|
1. Diabetic ketoacidosis is a potentially life-threatening medical condition thaT complicates insulin dependent diabetes. A true statement regarding diabetic ketoacidosis is: A. The metabolic acidosis is a ketoacidosis and hence is always a high anion gap metabolic acidosis B. The degree of acidosis is closely related to the degree of hyperglycemia C. The degree of anion gap bears no relationship to the degree of azotemia D. Patients presenting with diabetic ketoacidosis and a normal anion gap recover from acidosis more rapidly if bicarbonate is used in place of chloride in the intravenous fluids E. Because diabetic ketoacidosis is a catabolic state, it is accompanied by a shift of extracellular phosphate into the intracellular space 2. In children with established insulin dependent diabetes, the most common precipitating factor for diabetic ketoacidosis is: A. Inadvertent or deliberate omission of insulin B. Severe emotional stress C. Infection D. Use of drugs E. None of the above 3. The degree of cerebral obtundation during diabetic ketoacidosis correlates most closely with the degree of: A. Hyperosmolality B. Hyponatremia C. Acidosis D. Hypophosphatemia E. Hyperapnea 4. A 4-year-old with insulin dependent diabetes presented to the emergency department with fever and Kussmaul respirations; blood glucose is 600mg/dl and arterial blood gases show: pH of 7.1, bicarbonate of 7 mEq/l, serum sodium is 129 mEq/l. Therapy with intravenous saline (0.9 NaCl) and insulin is initiated. Within a few hours clouded sensorium is noted. Appropriate statements pertaining to this clinical scenario include: A. Deepening coma during diabetic ketoacidosis treatment is more likely in children B. Antibiotics should be given during the initial resuscitation phase in this patient C. If the patient’s neurologic status fails to improve, a cranial CT scan of the head needs to be done D. Intracranial pressure monitoring need not be instituted at this time E. All of the above 5. Which of the following has been shown to occur in proportion to the severity of brain injury: A. Hyperglycemia B. Coagulopathy C. Both D. Neither 6. Hypoglycemia is a life-threatening medical emergency that requires immediate attention. One measure used is the administration of glucagon. Glucagon is likely to be effective against hypoglycemia in which of the following clinical conditions: A. Starvation B. Ketotic hypoglycemia C. Glycogen storage disease D. Cirrhosis with hepatocellular failure E. None of the above 7. Which of the following statements is true regarding hypoglycemia in newborns, infants and children: A. A neonate may need up to 20 mg/kg/min of glucose in the perioperative period to maintain normoglycemia B. Hepatic glycogen stores fall by 90% in the first 3 postnatal hours C. Hypoglycemia due to documented high insulin levels that is resistant to medical therapy warrants a consideration for laparotomy D. Ketotic hypoglycemia is the most common form of childhood hypoglycemia E. All of the above 8. Regarding water homeostasis, which of the following statements is inaccurate: A. The maximum effect of arginine-vasopressin is to produce a urine osmolality of 1400 mOsmol/l and a urine output of 0.5 ml/kg/hr B. In the absence of arginine-vasopressin, urine flow will stabilize at 5 ml/kg/hr and with an osmolality of 300 mOsmol/l C. An infusion of DDAVP should be initiated as soon as the diagnosis of diabetes insipidus is made with the goal of establishing a urine osmolality double that of plasma and a urine output of 2 ml/kg/hr D. In the setting of global cerebral insult, the development of diabetes insipidus will most likely be followed by death in 1-5 days E. In the absence of osmotic diuretics, urine osmolality of < 300 mOsmol/l when the serum osmolality is > 295 mOsmol/l is high suggestive of diabetes insipidus 9. Match the diagnosis with its most likely description from below: A. Diabetes insipidus B. Osmotic diuresis C. Non-oliguric renal failure D. Fluid overload ____ Urine osmolality is 268 mOsmol/l and plasma osmolality is 327 mOsmol/l ____ Polyuria with a urine specific gravity of 1.008 and a plasma osmolality of 275 mOsmol/l ____ Urine osmolality of 297 mOsmol/l and plasma osmolality of 299 mOsmol/l ____ Fraction of excretion of sodium of 3 10. Match the most likely diagnosis with the following urine measurements: Urine Urine Urine/Plasma Na+ (mEq/l) FENA+(%) Osmolality Osmolality
