Case 16: 7yo - DM Flashcards

1
Q

how to test for Celiac

A

TTG IgA > 100
Total IgA
(if low total IgA, normal TTG –> false negative)

  • endomesial antibody = 100% specificity

gold standard = Biopsy

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2
Q

when can you NOT test for Celiac’s

A

already gluten free
(can’t get IgA antibodies, or scope/biopsy)

–> need to introduce celiac’s for 4w (1 slice of bread per day)

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3
Q

treatment for Celiac’s

A

Remove gluten - low FOD-MAP diet

  • trend TTG IgA q3-6mo for 1 year (==> takes 1y for antibodies to decrease)
  • q1y after that = to test for accidental ingestion
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4
Q

when do you use a genetic test for Celiac’s disease?

A

1) when gluten-free and don’t want to re-introduce
- useful only when negative
- b/c if positive = 20-30% of population has it

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5
Q

differentiate
= Celiacs
= gluten allergy
= gluten sensitivity

A

1) Celiac’s = IgA
- sxs: diarrhea, malabsorption

2) gluten allergy = IgE
- sxs: hives, swelling
- exercise induced wheat anaphylaxis = if eat wheat, then exercise within next hour ==> anaphylaxis

3) non-celiac gluten sensitivity
- rule out Celiac’s, rule out glutenallergy
- tx: decrease gluten to tolerable levels

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6
Q

What is the most common age group for significant vomiting

A

Kids <3yo ==>viral gastroenteritis, dehydration

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7
Q

Why do children have an increased risk of dehydration?

A

Kids <4yo v. adults

  • higher surface areas:body mass ratio == greater relatively area for evaporation
  • higher BMR == increased heat, loss of water
  • higher % body weight that is water (infants = 70%; children = 65%; adults = 60%)
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8
Q

How do diagnose DM?

A

Sxs = polyuria, polydyipsia, unexplained weight loss

1) sxs of DM + random BG > 200
2) fasting BG > 126
3) Oral glucose tolerance test: 2-h postload glucose >200
4) HbA1c >/= 6.5%

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9
Q

How to diagnose DKA?

A

Sxs = vomiting, tachycardia, mental status changes, dehydration

1) random BG > 200
2) venous pH < 7.3 OR serum bicarb < 15
3) moderate/large ketonuria/ketonemia

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10
Q

Diabetic ketoacidosis (DKA)

  • epidemiology:
  • pathophysiology:
  • LABS:
A

EPIDEMIOLOGY: T1DM&raquo_space;> T2DM

PATHOPHYSIOLOGY: T1DM == relative/abs insulin deficiency (insulin = glucose entry into peripheral tissues; inhibited lipolysis, glycogenolysis, tissue catabolism)

1) HYPERGLYCEMIA: lack of insulin + excess counterregulatory hormones (glucagon, catecholamines, cortisol, GH) –> catabolic state = increased gluconeogenesis, lipolysis, glycogenolysis, inhibited glycolysis
2) KETOGENESIS: increased lipolysis –> mobilized FFAs ==>ketones (acetoacetic, beta-hydroxybutyric acids)
3) METABOLIC ACIDOSIS = increased production of ketones –>decreased Ph
4) + LACTIC ACIDOSIS = dehydration, poor tissue perfusion
5) HYPOVOLEMIA, DEHYDRATION, ELECTROLYTE LOSS (Na, K, PO4) = when BG ~180 –> OSMOTIC DIURESIS

==> further LIPOLYSIS - d/t intravascular volume depletion –>catecholamine release
==>HYPEROSMOLALITY – d/t osmotic diuresis, hyperglycemia
==> RENAL IMPAIRMENT, HYPERGLYCEMIA – d/t dehydration

