortness of breath, abdominal pain, or a change in the level of consciousness

Front 13

diabetes vs prediabetes
nml A1c

Back 13

FBG 100-125 mg/dL = “impaired fasting glucose”
2-hour postload glucoses140-199 mg/dL= impaired glucose tolerance
no formal recognition of “prediabetes” w HbA1c
above the laboratory “normal” but below the diagnostic cut point for diabetes (6.0 to <6.5%) 10x risk of developing diabetes

use of HbA1c values in the diagnosis of diabetes in the pediatric age group has not yet been routinely accepted

Front 14

bicarb should not be given in DKA b/c

Back 14

well-described paradoxical CNS acidosis and hypokalemia from rapid correction of acidosis

increased risk of cerebral edema, which is the most common cause of diabetes-associated death in children (along w insulin bolos= glu drop too fast)

Front 15

DKA mgmt that I forget

Back 15

aseline serum osmolality should be measured prior to initiation of treatment. Isabella should have a baseline CBC with differential to help identify an infection as a precipitating factor, but this should be interpreted with caution, recognizing that the WBC count might be elevated with a left shift due to the stress of DKA alone. Blood and/or urine cultures should be considered, especially with Isabella's mental status changes, borderline hypotension and tachycardia. Blood lactate, pyruvate, and ammonia levels are not necessary because we have an explanation for her altered mental status.
In addition, measurement of blood beta-hydroxybutyrate concentrations, when available, are useful to confirm ketoacidosis, and can be used to monitor response to therapy.

Front 16

Kussmaul respirations

Back 16

pattern of rapid and deep breathing because the patient is attempting to blow off the excess CO2 caused by their metabolic acidosis.

distinctive because other causes of tachypnea such as heart and lung disease reduce vital capacity, leading to rapid, shallow respirations, not deep.

Front 17

T1D

Back 17

relative or absolute deficiency of insulin
Insulin facilitates entry of glucose into peripheral tissues, inhibits lipolysis, glycogenolysis, and tissue catabolism.

lack of insulin and excess counterregulatory hormones (glucagon, catecholamines, cortisol, and growth hormone) causes a catabolic state characterized by increased gluconeogenesis, lipolysis, and glycogenolysis, and an inhibition of glycolysis, which result in hyperglycemia and ketogenesis.

increased mobilization of free fatty acids, converted into ketones (acetoacetic and beta-hydroxybutyric acids).
lowers the blood pH, and leads to metabolic acidosis, worsened by lactic acidosis from dehydration and poor tissue perfusion.

Front 18

osmotic diuresis

Back 18

uncontrolled diabetes, when circulating blood glucose levels reach ~180 mg/dL, an osmotic diuresis occurs, leading to hypovolemia, dehydration, and a loss of sodium, potassium, and phosphate in the urine.

Intravascular volume depletion stimulates catecholamine release, which causes further lipolysis.

osmotic diuresis and hyperglycemia cause serum hyperosmolarity. Dehydration can result in renal impairment, which will exacerbate hyperglycemia

Front 19

A. pH on a venous blood gas:

B. Serum sodium:

C. Potassium:

D. Bicarbonate:

E. Creatinine:

F. Serum glucose:
G. Serum ketones:

H. Urine ketones:

Back 19

A. pH on a venous blood gas: metabolic acidosis bc ketoacids in blood

B. Serum sodium: Hyponatremia bc osmotic movement of water into the extracellular space in response to the hyperglycemia and hyperosmolarity (dilutional hyponatremia),
increased renal sodium losses.
corrected sodium=[{(measured glucose-100)/100} x 1.6] + measured sodium

C. Potassium: depleted through urinary losses, but serum potassium level can be high, normal or low. This
acidosis and insulinopenia drivesK out of cells and into the serum.
acidosis is corrected= K drops
K added to her IVF after initial volume expansion and after urine output is established, unless EKG changes (peaked T waves).
given as potassium chloride, potassium acetate, and/or potassium phosphate.
potassium phosphate reduces the amount of chloride the patient is given, thus decreasing the risk for causing an iatrogenic hyperchloremic acidosis, and provides both potassium and phosphorus, both of whose total body stores are often low at presentation of DKA ."

