(Test Bank) Nelson Pediatrics Review Mcqs

Kliegman,Stanton,St. Geme,Behrman, 19

Nursing

Test Bank

19th Edition

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Author(s): Kliegman, Stanton, St. Geme, Behrman

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Nelson Pediatrics Review(MCQs) 19 Edition 1. Which of the following statements regarding foster care is true? □A permanency plan must be made for a child in foster care no later than 12 mo from the child's entry into care □A minority of children in foster care have a history of abuse or neglect □The mission of foster care is to safely care for children while providing services to families to promote reunification □Most (>70%) of children in foster care are reunited with their families ■ A and C description The mission of foster care is to provide for the health, safety, and well-being of children while assisting their families with services to promote reunification. Children entering foster care have frequently experienced early childhood trauma. More than 70% have a history of abuse, neglect, or both. Only about 50% of children achieve reunification. In the USA, the Adoption and Safe Families Act (P.L. 105-89) passed in 1997 requires that a permanency plan be made for each child no later than 12 mo after entry to foster care and that a petition to terminate parental rights typically must be filed when a child has been in foster care for at least 15 of the previous 22 mo. (See Chapter 35, page 134, and e35 -1.) 2. A 4 yr old girl is admitted to the hospital for her third evaluation for vaginal bleeding. The mother noted bright red blood on the child's underwear. Previous examinations revealed a normal 4 yr old girl, Tanner stage 1, with normal external genitalia. Pelvic ultrasound results were normal, as was the serum estradiol level. The hemoglobin and platelet counts were normal, as were the bleeding time and coagulation studies. Findings on pelvic examination conducted under anesthesia also were normal. The next step in the examination is to: ■ Determine the blood type of the blood on the underwear □Interrogate the father □Isolate the parents and child □Determine von Willebrand factor levels □Measure fibronectin in the vagina description Consideration of factitious disorder by proxy should be triggered when the reported symptoms are repeatedly noted by only one parent, appropriate testing fails to confirm a diagnosis, and seemingly appropriate treatment is ineffective. At times, the child's symptoms, their course, or the response to treatment may be incompatible with any recognized disease. Preverbal children are usually involved. Bleeding is a particularly common presentation. This may be caused by adding dyes to samples, adding blood (e.g., from the mother) to the child's sample, or giving the child an anticoagulant (e.g., warfarin). (See Chapter 37, page 146.) 3. Munchausen syndrome by proxy is characterized by all of the following EXCEPT: □Mother who appears devoted and wins over members of care team □Multiple hospitalizations and investigations without diagnosis □Symptoms on history but not witnessed by medical team ■ Symptoms occurring in presence of different caregivers (e.g., while mother is out of town) □Use of medications or toxins description Symptoms in young children are mostly associated with proximity of the offending caregiver to the child. The mother may present as a devoted or even model parent who forms close relationships with members of the health care team. While appearing very interested in her child's condition, she may be relatively distant emotionally. (See Chapter 37, page 146.) 4. Which statement is false? ■ Malnutrition is the second leading cause of acquired immune deficiency worldwide behind HIV infection □Zinc is important in immune function and linear growth □Kwashiorkor and marasmus are rare in developed countries □The Western diet is associated with increased noncommunicable disease description The significant global burden of malnutrition and undernutrition is the leading worldwide cause of acquired immunodeficiency and the major underlying factor for morbidity and mortality globally for children <5 yr of age. Zinc is a micronutrient that supports multiple metabolic functions in the body, is essential for normal immune functioning, and is required to support linear growth; zinc deficiency is associated with impaired immune functioning and poor linear growth. In parallel to the risk for nutrient and energy deficiencies, issues relating to excesses pose important challenges because of their negative health effects, such as obesity or cardiovascular disease risk factors. The nutrition transition under way in the developing world from traditional diets to the Western diet has been associated with increases in noncommunicable diseases, often coexisting with undernutrition and malnutrition, observed sometimes in the same communities or even the same families. (See e41-1.) 5. Components of energy expenditure in children include: □Thermal effect of food □Basal metabolic rate □Energy for physical activity □Energy to support growth ■ All of the above description The 3 components of energy expenditure in adults are the basal metabolic rate, the thermal effect of food (energy required for digestion and absorption), and energy for physical activity. Additional energy intake and expenditure are required to support growth and development for children. (See e41-4.) 