LABS

  • pH(decreased) == metabolic acidosis d/t elevated ketoacids, lactic acid
  • serum Na (decreased) == (1) osmotic movement of water into extracelluar space d/t hyperglycemia, hyperosmolarity [dilutional hyponatremia]; (2) renal sodium losses in urine
  • serum K (normal) [with total body K decreased] == (1) hyperkalemia d/t acidosis and low insulin driving K out of cells; (2) expected hypokalemia with correction of acidosis and low insulin.
  • bicarbonate (decreased) == d/t metabolic acidosis, d/t elevated ketoacids, lactic acid
  • creatinine (elevated) ==d/t severe dehydration (prerenal azotemia)
  • serum glucose (elevated) == in DM, DKA
  • serum, urine ketones (elevated) == d/t increased lipolysis from low insulin
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11
Q
Diabetic ketoacidosis (DKA)
- presentation:
A

PRESENTATION: known T1DM + vomiting = assumed DKA until proven otherwise

  • vomiting
  • tachycardia
  • mental status changes
  • dehydration
  • weight loss
  • SOB
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12
Q

What kinds of potassium can be used during treatment of DKA?

A

KCl
K acetate
K phosphate == less Cl given; decreased risk for iatrogenic hyperchloremic acidosis; more K and PO4 given (both depleted during DKA)

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13
Q

How to monitor for treatment response in DKA?

A
  • rehydration status
  • serum, urine glucose levels
  • serum, urine ketone levels
  • K levels
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14
Q

Types of dehydration

  • causes:
  • how to replace the deficit:
  • complications of treatment:
A

==>based on serum Na

1) ISOTONIC/ISONATREMIC (Na nml) == losses: Na and H2O balanced
- causes: acute gastroenteritis, diarrhea
- how to replace the deficit: NS over 12h
- complications of treatment: none

2) HYPOTONIC / HYPONATREMIC (Na < 130) == losses: Na&raquo_space; H2O / dilutional
- causes: pts drink diluted fluids / water in setting of dehydration; adrenal insufficiency (low mineralocorticoids)
- how to replace the deficit (= Na deficit): NS or hypertonic saline over 24h
- complications of treatment: central pontine myelinolysis (d/t rapid correction == rapid shrinking of brain, esp. pons)

3) HYPERTONIC / HYPERNATREMIC (Na>150) == losses: H2O&raquo_space; Na ==>highest mortality
- causes: breastfeeding failure; use of inappropriate rehydration solutions; diabetes insipidus; DKA (osmotic diuresis, hyperosmolarity == although hyponatremic 2/2 hyperglycemia)
- how to replace the deficit (= free water deficit): NS over 48h
- complications of treatment: cerebral edema

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15
Q

Which type of dehydration is associated with the highest mortality?

A

HYPERTONIC / HYPERNATREMIC (Na>150) == losses: H2O&raquo_space; Na

  • breastfeeding failure
  • diabetes insipidus
  • DKA ==> osmotic diuresis, hyperosmolarity == although hyponatremic 2/2 hyperglycemic
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16
Q

Cerebral edema

  • epidemiology:
  • timing:
  • pathophysiology:
  • prognosis:
A

epidemiology: 0.5-1% of pediatric DKA epiodes

timing: even before
treatment is initiated and up to 24 hours after initiation of treatment.

pathophysiology RFs

  • high BUN at presentation
  • profound acidosis + hypocapnia
  • increased serum Na with treatment
  • administration of bicarb

prognosis: 21-24%rate of mortality

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17
Q

T2DM

  • epidemiology:
  • pathophysiology:
  • RFS:
  • screening indication
  • management
A
  • epidemiology: up to 50% of all new cases of DM; 10x increase in past 20y
  • pathophysiology: insulin resistance (nml / high levels of insulin) in peripheral tissues –> hyperglycemia
  • RFS: obesity (BMI>95%ile), ethnicity (Native A., African A., Latino A., Asian A.); age (12-16y); female sex; sedentary lifestyle; hyperglycemia over long periods of time