______________ ____________
_____________ ________________ A. < 10 < 1 > 500 > 1.59 B. > 60 > 2.98 298 1.008 C. > 80 > 1.98 695 2 ____ Rotavirus gastroenteritis with profuse diarrhea ____ Hemolytic uremic syndrome (HUS) ____ Syndrome of inappropriate anti-diuretic hormone secretion (SIADH) 11. A newborn is admitted to the Pediatric ICU for hypoglycemia. Physical examination is significant for hepatomegaly. The urine does not reveal ketonuria and toxic screening is reported to be negative. The most likely etiology for this patient is: A. Endocrinopathies B. Storage disease C. Chemicals/toxins D. Ketotic hypoglycemia 12. Precautions that must be taken when measuring ionized Calcium include all of the following except: A. Blood must be collected aerobically B. Blood must be collected anaerobically C. Red blood cells must be quickly removed D. Anti-coagulants that complex with calcium must be avoided Click here for answer13. With regard to hypercalcemia in the Pediatric ICU, all of the following statements are true except: A. Lack of weight-bearing is the most important factor in the hypercalcemia associated with immobility and is more severe in children B. Total serum calcium of < 15 mg% is regarded as “not acutely life-threatening” C. Hypercalcemia is protective against digitalis toxicity D. When hyperparathyroidism is suspected as the etiology of the hypercalcemia, mithromycin should be avoided if surgery is anticipated E. When using phosphate for treatment of hypercalcemia, the product of the concentration of calcium and phosphorus should be kept below 60 14. A 9-year-old boy is admitted to the Pediatric ICU with hypocalcemia with an ionized calcium level of 0.7 mmol/L. The hypocalcemia has been resistant to administration of repeated doses of intravenous calcium chloride. Under these circumstances, which of the following management strategies would be considered least appropriate: A. Hypomagnesemia must be considered B. Hypoparathyroidism must be considered C. Vitamin D insufficiency must be considered D. Mg SO4 is preferred to MgCl in this setting E. Rapid magnesium infusion leads to a poor clinical response since peak magnesium level is associated with a peak in renal excretion 15. Appropriate statements regarding treatment of hypomagnesemia in the intensive care setting include all of the following except: A. The daily requirement is in the range of 0.3 – 0.4 mEq/kg/day intravenously B. If the glomerular filtration rate is reduced, magnesium replacement may result in hypermagnesemia C. Intravenous magnesium is best delivered as a rapid bolus to achieve a high peak serum level D. Aminoglycosides are a recognized cause of hypomagnesemia 16. Clearance of which of the following drug(s) is/are dependent on hepatic blood flow: A. Propranolol and labetalol B. Lidocaine and nitroglycerine C. Morphine and verapamil D. All of the above E. None of the above 17. Regarding intravenous steroid preparations, which of the following is the most appropriate statement: A. Dexamethasone has the largest sodium retaining property and hydrocortisone the least B. When anti-inflammatory properties and relative hypovolemia are desired, dexamethasone is the agent of choice C. The anti-inflammatory properties of hydrocortisone do not increase when higher doses of hydrocortisone are used D. For the patient in shock and adrenal insufficiency, hydrocortisone is inappropriate E. Synthetic steroids compared with hydrocortisone are more avidly protein-bound and undergo faster hepatic degradation A. Congenital adrenal hypoplasia B. Pyloric stenosis C. Both D. Neither 18. ____ Hyponatremia ____ Metabolic acidosis ____ Emergency administration of “stress” doses of glucocorticoids is unlikely to be detrimental 19. Drugs known to cause adrenal suppression include: A. Ketoconazole B. Bactrimâ C. Etomidate D. All of the above 20. A 12-year-old is admitted to the Pediatric ICU with intractable shock, with a poor response to volume administration. You suspect adrenal insufficiency. All of the following statements pertaining to this diagnosis are true except: A. With long term steroid use, hypothalamic-pituitary-adrenal axis suppression can be minimized by steroid administration in the morning B. Reliable evidence regarding adrenal suppression can be obtained by the 30-minute ACTH stimulation test C. Clinically significant hypothalamic-pituitary-adrenal axis suppression does not occur with prolonged use of 12 mg/m2/day of cortisol D. Dexamethasone administration will interfere with subsequent measurement of cortisol E. Methyl prednisolone interferes with the protein displacement method but not with the common radioimmune assay method of cortisol determination 1.