D. Bicarbonate: low because of the metabolic acidosis caused by the elevated ketones and lactic acid

E. Creatinine: elevated secondary to the severe dehydration, also termed prerenal azotemia."

F. Serum glucose: elevated

G. Serum ketones: serum beta-hydroxybutyrate elevated. follow to determine how responding to insulin therapy."

H. Urine ketones: serum ketones will spill over into her urine

Front 20

3 types of dehydration depending on serum Na

Back 20

1) Isotonic/Isonatremic (Na = 130-150 mEq/L).
most common type in children
sodium and water losses are balanced
ex acute gastroenteritis and diarrhea.
deficit replaced over 12 hours.

2) Hypotonic/Hyponatremic (Na<130 mEq/L)
sodium losses exceed that of water
when pts consume diluted fluids or water in dehydration.
also result of adrenal insufficiency
deficit replaced evenly over 24 hours.
Rapid correction of hyponatremia= central pontine myelinolysis.

3) Hypertonic/Hypernatremic (Na>150 mEq/L)
water losses exceed that of sodium= highest mortality. causes: breastfeeding failure, use of inappropriate rehydration solutions (boiled milk), and diabetes insipidus.
deficit replaced evenly over 48 hours
Too rapid correction= of cerebral edema.

Although our patient is hyponatremic secondary to hyperglycemia, she best fits into hypertonic dehydration secondary to the osmotic diuresis and the resulting hyperosmolarity. Therefore, patients with DKA typically have their fluid deficit replaced evenly over 48 hours.

Front 21

3 bag approach
fluid management in the resuscitation of children presenting in DKA

Back 21

1) IV insulin
2) Dextrose free IV fluid containing a slightly more isotonic solution (0.675% saline) than is considered the norm, with appropriate amounts of potassium and phosphorus
3) a third fluid identical to the 2nd except that it contains 10% dextrose as well.

rate tapered up and down as needed to meet glucose targets while insulin is delivered at a constant rate of 0.1 units/kg/hour

protocol associated with a more rapid correction of acidosis when compared to traditional protocols.

Front 22

cerebral edema

Back 22

rare but (0.5-1% of pediatric DKA episodes) high rates of mortality (21-24%) and morbidity.
can occur at any point during the management even before treatment is initiated and up to 24 hours after initiation of treatment.

pathophysiology poorly understood
risk factors: high BUN concentration at presentation,
profound acidosis with hypocapnia,
attenuated rise in the measured serum sodium with treatment,
administration of bicarbonate

sx:
Headache
Recurrence of vomiting
Inappropriate slowing of heart rate (bradycardia)
Rising blood pressures (hypertension)
Decreased oxygen saturation (hypoxia)
Restlessness, irritability
Increased drowsiness (lethargy)
Cranial nerve palsies: CN VI - Abducens nerve
Abnormal pupillary responses: unequal pupils, fixed dilated pupils, absent response unilaterally or bilaterally

Front 23

components of admission order

Back 23

ADC Van Dismal

Admit to Diagnosis Condition Vital signs Allergies Nursing Diet IV fluids Special instructions Medications Activity Labs

Front 24

orders for DKA

Back 24

A. Continuous monitoring of vitals: rehydrated and their electrolytes correct

B. Perform neuro checks every hour: cerebral edema

C. Monitor fluid ins and outs: hydration status.

D. Diabetic diet: NPO until her blood sugars, neurologic status, and vomiting resolve. clears by mouth in a few hours we need to be sure to account for that in her IVF orders

E. Chest X-ray. no, clear explanation for her tachypnea."

F. EKG: no, only if K changes dramatically

G. Oral hypoglycemic agent: no

H. Insulin orders. until acidosis resolves (bicarbonate >15 mEq/L or normal anion gap) and ready to transition to subcutaneous insulin.

I. Serum electrolytes every 12 hours: "No, her electrolytes must be monitored every hour because important shifts can occur. 2-4 hours as she stabilizes."

J. Serum glucose every 60 minutes: "Yes,

K. Serum calcium, magnesium, and phosphorus now: phosphorus- and magnesium-depleted due to urine losses. As phosphorus is added, calcium must be monitored too.

L. Check serum pH (VBG) every 60 minutes: "Yes, due to the metabolic acidosis the serum pH is generally monitored with a venous blood gas. serum bicarbonate, anion gap, and urinary and/or serum ketones."

