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CASE PRESENTATION. CATALINA RUIZ MESA, MD PL 1 SBH. CASE. 17 yo, FEMALE 1 week history of polyuria, polydispsia, weight loss. PMH: negative FHX: type 1 and 2 DM in the maternal side, mom had gestational diabetes. COURSE. At home: CBG: 300. At clinic: PE and VS: WNL.

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Case presentation

CASE PRESENTATION

CATALINA RUIZ MESA, MD

PL 1

SBH


CASE

  • 17 yo, FEMALE

  • 1 week history of polyuria, polydispsia, weight loss.

  • PMH: negative

  • FHX: type 1 and 2 DM in the maternal side, mom had gestational diabetes


Course
COURSE

  • At home: CBG: 300.

  • At clinic: PE and VS: WNL.

    CBG:320, UA: glucosuria

  • ER: PE and VS: WNL.

    UA: prot: Neg, glu: 1000, ketone: 10, LE: TR, RBC: 0, Sq cells: 3, bact: few.

    CBC: WBC: 8.6, HB: 14.2, Hto:39.9, plat: 231. N: 72.2, L:21.7


Con t
Con’t

  • CMP: 133 101 10 283 4.1 14 0.7

    4.4 23 0.5 9.1 6.9 23 112

  • VBG: pH: 7.4, PCO2: 40, PO2: 54.8, O2Sat: 89.8, base ex: 0, bicarb: 24,3.


Type 1 dm
TYPE 1 DM

  • DM DEFINITION:

    Disorder of the metabolic homeostasis controlled by insulin, resulting in abnormalities of carbohydrate and lipid metabolism.

    TYPE 1: absolute insulin deficiency

    TYPE 2: Insulin resistance


  • PATHOGENESIS

    Autoimmune destruction of beta cells (T cell mediated) induced by environmental triggers.

    High risk:

    Major Histocompatibility Complex on chromosome 6.

    DR3-DQ2 allele

    DR4-DQ8 allele

    Family history: 10-20% have a family member with DM


  • TRIGGERS

    Congenital Rubella: up to 20% develop type 1 DM.

    No other specific environmental factors are confirmed.


AUTOANTIBODIES AGAINST BETA CELL

AB against whole islets

AB against specific proteins such as insulin, glutamic acid decarboxylase, tyrosine phosphatase, insulinoma- associated prot. 2.

No specific role in Beta cell damage, not everyone with this AB develop DM, but they are at risk.


More than 80% of beta cell must be lost before glycemic control is impaired significantly. At that point insulin is insufficient to maintain glucose and lipid homeostasis.

Blood glucose >180mg/dl glucosuria osmotic diuresis polyuria Polydipsia to maintain euvolemia.

Decreased insulin lipolysis and protein breakdown


Glucosuria, lipolysis and protein breakdown (caloric loss) weight loss and hyperphagia.

SYMPTOMS

Polydipsia

Polyuria usually < 1 month

Polyphagia

Weight loss


Diagnosis
DIAGNOSIS weight loss and hyperphagia.

  • Symptoms + random plasma glucose >200mg/dl OR

  • Fasting glucose > 126mg/dl

    Symptoms and glucose 100-125mg/dl should have an oral glucose tolerance test


Complications
COMPLICATIONS weight loss and hyperphagia.

  • ACUTE: DKA

    Hypoglycemia

  • LONG TERM: damage to microcirculation (blindness, end-stage renal disease, neuropathy), macrovascular complications/lipids


Acute complications
ACUTE COMPLICATIONS weight loss and hyperphagia.

  • HYPOGLYCEMIA < 60mg/dl

    Sweating, trembling, hunger and palpitations, headache, light headness, dizziness, diplopia, confusion. Seizures.

    Mild to moderate: 10-15gr glucose (4oz juice)

    Severe: IM or SC glucagon (1mg, except infants <10kg in whom 0.5mg is given)


Acute complications1
ACUTE COMPLICATIONS weight loss and hyperphagia.

  • DKA

    Vomiting, dehydration, abdominal pain, presence of an altered sensorium.

    Hyperglycemia: >200mg/dl

    Acidosis: pH <7.3, HCO3 <15meq/L

    Ketonemia


Dka con t
DKA CON’T weight loss and hyperphagia.