D An increased anion gap is usually
present with greater pre-renal azotemia, and not directly related to
hyperglycemia. The shift of
extracellular phosphate into the intracellular space does not occur until
diabetic ketoacidosis is reversed by the administration of insulin and fluids.
(Rogers MC, et al. Textbook of
Pediatric Intensive Care, 3rd Edition; pp 1263-1264; Adrogue H,
Wilson H, Boyd A. Plasma acid-based patterns in diabetic ketoacidosis.
N Engl. J Med 1982; 307:1603) 2.
A In most children with a diagnosis
of diabetes mellitus who develop diabetic ketoacidosis, the precipitating event
is an omission of insulin, whether inadvertent or deliberate.
The other causes are also possible, but not as likely.
(Rogers MC, et al. Textbook
of Pediatric Intensive Care, 3rd Edition; pp 1261) 3.
A
Hyperosmolality has also been
associated with EEG changes during diabetic ketoacidosis.
The mortality in children with cerebral edema from diabetic ketoacidosis
can approach 80%. An increased risk
is present for children less than 5 years of age who have a new diagnosis of
diabetes mellitus complicated by a prolonged untreated case of diabetic
ketoacidosis. Aggressive
rehydration, especially with hypotonic fluids, may acutely decrease an already
hyperosmolar state in the child precipitating a picture of cerebral edema.
(Rogers MC, et al. Textbook of
Pediatric Intensive Care, 3rd Edition; pp 1266-1267; Krane EJ, Walman
JK, Walsdorf JI. Some clinical
brain swelling in children during treatment of diabetic ketoacidosis. N Engl J Med 1985; 316:857) 4.
E Intravenous antibiotics should be
administered pending lumbar puncture. Progressive deterioration of mental status
in this patient would be an indication to obtain a cranial CT scan to evaluate
for cerebral edema. As stated in
the rationale in Question 1 above, children under the age of 5 newly diagnosed
with diabetes mellitus and who also have a complicated course of diabetic
ketoacidosis, have an increased risk of cerebral edema. Airway
and primitive reflexes should be monitored with the possibility of early
intubation, if any question of those is compromised.
(Rogers MC, et al. Textbook
of Pediatric Intensive Care, 3rd Edition; pp 1267-1269) 5.
C It is not uncommon to have
hyperglycemia in association with a head injured child.
Most likely, as a result of an increase in catecholamines and
corticosteroids, there is an increase in blood sugar. Hyperglycemia has already been shown to be associated with
the degree of severity in brain injury. Some
data suggests that ischemic brain injury may be worse in those patients who have
hyperglycemia in their recovery phase as opposed to those patients who had
normoglycemia. Any coagulopathy
which may exacerbate an ischemic picture also may worsen the severity of brain
injury. (Rogers MC, et al. Textbook
of Pediatric Intensive Care, 3rd Edition; pp 1271-1272; Pulsinelli W,
Levy D, Sigsbee B, et al. Increased damage after ischemic stroke in patients with
hyperglycemia with or without established diabetes mellitus.
Am J Med 1983; 74:540) 6.
E The first step in the treatment of
hypoglycemia in a child is initiation of dextrose bolus followed by an infusion
of 10% dextrose. All of these
conditions are characterized either by the inability to release glycogen from
the liver or depletion of glycogen from the liver, and therefore, glucagon is
unlikely to be effective. (Rogers MC, et al.