Screening indication: 10yo or puberty, q3y for overweight kids (BMI > 85%ile)
PLUS
- maternal hx of DM or GDM
- Fhx of T2DM in first-degree relative
- race/ethnicity
- signs/conditions of insulin resistance == acanthosis nigricans, HTN, dyslipidemia, PCOS

Management

  • insulin for kids with random BG> 250; HbA2c values > 9%
  • medical therapy + diet, exercise from time of diagnosis
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18
Q

Adjusted Glasgow coma scale for kids <5yo

A

A. Adjusted verbal response criteria [v. adult]
5 - Smiles, orientated to sounds, follows objects, interacts [oriented]
4 - Cries but consolable, inappropriate interactions [confused but able to answer questions]
3 - Inconsistently inconsolable, moaning [inappropriate words]
2 - Inconsolable, agitated [incomprehensible sounds]
1 - No verbal response

Others as normal: 
B. eye-opening response
4 - Eyes open spontaneously
3 - Eyes open to verbal command
2 - Eyes open to pain
1 - No eye opening

C. 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

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19
Q

What is the threshold for treatment in Glasgow score?

A

Total score = 15

GCS = 8 –> may require aggressive intervention and management

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20
Q

Differential diagnosis of vomiting, altered mental status

  • hx:
  • presenting sxs:
  • other sxs:
  • sxs that would NOT be seen:
A

LETHAL

1) DKA
- hx: enuresis, polydipsia
- presenting sxs (d/t acidosis): vomiting, tachypnea, vague diffuse abd pain
- other sxs: dehydration (vomiting, osmotic diuresis); altered mental status (dehydration, electrolyte abn); +/- concurrent cerebral edema
- sxs that would NOT be seen: fever

2) Toxic ingestion
- hx: got into the medicine cabinet.
- presenting sxs: vomiting, altered mental status, obtundation
- other sxs: dehydration (d/t vomiting), impaired oral intake (d/t AMS); tachypnea (if ASPIRIN); abd pain (Fe)

3) GI obstruction
- hx:
- presenting sxs: vomiting (+/- bilious); abd pain
- other sxs: dehydration (d/t vomiting)
- sxs that would NOT be seen: AMS (unless SEVERE dehydration)

4) increased intracranial pressure (ICP) ==> possible tumor causing central DI
- presenting sxs: vomiting
- other sxs: AMS, HA (prior to, accompanying)

5) pyelonephritis
- presenting sxs: vomiting
- other sxs: dehydration, urinary frequency
- sxs that would NOT be seen: polyuria (b/c the kidneys are being damaged)

LIKELY

1) gastroenteritis = most common cause of vomiting (viral/bacterial)
- presenting sxs: fever, colicky abd pain, diarrhea
- other sxs: dehydration

2) appendicitis
- presenting sxs: abd pain –>migrating to RLQ
- other sxs: vomiting

3) bacterial pneumonia ==> inflammation of pleura
- hx: for any child presenting with abd pain
- presenting sxs: abd pain
- other sxs: mild dehydration; diminished consciousness (if septic)

21
Q

A 9yo pt presents in DKA, with tachypnea. What is her acid-base status?

A

Purely metabolic acidosis

==> tachypnea as a normal physiologic response for acidosis in DKA (Kussmaul respirations)

22
Q

What further evaluation does a pt with newly diagnosed DM need?

A

==>increased risk of other autoimmune related dz

1) annual thyroid fx tests [AUTOIMMUNE THYROID DZ]
- -> once metabolic control has been established for several weeks –> can initially have baseline abn thyroid fx 2/2 non-thyroidal illness

2) TTG-IgA screening [CELIAC DZ]

23
Q

Management of vomiting, altered mental status and blood glucose abnormalities

A

1) ABCs
2) fluid bolus of NS at 20mL/kg over 60min

3) r/out LETHAL considerations on diffdx
- bedside fingerstick blood glucose ==> hypoglycemia, hyperglycemia d/t metabolic abnormality, toxic ingestion
- continuous CV monitor ==> response to therapy, monitor for cardiac rhythm problems
- UA ==> glucosuria, ketonuria for UTI/pyelo; toxins
- blood gas; electrolyte panel ==> metabolic abnormalities that need immediate correction