Acidosis and ketosis cause an ileus that can lead to abdominal pain, can be severe.

Elevation of stress hormones, epinephrine and cortisol, can lead to an elevation in the WBC.

CAUSES

  • Omission of insulin dose

  • Intercurrent illness increased in insulin requirements


Dka con t1
DKA CON’T weight loss and hyperphagia.

TREATMENT

1 HOUR:

Fluid resuscitation 10ml/kg (0.9% NS)

AFTER 2 HOUR:

  • Maintenance requirements + replacement of the deficit ever 48H. ( 0.9%NS + 20meq/L K phos + 20meq/L KCL or K acetate)

    Total fluid no more than 1.5 or 2 times maintenance fluid rate.


Dka con t2
DKA CON’T weight loss and hyperphagia.

When blood glucose < 300mg/dl 0.9%NS is changed to D5 0.45% saline + K.

If blood glucose < 150mg/dl the dextrose content may need to be increased to 10% or even 12.5%.


Dka con t3
DKA CON’T weight loss and hyperphagia.

REMEMBER

  • Insulin treatment and correction of acidosis cause the K to move intracellularly. Unless hyperkalemia or anuria, K should be added to IV fluids after the 2 hour.

  • Patient in DKA also has phosphate depletion

  • HCO3 treatment is associated with cerebral edema. Only if pH <6.9 or for life threatening hyperkalemia. (1-2mmol/kg in 0.45% saline over 1-2h)


Dka con t4
DKA CON’T weight loss and hyperphagia.

  • IV insulin 0.1 Units/kg/hour

    Until acidosis resolves (pH >7.3, HCO3 >15meq/L).

    Increased dose to 0.15 or 0.2U/kg/h if acidosis is not resolving.

    GOALS:

    -Decrease glucose at a rate of 100mg/dl/h

    - After the 1 hour pH should increase at least 0.03 units/hour.


Dka con t5
DKA CON’T weight loss and hyperphagia.

MONITOR:

  • VS, PE, neurologic evaluation

  • I’s and O’s every hour

  • Serum glucose, pH, at presentation and every hour.

  • Electrolytes, BUN, creat. At presentation and then every 2-3h with urine ketones.


Dka con t6
DKA CON’T weight loss and hyperphagia.

RESOLUTION:

Normal sensorium, normal VS, ability to tolerate PO, no acidosis (normal pH, HCO3 >18, normal anion Gap)

D/C IV insulin at time of SC rapid acting insulin or 30 minutes AFTER SC insulin.


Management of dm
MANAGEMENT OF DM weight loss and hyperphagia.

GOALS:

  • As close to metabolic normalcy as possible

  • Avoid acute complications

  • Minimize the risk of long term micro and macro vascular complications

  • F/U by diabetes team every 3 months


Insulin
INSULIN weight loss and hyperphagia.

  • RAPID ACTING

    LISPRO (HUMALOG)

    ASPART (NOVOLOG)

    GLULISINE (APIDRA)

    Onset: 0.25h

    Peak: 0.5- 1h

    Duration: 3-4h


Insulin con t
INSULIN weight loss and hyperphagia.Con’t

  • SHORT ACTING

    REGULAR INSULIN (is used IV in DKA)

    Onset: 0.5-1h

    Peak: 2-3h

    Duration: 4-6h


Insulin con t1
INSULIN weight loss and hyperphagia.Con’t

  • INTERMIDIATE

    NPH

    DETEMIR (LEVEMIR) time of action depends on the dose

    Onset: 2-4h

    Peak: 6-10h

    Duration: 14-16h


Insulin con t2
INSULIN weight loss and hyperphagia.Con’t

  • LONG ACTING:

    GLARGINE (LANTUS)

    Onset: 2-3h

    Peak: NO PEAK

    Duration: 20-24h


Insulin1
INSULIN weight loss and hyperphagia.

DAILY REQUIREMENTS (Units/kg/day)

<3y - 0.3- 0.4

3-6y - 0.5

7-10y - 0.6- 0.8

11-14y - 0.8- 1

>14y - 1- 1.5


Treatment
TREATMENT weight loss and hyperphagia.