Textbook of Pediatric Intensive Care, 3rd Edition; pp
1273-1274; Kogut M. Hypoglycemia:
pathogenisis, diagnosis and treatment. In Gluck L, Kone T, Dodge P, eds.
Current problems in pediatrics. Chicago:
Yearbook, 1974, 3) 7.
E The stimulus for the mechanisms
which elevate blood glucose in the setting of hypoglycemia is primarily CNS
hypoglycemia. The body’s measures
which help to remedy hypoglycemia are primarily the release of epinephrine and
glucogon with their effects being additive.
The neonate requires a considerable amount of glucose, especially in the
perioperative period. There is a
significant decline in glycogen storage within the liver within the first 3
post-natal hours. If hypoglycemia
is resistant to medical therapy, a laparotomy may be indicated to determine the
presence of a tumor or subtotal pancreatectomy. Ketonic hypoglycemia is the most common form in children.
(Rogers MC, et al. Textbook of
Pediatric Intensive Care, 3rd Edition; pp 1272-1275; Mozam F, Rodgers
B, Talbert J et al. Near-total
pancreatectomy in persistent infantile hypoglycemia. Arch Surg 1982; 117:1151) 8.
B Maximum effects of arginine
vasopressin result in an osmolality of 1400 mOsmol/l with a urine output of 0.5
ml/kg/hr. It is important to
initiate DDAVP treatment as soon as diabetes insipidus is made as the diagnosis,
to prevent large surges in fluid loss. The
goal is to double the urine osmolality in comparison to the plasma and obtain a
urine output of 2 ml/kg/hr. Death
can occur within 1-5 days after the presentation of diabetes insipidus with
cerebral insult. Low urine
osmolality (< 300 mOsmol/l) and serum osmolality > 295 mOsmol/l is
consistent with a diagnosis of diabetes insipidus without the presence of any
osmotic diuretics. In the
absence of ADH hormone, the urine flow will continue to increase in the range of
15-20 ml/kg/hr with a significant increase in serum osmolality. (Rogers MC, et
al. Textbook of Pediatric Intensive
Care, 3rd Edition; pp 1275-1280) 9.
A, D, B, C Fluid overload leads to
polyuria accompanied by plasma hypoosmolality.
With osmotic diuresis, the urine osmolality remains close to that of
plasma. In the absence of osmotic
diuretics, when the plasma osmolality is more than 295 mOsmol/l, while the urine
osmolality remains 300 mOsmol/l or less, the diagnosis of DI is very likely.
(Rogers MC, et al. Textbook of
Pediatric Intensive Care, 3rd Edition; pp 1275-1280) 10.
A, B, C Gastroenteritis has minimal
urine sodium losses. It maintains a
relatively high urine/plasma osmolality. There
is a significant degree of urine sodium losses in hemolytic-uremic syndrome.
With a high FEna (>3%), a urine osmolality of approximately
300 mOsmol/l and a 1:1 urine/plasma osmolality, a syndrome of inappropriate
antidiuretic hormone secretion has the highest amount of urine sodium losses
with a very high urine osmolality, and 2:1 urine/plasma osmolality. (Rogers MC,
et al. Textbook of Pediatric Intensive Care, 3rd Edition;
pp 1276-1278) 11.
B
With the lack of ketonuria, a
negative toxicology screen and significant hepatomegaly on exam, the diagnosis
is most likely the result of a storage disease. (Rogers MC, et al.
Textbook of Pediatric Intensive Care, 3rd Edition; pp
1272-1275) 12.
A Blood should be collected
anaerobically because CO2 loss can alter the pH, and therefore,
affect the binding of albumin. Red
blood cells, if not removed, may cause acidosis as a result of lactate
production. Some anticoagulants may
attach to calcium and cause misinterpretation of calcium levels. (Rogers MC, et
al. Textbook of Pediatric Intensive
Care, 3rd Edition; p 1281) 13.
