16: 7-year-old female with abdominal pain and vomiting Flashcards

1
Q

Children have a higher risk of dehydration than adults because they have

A
  • Higher surface area:body mass ratio; hence, a greater relative area for evaporation to occur
  • Higher basal metabolic rates than adults, which generates heat and expends water, and
  • Higher percentage of body weight that is water (in infants, 70% of body weight is water; in children, 65%; and in adults, 60%).
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2
Q

The diagnostic criteria for DKA are:

A
  • A random blood glucose of > 200 mg/dL (> 11.1 mmol/L)
  • A venous pH < 7.3 or serum bicarbonate < 15 mEq/L (< 15 mmol/L), and
  • Moderate or large ketonuria or ketonemia.
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3
Q

four ways to diagnose diabetes mellitus

A
  1. A patient may be diagnosed with diabetes if he/she has symptoms of diabetes (polyuria, polydipsia, and unexplained weight loss) plus a random (any time of day, without regard to time since last meal) plasma glucose concentration > 200 mg/dL (11.1 mmol/L).
  2. A patient can also be diagnosed with diabetes mellitus with a fasting (no caloric intake for at least 8 hours) blood glucose > 126 mg/dL (7.0 mmol/L).
  3. A patient can also be diagnosed with diabetes mellitus with a 2-hour postload glucose of > 200 mg/dL (11.1 mmol/L) during an oral glucose tolerance test.
  4. A HbA1c ≥ 6.5% in an adult is diagnostic of diabetes. T
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4
Q

DKA should be suspected in pediatric patients who present with the following signs and symptoms

A
Vomiting
Weight loss
Dehydration
Shortness of breath
Abdominal pain, or
Change in the level of consciousness.
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5
Q

When circulating blood glucose levels reach ~180 mg/dL

A

an osmotic diuresis occurs, leading to hypovolemia, dehydration, and a loss of sodium, potassium, and phosphate in the urine

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6
Q

Laboratory Abnormalities in DKA

A
  • pH on a venous blood gas dec
  • serum Na dec
  • K nml
  • bicarb dec
  • Cr elevated
  • serum glucose elevated
  • serum ketones and urine ketones elevated
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7
Q

Types of dehydration: Isotonic/Isonatremic (Na = 130-150 mEq/L [130-150 mmol/L])

A
  • This is the m/c type of dehydration in children and occurs when sodium and water losses are balanced, including children presenting with acute gastroenteritis and diarrhea.
  • Typically the deficit in isonatremic dehydration can be replaced over 12 hours.
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8
Q

Types of dehydration:

Hypotonic/Hyponatremic (Na < 130 mEq/L [< 130 mmol/L])

A
  • This type of dehydration occurs when sodium losses exceed those of water.
  • This most commonly occurs when patients consume diluted fluids or water in the face of dehydration.
  • Hyponatremia may also be the result of adrenal insufficiency.
  • The deficit in hyponatremic dehydration is typically replaced evenly over 24 hours.
  • Rapid correction of hyponatremia is associated with central pontine myelinolysis (a neurologic disease caused by damage of the myelin sheath of nerve cells in the brainstem, more precisely in the area termed the pons, the most common cause of which is the too-rapid correction of hyponatremia.
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9
Q

Types of dehydration: Hypertonic/Hypernatremic (Na > 150 mEq/L [> 150 mmol/L])

A
  • This type of dehydration occurs when water losses exceed that of sodium and is associated with the highest mortality.
  • Possible causes of hypernatremic dehydration include breastfeeding failure, use of inappropriate rehydration solutions (boiled milk), and diabetes insipidus.
  • The deficit in hypernatremic dehydration is typically replaced evenly over 48 hours.
  • Too-rapid correction of hypernatremia is associated with the development of cerebral edema.
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10
Q

The pathophysiology of cerebral edema is poorly understood, but epidemiologic research has identified several risk factors:

A
  • High BUN concentration at presentation
  • Profound acidosis with hypocapnia
  • Attenuated rise in the measured serum sodium with treatment, and
  • Administration of bicarbonate.
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11
Q

T2DM Risk Factors

A
  • 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
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12
Q

Using the Glasgow Coma Scale, a score is assigned in each of three categories

A

Best eye-opening response
Best verbal response
Best motor response

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13
Q

Adjusted verbal response criteria for children under the age of 5 years:

A

5 - Smiles, orientated to sounds, follows objects, interacts
4 - Cries but consolable, inappropriate interactions
3 - Inconsistently inconsolable, moaning
2 - Inconsolable, agitated
1 - No verbal response

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14
Q

In a patient with dehydration and tachycardia

A

resuscitation with an IV fluid bolus is crucial. Fluid resuscitation should begin quickly with an IV fluid bolus of isotonic (0.9%, aka normal, saline) at 20 mL/kg over 60 minutes to begin to restore intravascular volume.