INSULIN

ADMINISTRATION

  • Twice daily injections:

  • 2/3 total dose AM: 1/3 lispro, 1/3 NPH

  • 1/3 total dose PM: ½ lispro, ½ NPH


Administration con t
ADMINISTRATION CON’T weight loss and hyperphagia.

2. Basal bolus regimen:

  • ½ of total daily dose: one time Lantus OR

    If pump the basal insulin can be short acting insulin (#units/hour)

  • Other ½ of total daily dose: short acting (Lispro) with meals based on carbohydrate intake.


Bolus: weight loss and hyperphagia.

  • Amount of insulin needed to cover the cabs in the meal.

    2. Amount of insulin needed to correct for a blood glucose concentration outside of the target range. (80- 120mg/dl day time, 100-150mg/dl at bed time)


Treatment1
TREATMENT weight loss and hyperphagia.

DIET

Caloric requirements:

<10y: 1000kcal + 100kcal/year

>10y: female: 45kcal/kg/day

male: 55kcal/kg/day

50-55% carbohydrate calories, 20% protein, and approximately 30% fat


Treatment2
TREATMENT weight loss and hyperphagia.

EXERCISE

Regular exercise should be encouraged.

During exercise increase cals or decrease insulin


F u and monitoring
F/U AND MONITORING weight loss and hyperphagia.

CBG:

Before meals, bedtime, overnight (2am). If basal/bolus regimen more often, also in exercise, illnesses.

During illnesses: insulin requirement increases. Extrafluids to avoid dehydration, if no solids are tolerated, sugar containing foods can be given to maintain some caloric intake and prevent hypoglycemia. If no PO or vomiting ER


F u and monitoring1
F/U AND MONITORING weight loss and hyperphagia.

HBA1C

Every 3 months

Values depend on age:

7.5- 8.5% toddlers and preschoolers (<6y)

<8% school age children (6- 12y)

<7.5% adolescents and young adults (13-19y)


F u and monitoring2
F/U AND MONITORING weight loss and hyperphagia.

URINE OR BLOOD KETONES

should be monitored when blood glucose values are elevated (>250-300), when children have a fever, or when they are not feeling well.


F u and monitoring3
F/U AND MONITORING weight loss and hyperphagia.

  • TSH

    At Dx of DM and then every 1-2y because of the association with other autoimmune disease.

  • Screen for CELIAC DISEASE at least one time, or if poor growth and GI symptoms. Tissue transglutaminase and antiendomysial antibodies.


F u and monitoring4
F/U AND MONITORING weight loss and hyperphagia.

  • OPHTHALMOLOGY

    Once the child is 10y and has had DM for 3-5years. Yearly F/U. Retinopathy not seen before 5-10 years.

  • MICROALBUMIN

    After the child is 10y and has had DM for 5years.

  • NEUROPATY

    Changes in nerve conduction may be seen after 4-5 years


F u and monitoring5
F/U AND MONITORING weight loss and hyperphagia.

  • LIPIDS <100mg/dl

    If >10y treat with statins if LDL >160mg/dl

    Consider treatment if LDL > 130mg/dl and other risk factors.

  • EDUCATION

    Life long process to the patient and families.


Back to the case
…BACK TO THE CASE weight loss and hyperphagia.

  • FLOOR: PE and VS: WNL

    Plan: - CBG before meals, bedtime, 2am

    Insulin Lantus 20Units SC daily

    - Humalog SS:

    71-100 4U

    101-150 6U

    151-200 8U

    201-300 10U

    301-400 12U

    >400 13U


Case con t
CASE weight loss and hyperphagia.Con’t

LABS

  • Gc Chlamydia: not detected

  • Islet cell ab: neg

  • GAD 65 ab: >30 (high) ref: <1.

  • C-peptide: 2.1

  • Insulin: <2 ref: <17

  • HBA1C: 8.2


REFERENCESS weight loss and hyperphagia.

  • Cooke DW, Plotnick L. Type 1 diabetes mellitus in pediatrics. Pediatr Rev. 2008;29:374-385

  • Cooke DW, Plotnick L. management of diabetic ketoacidosis in children and adolescent. Pediatr Rev 2008;29;431-436

  • The Washington Manual of Pediatrics, 2009 by Department of Pediatrics, Washington University on behalf of the School of medicine.


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