C
Lack of weightbearing is more
severe in children as a result of hypercalcemia and immobility. Levels of total serum calcium > 15 mg% may be
lifethreatening. Digitalis toxicity
increases in the setting of hypercalcemia.
Mithramycin should be avoided if surgery is anticipated because of the
possibility of severe marrow suppression as a result of its administration, and
therefore, complicating thrombocytopenia which could lead to significant
bleeding. The product of the
concentration of calcium and phosphorus should be kept below 60 when treating
hypercalcemia. (Rogers MC, et al.
Textbook of Pediatric Intensive Care, 3rd Edition; pp
1282-1285) 14.
D
For any patients admitted to the
ICU with hypocalcemia, treatment should be initiated unless the hypocalcemia is
borderline and without symptoms. Hypocalcemia,
which is resistant to the administration of repeated doses of intravenous
calcium chloride may be an indication of hypomagnesemia, hypoparathyroidism, or
vitamin D insufficiency. Magnesium sulfate should not be used since the possibility
exists for a complex to be formed between magnesium sulfate and calcium.
A rapid magnesium infusion leads to a peak adrenal excretion. (Rogers MC,
et al. Textbook of Pediatric
Intensive Care, 3rd Edition; pp 1283-1285) 15.
C The daily requirement is
approximately 0.3-0.4 mEq/kg/day IV. With
a decrease in glomerular filtration rate, magnesium replacement may precipitate
hypermagnesemia. Intravenous
magnesium should not be rapid bolus as discussed previously. Magnesium chloride is preferable to magnesium sulphate, since
the sulphate can bind calcium. Rapid
magnesium infusion leads to a poor clinical response since peak magnesium levels
are associated with peak renal excretion. Aminoglycosides have been known to
cause hypomagnesemia. (Rogers MC, et al. Textbook of Pediatric Intensive Care, 3rd Edition;
pp 1285-1288; Chernow B, Smith J, Rainey T, et al. Hypomagnesemia: indications
for the critical care specialist. Crit Care Med 1982; 10:193) 16.
E Propranolol, labetalol, lidocaine, nitroglycerine, morphine and
verapamil are not dependent on hepatic blood flow. (Rogers MC, et al.
Textbook of Pediatric Intensive Care, 3rd Edition; pp
1200-1205) 17.
B
Dexamethasone has the least sodium
retaining properties and therefore, it is very appropriate for clinical
situations where relative hypovolemia is desired.
Prednisone and methylprednisolone are intermediate in terms of their salt
retaining properties. Synthetic
steroids are less avidly bound to protein and they undergo slower hepatic
degradation, which makes them very effective in clinical practice. (Rogers MC,
et al. Textbook of Pediatric
Intensive Care, 3rd Edition; pp 1249-1252) 18.
A, A, C Pyloric stenosis usually
induces metabolic alkalosis rather than metabolic acidosis, and CAH is
associated with hyponatremia in the presence of hyperkalemia. (Rogers MC, et al.
Textbook of Pediatric Intensive Care, 3rd Edition; pp
1252-1254) 19.
D
Ketoconazole, Bactrimâ,
and Etomidate are all known to cause adrenal suppression. (Rogers MC, et al.
Textbook of Pediatric Intensive Care, 3rd Edition; pp
1252-1254) 20.
D With long-term steroid use,
morning administration will minimize hypothalamic-pituitary-adrenal axis
suppression. Also, with prolonged
use of the administration of steroids, it is best to administer the dose in the
morning, since this will coincide with peak diurnal variation in the endogenous
steroid levels. The 30-minute ACTH
administration test is a reliable test for adrenal suppression.
Prolonged use of 12 mg/m2/day cortisol does not cause clinical
significant hypothalamic-pituitary-adrenal axis suppression.
Methylprednisolone does not interfere with the common radioimmune assay
method of cortisol administration. Dexamethasone
administration will not interfere with subsequent measurement of cortisol, and
therefore, it is used in the so-called dexamethasone suppression test. (Rogers
MC, et al. Textbook of Pediatric
Intensive Care, 3rd Edition; pp 1251-1256) |