24
Q

DKA

  • management
  • treatment
A

HOSPITAL ADMISSION

  • baseline serum osmolality
  • baseline CBC + diff (b/c infection can precipitate DKA; nml increased WBC + left shift d/t DKA alone0
  • blood and/or urine Cx –> esp. with AMS, borderline hypotension, tachycardia
  • beta-hydroxybutyrate conc. –> to confirm ketoacidosis

NPO = until blood sugars, neurologic status, vomiting resolve.

1) continuous monitoring of vitals == during rehydration, electrolyte correction
2) q1h neuro checks == for cerebral edema
3) Strict I’s and O’s == hydration
4) insulin drip until acidosis resolved (bicarb >15, or normal AG) ==> then transition to subcutaneous insulin
5) LAB: Serum glucose q60min
6) LAB: Serum Ca, Mg, PO4 draw ==> usually depleted d/t urine losses; and monitor Ca as PO4 replenished
7) LAB: serum pH q60min ==> d/t metabolic acidosis; pH slowly rises with insulin +/- bicarb, AG, urinary and/or serum ketones
8) Urine dipstick for ketones ==> d/t metabolic acidosis; ketones slowly decreases with insulin

TREATMENT
1) IVF BOLUS with NS @ 20ml/kg over 60 min (any further would be at lower doses)
+
2) MIVF with NS, K == to correct low serum sodium, total K depletion (once know K levels)

3) IV Insulin drip (NOT BOLUS) ==> suppress lipolysis, ketogenesis
4) careful monitoring of glucose levels q30min - q1h –> ICU: altered mental status, persistent hypovolemia, increased risk of cerebral edema

5) dextrose free IV fluids + more isotonic solution + K + PO4
6) D10W, in isotonic

  • K repletion earlier IF –> EKG changes (peaked T waves)
25
Q

DKA

- treatment - WHAT NOT TO GIVE

A

bicarbonate; insulin bolus

==> paradoxical CNS acidosis and hypokalemia from rapid correction of acidosis
==> increased risk of cerebral edema

26
Q

most common cause of diabetes-associated death in children

A

cerebral edema d/t to DKA itself or from rapid overcorrection of dehydration

27
Q

fluid management: restoration of intravascular volume

A

==> 10-20mL/kg bolus of NS until patient urinates and/or improvement of VS (HR, BP) and mental status

28
Q

why do patients in DKA typically start urinating very shortly after providing fluid boluses? do you fix their dehydration that quickly?

A

NO
–> d/t osmotic diuresis (as occurs in DM when serum glucose > 180) ==> glucosuria, obligate loss of water, Na, K

so it’s WORSE b/c they’re in uncompensated diuresis

29
Q

fluid management: correct dehydration

A

degree of dehydration
mild = 3-5%
moderate = 6-10%
severe = 11-15%

rate of infusion determined by serum Na concentration/osmolarity

30
Q

fluid management: maintenance fluids

A

to replace daily insensible losses (perspiration, respiration) [40%]
+ normal urine output (2ml/kg/h for children <15kg; 1ml/kg/h for children > 15kg) [60%]

= 1/4 NS or 1/2 NS + D5W

31
Q

fluid management: replace ongoing losses

A

-monitor output (urine, stool, vomit and/or NGT), insensible losses (fever, tachypnea), vital signs

DIARRHEA == q4-6h with 1/2 NS

32
Q

insulin therapy regimens

A

1) BASAL INSULIN = intermediate / long-acting –> suppress hepatic glucose production, maintain normoglycemia in fasting state
2) PRANDIAL INSULIN = short-acting insulin just before meals and/or snacks for carb load

TRADITIONAL

  • 2/3 total dose in AM (1/3 short-acting, 2/3 intermediate-acting)
  • 1/6 of total at dinner (short-acting)
  • 1/6 of total before bed (intermediate-acting)

BASAL-BOLUS THERAPY

  • 1/2 total dose in PM (ultra-long-lasting = glargine)
  • 1/2 split among 3 meals

adjustments to insulin dosages needed during first weeks to months –> d/t “honeymoon period”

MEAL STRATEGIES –> improve blood sugar; decrease long-term complications.