M. Urine dipstick for ketones: "Yes, checked quickly at the bedside with a dipstick or a formal urinalysis

Front 25

Other ways to manage T1D

Back 25

Metformin, classically first line for type 2 diabetes, adjunct therapy, for type 1 diabetes w insulin resistance.

Pramlintide, a synthetic analog of human amylin, conjunction w insulin to delay gastric emptying and inhibit release of glucagon,

Trials in children with both pramlintide and glucagon-like peptide agonists (endogenous peptides with actions similar to amylin) ongoing

bc is autoimmune disease, immunotherapies for children also under intense investigation.

Front 26

tests for new diabetic

Back 26

increased propensity for insulin in Latino pop and the increasing T2D even very young children,
typically present with hyperglycemia not ketoacidosis, and generally overweight

T1D inc risk of other autoimmune dx- autoimmune thyroid disease and Celiac disease most common
Annual thyroid function testing but NOT until metabolic control has been established for several weeks (first outpatient visit) bc new-onset diabetes and DKA often will have abnormal thyroid function secondary to non-thyroidal illness

every child with new-onset type 1 diabetes be screened for Celiac disease at diagnosis.

antibody measures to screen for risk of thyroid disease and celiac disease while Isabella is in the hospital, while putting off actual thyroid function tests until the first follow-up visit.

Anti-pancreatic antibodies including insulin, GAD, and IA2
Thyroid antibodies
Anti-endomysial and tissue transglutaminase antibodies with a serum IgA level

Front 27

concordance rate
multifactorial

Back 27

chance that identical twins have the same dx
if a disease is multifactorial, it is more likely that a person's twin (mono- or dizygotic) will have the disease than the person's sibling. This is simply because twins tend to be raised in more similar environments than siblings

multifactorial inheritance. For type 1 diabetes, the concordance rate for monozygotic twins has been estimated as 21-53%, with most estimates ranging from 30% to 50%.
risk of diabetes in the general population is only 0.4% (obviously, this depends on the specific population). The chance that a dizygotic twin will have type I diabetes is about 13%. And the chance that the sibling of an affected person has Type 1 diabetes is 6-7%.

Front 28

insulin regimen

Back 28

2/3 of the total dose in the morning (1/3 rapid or short-acting, 2/3 intermediate-acting (such as NPH)); 1/6 of the total at dinner as rapid or short-acting insulin; and 1/6 of the total before bed as intermediate-acting insulin.

some benefit to institution of “basal-bolus” therapies immediately after diagnosis of diabetes,
½ of the total daily dose is given in the form of an “ultra-long-acting” basal insulin given at bedtime (such as insulin glargine, which lasts for upwards of 24 hours), and the other half is split evenly amongst all 3 meals.
ultra-long-acting insulins has given children with type 1 diabetes greater flexibility in their day to day schedules, as their meal times are no longer predetermined by the timing of their intermediate-acting insulin dose several hours prior to their meal.

The initial total daily dose of 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 without DKA at presentation may be treated with 0.25 to 0.75 unit/kg per day, depending on age and pubertal status

Front 29

honey moon phase

Back 29

Within 1 month of diagnosis, most pediatric patients have a temporary remission of diabetes and require little exogenous insulin
parents may assume child is cured

Front 30

T2D

Back 30

Usually normal or high levels of insulin, but hyperglycemia exists due to insulin resistance (IR) of peripheral tissues.
risks: genetics, obesity, increasing age, and hyperglycemia over long periods of time.

Epidemiology/Risk Factors:

Obesity: Type 2 DM in children is more strongly associated with obesity than with any other clinical condition. Most studies have found that mean body mass index (BMI) among children with type 2 DM is >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)
Sedentary lifestyle

Screening: The ADA recommends a fasting plasma glucose level, beginning at 10 years of age or at onset of puberty and then every 3 years thereafter, in children who meet the following criteria:

Overweight (BMI >85th percentile for age and sex, weight for height >85th percentile, or weight >120% of ideal for height)
PLUS
Any two of the following risk factors:

Maternal history of diabetes or gestational diabetes during the child’s gestation.
Family history of type 2 diabetes in a first- or second-degree relative
Race/ethnicity (Native American, African American, Latino, or Asian American, Pacific Islander)
Signs of insulin resistance or conditions associated with insulin resistance (acanthosis nigricans, hypertension, dyslipidemia, polycystic ovary syndrome).

Front 31

ages most able to become fluent in nonnative languages

Back 31

4-8y/o