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15
Q

next step is to try to identify or exclude the potentially life-threatening conditions on the differential diagnosis

A
  • -A bedside capillary blood glucose measurement (fingerstick) will quickly identify two treatable causes of altered mental status, hypo- and hyperglycemia. The presence of hypoglycemia could point to a metabolic abnormality or toxic ingestion as potential causes.
  • -Placing such a pt on a continuous CV monitor is important for monitoring response to therapy and identifying potentially lethal cardiac rhythm disturbances
  • -A UA will be helpful in quickly identifying glucosuria or ketonuria or suggesting urinary tract/kidney infection. Urine may also be sent for evaluation of toxins.
  • -A blood gas and electrolyte panel will identify metabolic derangements that need immediate correction, and may also help to make the diagnosis.
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16
Q

Insulin Administration

A
  • An insulin drip (0.1 units/kg/hour) should be started after the patient has received initial volume expansion, usually about 1 hour after starting fluids. (An insulin drip is typically started at the same time as maintenance plus replacement IV fluids.)
  • Bicarbonate should not be given routinely because of the well-described paradoxical CNS acidosis and hypokalemia from rapid correction of acidosis. In addition, bicarbonate administration has been associated with an increased risk of cerebral edema, the most common cause of diabetes-associated death in children.
  • Although K should be added eventually to the IV fluids, it should not be added until the serum K level is known.
  • An insulin bolus is generally not recommended in children because it has also been associated with an increased risk of cerebral edema and could cause the glucose to drop too rapidly.
  • After the initial fingerstick, glucose levels should be monitored carefully (every 30 minutes to 1 hour initially).
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17
Q

Provide bolus fluids to restore intravascular volume

A

This is accomplished with a 10-20 mL/kg bolus of 0.9% saline (isotonic or “normal” saline). The general recommendation for patients who are not in DKA or renal failure is to provide serial boluses until the patient urinates. However, patients in DKA typically start urinating very shortly after providing fluid boluses due to osmotic diuresis (this occurs in diabetes when the serum glucose concentration exceeds the renal threshold for glucose reabsorption [> 180mg/dL], leading to glucosuria and obligate loss of water, sodium and potassium, not because they have received enough resuscitation fluids. Therefore, patients in DKA should be monitored for improvement of their vital signs (normalized heart rate and blood pressure) and mental status.

18
Q

correct dehydration

A

The amount of fluid required to replace the patient’s deficit is dictated by your assessment of the degree of dehydration (3-5%, 6-10% or 11-15%). The composition of fluid (0.3% saline, 0.45% saline, 0.9% saline, etc.) and rate of infusion is 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.

19
Q

Provide maintenance fluids

A

In addition to the fluids required to replace the fluid deficit, patients with dehydration must also be provided with maintenance fluids. Maintenance fluids replace daily insensible losses (perspiration and respiration) and normal urine output (approximately 2.0 mL/kg/hr for children < 15 kg and 1.0 mL/kg/hr for children > 15 kg and adults). Insensible losses account for approximately 40% of daily maintenance needs, while normal urine output accounts for about 60%. In general, 0.25% saline (1/4 normal saline) or 0.45% saline (1/2 normal saline) with 5-10% dextrose is used to provide maintenance fluids.

20
Q

Replace ongoing losses

A

In many patients with dehydration, the losses may continue, even after replacement therapy has begun. Therefore, careful attention must be paid to monitoring the patient’s output and vital signs, to determine the need for additional replacement. The amount and type of replacement fluid is determined by the source of the losses. For example, in gastroenteritis with ongoing diarrhea, stool output that exceeds 1.0 g/kg/hr should be replaced every 4 to 6 hours with 0.45% saline (1/2 normal saline). Additional examples of ongoing losses are emesis, nasogastric tube output, increased insensible losses due to fever, and tachypnea.

21
Q

There are three methods of calculating maintenance fluids

A

By caloric expenditure
By body surface
The Holliday-Segar method

22
Q

The Holliday-Segar method is probably the easiest to remember.