  • ADA diet
  • carb counting
  • carb exchanges
33
Q

define: “honeymood period” of insulin treatment for diametes

A

T1DM = within 1 month of diagnosis and treatment ==> temporary remission of diabetes, where require little exogenous insulin

34
Q

in a child who may have an acute abdomen, Why should you ask mom to refrain from giving anything to the child by mouth? (Check all that apply.)

Multiple Choice Answer:
A she might need surgery
B Additional vomiting may worsen metabolic abnormalities
C Risk of aspiration

A

all of the above

risk of aspiration due to altered mental status

35
Q

define: Kussmaul resipration

A

classic pattern for DKA

pattern of rapid and DEEP breathing pattern d/t pt attempting to blow off excess CO2 in metabolic acidosis

==> most other causes of tachypnea (heart and lung disease) == reduced vital capacity == rapid, shallow respirations

36
Q

how to calculate adjusted serum sodium in presence of hyperglycemia

A

REASONS

1) will guide choice of fluid resuscitation
2) determine if hyperglycemia fully accounts for dilutional hyponatremia
3) combo of attenuated increase in measured Na and decrease in corrected Na ==> risk factor for developing cerebral edema

Corrected Na = {[(measured BG-100)/100]*1.6} + measured Na

37
Q

Isabella weighs 22 kg and is approximately 10% dehydrated. She then asks you: “So how much fluid will Isabella need over the next 24-48 hours in order to replace her current fluid deficit?”

A

If her currently weight is 22 kg and she is 10% dehydrated, then her pre-illness weight can be calculated with the following formula:

Pre-illness weight = Current weight / [(100 - % dehydrated) x 0.01] = 22 / [(100-10) x 0.01] = 24.44 kg.

Deficit = 24.44 kg (pre-illness weight) - 22 kg (current weight) = 2.44 kg of body weight = 2440 mL of estimated free water deficit.

38
Q

over what period of time is fluid deficit replaced in DKA? why?

A

48h

d/t hyperosmolarity
and risk for cerebral edema

should limit IV fluids to 1.5-2x maintenance (max)

39
Q

in DKA, why should yo make sure to use NS in first 4-6h?

A

==> to help slow rapid drop in serum osmolarity that occurs as serum glucose is lowered with rehydration and insulin

then can add dextrose to IV fluids when glucose <300mg/dL

40
Q

Which of the following are common signs and symptoms of cerebral edema? (Select all that apply.)

Multiple Choice Answer:
A Headache
B Recurrence of vomiting
C Hypotension
D Inappropriate slowing of heart rate (bradycardia)
E Tachycardia
F Rising blood pressures (hypertension)
G Decreased oxygen saturation (hypoxia)
H Restlessness, irritability
I Increased drowsiness (lethargy)
J Cranial nerve palsies: CN VI - Abducens nerve
K Abnormal pupillary responses: unequal pupils, fixed dilated pupils, absent response unilaterally or bilaterally
L Abdominal pain

A
HA
persistent vomiting
bradycardia
hypertension
hypoxia
restlessness, irritability
lethargy
cranial nerve palsies (esp. CN6 - abducens n)
abnormal pupillary responses = unequal pupils, fixed dilated pupils, absent response U/L or B/L
41
Q

what are potential management alternatives for a child with T1DM and why would they be used?

A

1) METFORMIN –> adjunct therapy for adolescents with T1DM + significant insulin resistance
2) PRAMLINITIDE + insulin to delay gastric emptying and inhibit release of glucagon
3) Immunotherapies

42
Q

what other studies should be ordered at this time in a patient newly diagnosed with diabetes? (Select all that apply.)