6. Which of the following clinical scenarios increases the risk of vitamin A deficiency? □Vegetarian diet □Chronic intestinal disorders □Zinc deficiency ■ B and C □All of the above description Vitamin A is an essential micronutrient because it cannot be biogenerated de novo by animals. It must be obtained from plants in the form of provitamin -A carotenoids. In the USA, grains and vegetables supply approximately 55% and dairy and meat products su pply approximately 30% of vitamin A intake from food. Vitamin A and the provitamins -A are fat soluble, and their absorption depends on the presence of adequate lipid and protein within the meal. Chronic intestinal disorders or lipid malabsorption syndromes can result in vitamin A deficiency. In developing countries, subclinical or clinical zinc deficiency can increase the risk of vitamin A deficiency. There is also some evidence of marginal zinc intakes in children in the USA. (See Chapter 45, page 188.) 7. Which statement about vitamin A toxicity is NOT true? □Excess vitamin A in utero can cause congenital malformations □It may present as pseudotumor cerebri ■ An infant with a preference for carrots and butternut squash may develop toxicity □It may cause fissures at the corners of the mouth, pruritus, and alopecia □Symptoms subside rapidly after withdrawing the source of the vitamin description Excessive intake of carotenoids is not associated with toxicity but can cause yellow coloration of the skin that disappears when intake is reduced; this disorder (carotenemia) is especially likely to occur in children with liver disease, diabetes mellitus, or hypothyroidism and in those who do not have enzymes that metabolize carotenoids. (See Chapter 45, page 191.) 8. Which statement about vitamin E is false? □The most common form of vitamin E is tocopherol ■ Premature infants given formula with a high content of polyunsaturated fatty acids and iron supplementation are protected from deficiency □Cholestatic liver disease increases the risk of deficiency □Premature infants with vitamin E deficiency develop hemolysis, thrombocytosis, and edema □Prolonged vitamin E deficiency causes a severe, progressive neurologic disorder description Premature infants are particularly susceptible to vitamin E deficiency because there is significant transfer of vitamin E during the last trimester of pregnancy. Vitamin E deficiency in premature infants causes thrombocytosis, edema, and hemolysis, potentially causing anemia. The risk of symptomatic vitamin E deficiency was increased by the use of formulas for premature infants that had a high content of polyunsaturated fatty acids (PUFAs). These formulas led to a high content of PUFAs in red blood cell membranes, making them more susceptible to oxidative stress, which could be ameliorated by vitamin E. Oxidative stress was augmented by aggressive use of iron supplementation; iron increases the production of oxygen radic als. The incidence of hemolysis due to vitamin E deficiency in premature infants decreased secondary to the use of formulas with a lower content of polyunsaturated fatty acids, less -aggressive use of iron, and provision of adequate vitamin E. (See e49-1.) 9. Manifestations of hyperkalemia include all of the following EXCEPT: □Paresthesias □Weakness □Paralysis □Wide QRS complex ■ Tetany description The most important effects of hyperkalemia are due to the role of potassium in membrane polarization. The cardiac conduction system is usually the dominant concern. Changes in the electrocardiogram (ECG) begin with peaking of the T waves. This is followed, as the potassium level increases, by ST segment depression, an increased PR interval, flattening of the P wave, and widening of the QRS complex. This process can eventually progress to ventricular fibrillation. Asystole may also occur. Some patients have paresthesias, fasciculations, weakness, and even an ascending paralysis, but cardiac toxicity usually precedes these clinical symptoms, emphasizing the danger of assuming that an absence of symptoms implies an absence of danger. (See Chapter 52, page 221.) 10. Hyperkalemia may be associated with all of the following EXCEPT: □Succinylcholine use □Burns □Trauma □Chemotherapy ■ Metabolic alkalosis □Digitalis toxicity □Uremia description Many causes of hyperkalemia result in metabolic acidosis; a metabolic acidosis worsens hyperkalemia through the transcellular shift of potassium out of cells. Renal insufficiency is a common cause of the combination of metabolic acidosis and hyperkalemia. This association is also seen in diseases associated with aldosterone insufficiency or aldosterone resistance. (See Chapter 52, page 221.) 11. The best method to reduce the potassium level during hyperkalemia, by reducing the body burden of potassium, is: □Sodium bicarbonate infusion □Glucose and insulin infusion □Calcium infusion □Albuterol aerosol ■ Kayexalate enema description Treatment of hyperkalemia has 2 basic goals: (1) to stabilize the heart to prevent life-threatening arrhythmias and (2) to remove potassium from the body. The treatments that acutely prevent arrhythmias all have the advantage of working quickly (within minutes) but do not remove potassium from the body. Calcium stabilizes the cell membrane of heart cells, preventing arrhythmias. It is given intravenously over a few minutes, and its action is almost immediate. Several medications cause potassium to move intracellularly and thus rapidly reduce the plasma level to prevent