A
  • -100 mL/kg/day for the first 10 kg of body weight
  • -50 mL/kg/day for the second 10 kg of body weight
  • -20 mL/kg/day for each additional 1 kg of body weight
23
Q

Admission Orders for Patient in DKA

A
  • continuous monitoring of vitals
  • hourly neuro checks
  • monitors I and Os
  • insulin orders
  • –Patient will continue on the insulin drip until the acidosis has resolved (bicarbonate > 15 mEq/L [> 15 mmol/L] or a normal anion gap) and the patient is ready to transition to subcutaneous insulin.
  • serum glucose every 60 mins
  • serum ca, mg, and phosphorous now
  • check serum pH (VBG) every 60 mins
  • urine dipstick for ketones
24
Q

every insulin regimen has the same two components:

A
  • -Basal insulin: An intermediate- to long-acting preparation to suppress hepatic glucose production and maintain normoglycemia in the fasting state.
  • -Prandial insulin: Doses of short-acting insulin taken before meals and/or snacks to cover the expected carbohydrate load from the food intake.
25
Q

Traditional Regimen

A

2/3 of the total dose in the morning (1/3 rapid or short-acting, 2/3 intermediate-acting [e.g., 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.

26
Q

“Basal-bolus” Therapy

A
  • -Half of the total daily dose is given in the form of an “ultra-long-acting” basal insulin given at bedtime (e.g., insulin glargine, which lasts for upwards of 24 hours), and
  • -Half is split evenly among all 3 meals.
27
Q

The initial total daily dose of insulin varies with weight, age, pubertal status, and presence or absence of DKA.

A
  • -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.
28
Q

Patients with type 1 diabetes have an increased risk of

A

other autoimmune related diseases, with autoimmune thyroid disease and celiac disease being the most common

29
Q

Differential Diagnosis of Vomiting and Altered Mental Status: DKA (1/8)

A
  • -Vomiting-usually precipitated by the acidosis-is often a presenting symptom, as are increased respiratory rate and vague abdominal pain.
  • -A preceding history of enuresis and polydipsia is strongly suggestive of newly presenting diabetes.
  • -Unless a coincident infection precipitates ketosis and thus a presentation for medical evaluation, one does not expect to see fever in a child with DKA.
  • -Diffuse abdominal pain is characteristic, a consequence of the ongoing acidosis.
  • -Significant dehydration is a prominent feature due to a combination of vomiting and osmotic diuresis.
  • -AMS is often a result of dehydration and/or electrolyte abnormalities; its presence should make one consider whether or not there is concurrent cerebral edema.
  • -Tachypnea is a normal physiologic response to attempt to compensate for the acidosis in DKA, which is purely a metabolic acidosis.
30
Q

Differential Diagnosis of Vomiting and Altered Mental Status: Toxic ingestions (2/8)

A
  • -Toxic ingestion often results in 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.
  • -Aspirin overdose may present with tachypnea.
  • -Abdominal pain may be seen in toxic ingestions-in an overdose of iron, for example.
31
Q

Differential Diagnosis of Vomiting and Altered Mental Status: GI obstruction (3/8)

A
  • -Vomiting, sometimes bilious, is commonly seen in GI obstruction.
  • -Almost all patients with obstruction will be dehydrated; the degree of dehydration depends on degree of vomiting.
  • -Abdominal pain is a prominent feature of GI obstruction.
  • -Altered mental status is unlikely unless dehydration is severe.
32
Q

Differential Diagnosis of Vomiting and Altered Mental Status: Inc ICP (4/8)

A

> > Increased ICP often presents with vomiting.
Rarely, a tumor might cause a central diabetes insipidus.
A patient with increased ICP may exhibit an altered level of consciousness, often preceded/accompanied by headache.

33
Q

Differential Diagnosis of Vomiting and Altered Mental Status: Gastroenteritis (5/8)

A
  • -Gastroenteritis is the most common cause of vomiting; it may be viral or bacterial.
  • -It usually also presents with fever, colicky abdominal pain, and diarrhea.
  • -Dehydration is common in gastroenteritis.
34
Q

Differential Diagnosis of Vomiting and Altered Mental Status: Appendicitis (6/8)

A

–Abdominal pain is a prominent symptom of appendicitis, classically migrating to the RLQ

35
Q

Differential Diagnosis of Vomiting and Altered Mental Status: Bacterial PNA (7/8)

A
  • -The possibility of pneumonia should be investigated in any child presenting with abdominal pain (can be caused by inflammation of the pleura).
  • -If the patient becomes septic, can see a diminished level of consciousness.
  • -Signs of dehydration, if present, are mild.
36
Q

Differential Diagnosis of Vomiting and Altered Mental Status: Pyelonephritis (8/8)

A

> > Vomiting may be seen in pyelonephritis and may lead to dehydration.
It would be important to distinguish between urinary frequency-which one might expect in the case of pyelonephritis-and polyuria, which should not commonly be present.

37
Q

signs of cerebral edema

A

irregular respirations, headache, vomiting, third nerve palsy, and high blood pressure.

38
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?

A

This is the correct choice. 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.

39
Q

most common causes of a small bowel obstruction

A

adhesions from a previous surgery or a hernia

40
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?

A

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.

41
Q

Potassium in DKA

A

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.