Multiple Choice Answer:
A Anti-pancreatic antibodies including insulin, GAD, and IA2
B Thyroid antibodies
C Thyroid function tests
D Anti-endomysial and tissue transglutaminase antibodies with a serum IgA level

A

A. T1DM autoantibodies
B. thyroid disorder
D. celiac disease

==> to test for other autoimmune conditions

43
Q

other educational priorities that need to be addressed prior to discharge.

Multiple Choice Answer:
A Symptoms of hypo- and hyperglycemia
B Blood glucose monitoring
C Treatment of hypo- and hyperglycemia
D Checking for ketones
E Long-term complications of uncontrolled diabetes mellitus
F Benefits of an insulin pump
G Instruction on an individualized meal plan
H Pathophysiologic differences between type 1 and type 2 diabetes
I Sick-day management (e.g., when Isabella has the flu)
J Reasons for and ways to contact their diabetes team

A

other educational priorities that need to be addressed prior to discharge.

  • Symptoms / treatment of hypo- and hyperglycemia
  • Blood glucose monitoring
  • Checking for ketones
  • Instruction on an individualized meal plan
  • Sick-day management (e.g., when Isabella has the flu)
  • Reasons for and ways to contact their diabetes team

the rest are eventually important, but not right now.

44
Q

Luanne is a 15-year-old female with three hours of abdominal pain and two episodes of non-bilious, non-bloody vomiting. She rates her pain at 8/10 and describes it as constant and located mainly in the middle of her belly, but somewhat present throughout her abdomen. It is worse with coughing and moving. She has never had this pain before, and has had no appetite since the pain started. She is sexually active with her boyfriend of three months, always uses condoms, and has not been tested for STIs. Her last menstrual period was two weeks ago. Vitals: 37.9 C, HR 100 bpm, BP 120/85 mm Hg, RR 14 bpm. On exam, she exhibits involuntary guarding, mild rebound tenderness, and tenderness to palpation between her right anterior superior iliac spin and umbilicus. On pelvic exam, she reports tenderness when attempting to palpate her right adnexa, but no masses are appreciated and there is no cervical motion tenderness. Her WBC and CRP are within normal limits. Based on the information above, what is the most likely diagnosis?

 Multiple Choice Answer:
A		Ovarian torsion	
B		Pelvic inflammatory disease	
C		Ectopic pregnancy	
D		Appendicitis
A

D. Appendicitis is the most common condition in children requiring immediate surgical intervention, but often (especially in infants) presents differently than in adults. Aspects of their atypical presentation include lack of migration of pain to the RLQ, negative Rovsing’s sign, and involuntary guarding and fever without perforation. School-age children who can articulate the pain often describe pain with movement or coughing (cat’s eye sign). Also, rebound tenderness was found to be neither sensitive nor specific in the pediatric population, while in the adult population it is one of the most accurate PE findings (86%). Luanne is of the older pediatric population, and so will present with a more typical appendicitis. Her sudden onset of intense pain at the umbilicus with vomiting, anorexia, and tenderness at McBurney’s point are all classic findings. The more atypical signs include diffuse pain centered below the umbilicus, and rebound tenderness that might point to a perforation (more likely, it is part of the atypical pediatric presentation given her normal WBC). Another atypical aspect of her exam is her adnexal pain during the pelvic exam, which could be due to the degree of inflammation and the positioning of her appendix. The key take-away point is to have a high index of suspicion for appendicitis in pediatric patients with abdominal pain given their atypical presentation.