arrhythmias. These include bicarbonate, insulin and glucose, and nebulized albuterol. However, these medicines do not remove potassium from the body. To reduce the total body potassium, 3 options are avai lable. In patients who are not anuric, a loop diuretic increases renal excretion of potassium. A high dose may be required in a patient with significant renal insufficiency. Sodium polystyrene sulfonate (Kayexalate) is an exchange resin that is given either rectally or orally. Sodium in the resin is exchanged for body potassium, and the potassium -containing resin is then excreted from the body. Some patients require dialysis for acut e removal of potassium. Dialysis is often necessary if the patient has either severe renal failure or an especially high rate of endogenous potassium release, as is sometimes present with tumor lysis syndrome or rhabdomyolysis. (See Chapter 52, page 222.) 12. Clinical manifestations of hypokalemia include all of the following EXCEPT: □ECG changes □Paralysis □Urinary retention □Constipation □Muscle cramps ■ Blurry vision description The heart and skeletal muscle are especially vulnerable to hypokalemia. ECG changes include a flattened T wave, a depressed ST segment, and the appearance of a U wave, which is located between the T wave (if still visible) and the P wave. Ventricular fibrillation and torsades de pointes may occur, although usually only in the context of underlying heart disease. The clinical consequences of hypokalemia in skeletal muscle include muscle weakness and cramps. Paralysis is a possible complication, generally only at potassium levels <2.5 mEq/L. It usually starts in the legs and moves to the arms. Respiratory paralysis may require mechanical ventilation. Some patients have rhabdomyolysis; the risk increases with exercise. Hypokalemia slows gastrointestinal motility. This effect manifests as constipation; with potassium levels <2.5 mEq/L, an ileus may occur. Hypokalemia impairs bladder function, potentially leading to urinary retention. (See Chapter 52, page 224.) 13. From the following list, choose the route(s) by which insensible water loss may occur: 1. Sweat, 2. Fecal loss, 3. Evaporative loss from skin, 4. Respiratory water loss, 5. Obligate water for urinary solute excretion □1 and 3 □1, 2, and 3 □3 only ■ 3 and 4 □2 and 5 description Water is a crucial component of maintenance fluid therapy because of the obligatory daily water losses. These losses are both measurable (urine, stool) and not measurable (insensible losses from the skin and lungs). Failure to replace these losses leads to a child who is thirsty, uncomfortable, and, ultimately, dehydrated. (See Chapter 53, page 242.) 14. Which of the following is a goal of maintenance fluids? □Diminish protein degradation □Prevent dehydration ■ Prevent hunger □Prevent electrolyte derangements □Prevent ketoacidosis description The glucose in maintenance fluids provides approximately 20% of the normal caloric needs of the patient, prevents the development of starvation ketoacidosis, and diminishes the protein degradation that would occur if the patient received no calories. Glucose also provides added osmoles, thus avoiding the administration of hypotonic fluids that may cause hemolysis. Maintenance fluids do not provide adequate calories, protein, fat, minerals, or vitamins. This fact is typically not problematic for a patient receiving intravenous fluids for a few days. A patient receiving maintenance intravenous fluids is receiving inadequate calories and will lose 0.5-1% of weight each day. Table 53-1 summarizes the goals of maintenance fluids. (See Chapter 53, page 242.) 15. Which patient has an elevated risk of hyponatremia with standard maintenance fluid therapy (D5 ½ NS if >10 kg, D5 ¼ NS if <10 kg)? □6 mo old NPO for elective hernia repair □4 month old with bronchiolitis and poor oral intake □13 yr old status post motor vehicle accident with multiple fractures, requiring treatment with narcotics and antiemetics □8 yr old with nephrotic syndrome □A and D ■ B, C, and D description Patients who are producing antidiuretic hormone (ADH) may retain water, creating a risk of hyponatremia due to water intoxication. Patients who may be producing ADH owing to subtle volume depletion or other mechanisms (respiratory disease, stress, pain, nausea, medications such as narcotics) may be more safely treated with fluids that have a higher sodium concen tration, with a decrease in fluid rate, or with a combination of these strategies. Patients with persistent ADH production due to an underlying disease process (syndrome of inappropriate ADH secretion [SIADH], congestive heart failure, nephrotic syndrome, liver disease) should receive less than maintenance fluids. Treatment is individualized, and careful monitoring is critical. Special caution is needed in patients who are known to have low -normal serum sodium concentrations or hyponatremia. (See Chapter 52, page 243.) 16. In which patient is oral rehydration NOT indicated? □2 yr old with moderate hypernatremic dehydration □6 mo old with mild hyponatremic dehydration ■ 4 mo old with severe dehydration and normal serum sodium □3 yr old with moderate dehydration and normal serum sodium □A and C description Dehydration, most often due to gastroenteritis, is a common problem in children. Most cases can be managed with oral rehydration. Even children with mild to moderate hyponatremic or hypernatremic dehydration can be managed with oral rehydration. The infant with severe dehydration is gravely ill. The decrease in blood pressure indicates that vital organs may be receiving inadequate perfusion. Immediate and aggressive intervention is necessary. If possible, the child with severe dehydration initially should receive intravenous therapy. (See Chapter 54, page 245.) 