2 weeks ago (NOT likely ectopic ==> 6-8w after last menstrual period)
rebound tenderness = peritoneal signs

Ovarian torsion is more common in the post-menopausal population, though it can present in any age group. It is described as intermittent stabbing pain in the lower abdomen or pelvis. Torsion is often secondary to an ovarian mass, such as a neoplasm or corpus luteal cyst, which may occasionally be appreciated on exam. Nausea and vomiting are very common findings as well. Ultrasound is essential to initial workup. Given Luanne’s pain localized around her belly button, her tenderness at McBurney’s point, and lack of palpable masses on pelvic exam, ovarian torsion is a less likely diagnosis.

45
Q

A 4-year-old girl with a history of type 1 diabetes mellitus was admitted to a local hospital for treatment of DKA. A few hours after the treatment, she develops grunting, irregular respirations, and has vomited twice. On exam, her left eye is pointing downward and out on straight gaze. Her diastolic blood pressure is 90 mmHg. What is a likely diagnosis?

 Single Choice Answer:
Please select one answer.  
A		Hypoglycemia	
B		Hypokalemia	
C		Hyponatremia	
D		Pneumonia with possible sepsis	
E		Cerebral edema
A

E. DKA

irregular respirations

focal neurological deficits
cerebral edema?

Administration of bicarbonate during DKA treatment increases the risk of cerebral edema. Although symptomatic cerebral edema is rare (less than 1%), it is associated with a high mortality rate (over 20%). The signs of cerebral edema are described in the vignette, and include irregular respirations, headache, vomiting, third nerve palsy, and high blood pressure.

46
Q

A 9-year-old female is brought to clinic by her mother because of two days of abdominal pain and vomiting. She has vomited six times today and has had decreased appetite, but no diarrhea, fevers, sick contacts, or changes in diet. Her mom states that she has been otherwise healthy apart from increased thirst and occasional bedwetting over the last few weeks. Of note, patient’s maternal grandmother suffers from celiac disease. On exam, patient is afebrile and has a HR of 180 bpm, BP 90/60 mmHg, RR 50 bpm, and O2 saturation of 98%. She is lying in bed appearing slightly drowsy, taking rapid, deep breaths and is slow to respond to questions. Her heart and lung exams are normal apart from being tachycardic, and abdominal exam reveals mild diffuse tenderness to palpation with no rebound or guarding. Which of the following would be the most appropriate next step in management?

 Single Choice Answer:
Please select one answer.  
A		Chest x-ray	
B		Urine culture	
C		Fingerstick glucose	
D		Abdominal ultrasound	
E		Gastric lavage
A

C

thirst, bedwetting == T1DM + DKA
FHx Celiac
deep, slow breaths

Obtaining a fingerstick glucose is the diagnostic step with the highest yield since the patient’s clinical picture is strongly indicative of diabetic ketoacidosis (DKA). DKA is a condition more closely associated with type 1 (rather than type 2) diabetes, and is formally diagnosed if a random glucose is > 200 mg/dL, venous pH is < 7.3 and/or bicarbonate < 15 mEq/L and there is ketonemia or ketonuria. Patients in DKA can present with abdominal pain and vomiting secondary to metabolic acidosis that stems from ketonemia and lactic acidosis. Furthermore, osmotic diuresis from hyperglycemia may contribute to dehydration, which can manifest as tachycardia, hypotension, and altered mental status. In an attempt to compensate for the metabolic acidosis, the patient may also present as tachypneic with characteristic Kussmaul respirations (rapid, deep breaths). This patient’s history of polydipsia, enuresis, and family history of autoimmune disease (including celiac disease and Hashimoto’s thyroiditis) suggest that the patient has type 1 diabetes. Her current vital signs and general state of lethargy also point towards DKA and should be confirmed with a fingerstick glucose (in addition to other tests).

47
Q

A 9-year-old male presents to the ED in an ambulance after he was found unconscious at a local playground. In the ED he is arousable but extremely obtunded. He is able to minimally verbalize that his head hurts and his stomach feels uncomfortable. He states the pain is constant and non-radiating. He vomits clear liquid twice over the course of 30 minutes. Vital signs are as follows: T 37.6 C, P 66 bpm, BP 155/80 mm Hg, RR 18 bpm. You further notice that his breathing is irregular with brief episodes of apnea. On physical exam you are unable to reproduce the abdominal pain and there is no rebound tenderness or guarding. The rest of the physical exam is unremarkable. What is the most likely diagnosis?

 Single Choice Answer:
Please select one answer.  
A		DKA	
B		Appendicitis	
C		Intracranial hemorrhage	
D		Gastroenteritis	
E		Small bowel obstruction
A

C. Increased ICP can be secondary to epidural or subdural hemorrhage. It is possible the patient may have fallen while playing in the playground. Increased ICP can present as the classic Cushing’s triad: hypertension, inappropriate slowing of the heart rate, and irregular respirations (Cheyne-Stokes respiration). A further complication of increased ICP is epigastric discomfort. This is caused by the elevated ICP causing vagal stimulation, resulting in the secretion of gastric acid. Lastly, the patient’s headache and non-bilious vomiting can also be ascribed to the increased ICP.

unconscious, abdominal pain, vomiting
non-reproducible pain
Cheyne-stokes breathing pattern (NOT Kussmaul)

patient with DKA one would expect increased adrenergic tone leading to tachycardia, not inappropriate slowing of the HR. Secondly, the patient’s breathing pattern is more consistent with Cheyne-Stokes respirations, not Kussmaul breathing. Kussmaul breathing is typically characterized by deep breaths that may be rapid, normal or slow in rate without periods of apnea, often associated with metabolic acidosis. Lastly, one would expect signs or symptoms consistent with dehydration such as polyuria, polydipsia, decreased skin turgor, or skin tenting. However, the altered mental status, vomiting, headache, and abdominal pain could be seen in DKA.

48
Q

A 7-year-old boy is brought by ambulance to the ED with altered consciousness. The EMT said he found the boy in a pool of vomit. He is unable to answer questions coherently and he is alone. Physical exam findings indicate dry mucous membranes, tachypnea, tachycardia, and moaning on palpation of the abdomen. His physical exam is otherwise normal, including a normal blood pressure. What is the most likely cause of his condition?

 Single Choice Answer:
Please select one answer.  
A		Appendicitis	
B		DKA	
C		Narcotic overdose	
D		Non-accidental trauma	
E		Sepsis
A

B. DKA typically presents with altered mentation, vomiting, dehydration, and abdominal pain. The history will yield polydipsia and polyuria during the days preceding DKA. Metabolic acidosis causes tachypnea as the body tries to blow off CO2 through a compensatory respiratory alkalosis.

vomiting, obtunded
dehydrated

If narcotics pinpoint pupils, decreased RR, bradycardia

if appendicitis = abodminal pain
. Appendicitis would rarely present with altered consciousness. The usual history with appendicitis is onset of periumbilical pain that persists over hours, migrating to the right lower quadrant. Vomiting could be present, and tachycardia may be present due to pain or dehydration, but altered mental status would be unusual. On physical exam, peritoneal signs may be present as well as psoas, obturator, or Rovsing’s sign.

if sepsis =more hyperdynamic vitals

49
Q

A 9-year-old male is brought to the ED in a coma secondary to diabetic ketoacidosis. Which of the following laboratory results would NOT likely be found in this patient?

 Single Choice Answer:
Please select one answer.  
A		Anion gap of 20 mEq/L	
B		Potassium of 3.3 mEq/L	
C		Venous pH of 7.1	
D		Sodium of 132 mEq/L	
E		Creatinine of 1.0 mEq/L
A

B

anion  gap metabolic alkalosis
normal K
low venous pH
Low Na
High Cr (dehydrated), BUN

in diabetic ketoacidosis, the acidosis and lack of insulin cause potassium to leave cells and enter the serum, causing an elevated serum potassium level. However, as the DKA is corrected and insulin is administered, the potassium will re-enter the cells, causing a decreased serum potassium level, so potassium levels should be monitored closely when therapy is initiated