17. Which statement about pediatric poisoning is NOT true? □Most poisonings among young children involve a single substance and are unintentional □Poison prevention should be discussed at all well child visits beginning at 6 months □Pediatric poisonings occur most frequently in the toddler and adolescent age ranges ■ The toddler age group experiences the majority of poisoning deaths □Poison control centers are available via phone, 24-7, toll free description Although the majority of exposures are in children <6 yr, only 2% of the reported deaths occur in this age group. In addition to the exploratory nature of ingestions in young children, product safety measures, poison prevention education, early recognition of exposures, and around -the-clock access to regionally based poison control centers all contribute to the favorable outcomes in this age group. Exposures in the adolescent age group are primarily intentional (suicide or abuse or misuse of substances) and thus often result in more severe toxicity. Adolescents (ages 13 -19 yr) accounted for 74 of the 108 poison -related pediatric deaths in 2008 reported to the National Poison Data System. Pediatricians should be aware of the signs of drug abuse or suicidal ideation in this population and should aggressively intervene. (See Chapter 58, page 250.) 18. Quantitative levels of certain medications are helpful in the management of acute poisonings. For which of the following medications is this NOT true? □Salicylates □Acetaminophen □Iron □Carbon monoxide ■ Marijuana description For select intoxications (salicylates, some anticonvulsants, acetaminophen, iron, digoxin, methanol, lithium, theophylline, ethylene glycol, carbon monoxide), quantitative blood concentrations are integral to confirming the diagnosis and formulating a treatment plan. For most exposures, quantitative measurement is not readily available and is not likely to alter management. (See Chapter 58, page 253.) 19. The 4 principles of management of poisonings are what? ■ Decontamination, enhanced elimination, antidote, supportive care □Degradation, hydration, oxygenation, antidote □Ipecac, clinical monitoring, dialysis, reversal □Alkalinization, oxygenation, elimination, hydration description The 4 principles of management of the poisoned patient are decontamination, enhanced elimination, antidote, and supportive care. Few patients meet criteria for all of these interventions, although clinicians should consider each option in every poisoned patient so as not to miss a potentially lifesaving therapy. Antidotes are available for relatively few poisons, thus emphasizing the importance of meticulous supportive care and close clinical monitoring. (See Chapter 58, page 254.) 20. A 15 yr old boy is admitted to your care after the intentional ingestion of 2 g of his own amitriptyline in a suicide gesture. He received activated charcoal for gastrointestinal decontamination. The patient is placed in the ICU for monitoring and remains stable. He is receiving only 0.45% normal saline. You observe a change in his cardiac monitor display with a widening of his QRS complex to 0.12 second and occasional ectopic beat s. The most appropriate next step in management is to: □Ignore these changes because they are still within normal limits ■ Add sodium bicarbonate to his IV fluids to try to raise his serum pH above 7.4 □Repeat a dose of activated charcoal □Begin a lidocaine infusion at an appropriate dose □Order a chest radiograph description Sodium bicarbonate is the antidote of choice for TCA toxicity and works via overcoming the sodium channel blockade by providing a sodium load and via inducing an alkalosis to decrease drug binding to sodium channels. Indications for sodium bicarbonate include a QRS duration >100 msec, ventricular dysrhythmias, and hypotension. An initial bolus of 1-2 mEq/kg of sodium bicarbonate is given followed by initiation of a continuous infusion. Additional boluses may be given if the QRS duration continues to widen, with the goals of therapy being a serum pH of 7.45 -7.55, improved hemodynamic stability, and narrowing of the QRS complex. (See Chapter 58, page 264.) 21. A 2 yr old boy arrives in the emergency department after a seizure. On presentation his vital signs are: temperature 40.2°C, heart rate 200 beats/min, respiratory rate 52 breaths/min. His laboratory values are: arterial pH 7.2, serum bicarbonate 6 mmol/L, arterial PCO2 18 mm Hg, sodium 148 mmol/L, potassium 3.1 mmol/L, WBC count 10,200/mm3. On the basis of the history obtained and the presentation, you suspect that an accidental ingestion has occurred. The most likely toxin is: □A tricyclic antidepressant □Acetaminophen □Cocaine □An organophosphate insecticide ■ A salicylate description Salicylate ingestions are classified as acute or chronic, and acute toxicity is far more common in pediatric patients. Early signs of acute salicylism include nausea, vomiting, diaphoresis, and tinnitus. Moderate salicylate toxicity can manifest as tachypnea and hyperpnea, tachycardia, and altered mental status. The tachycardia results in large part from marked insensible losses from vomiting, tachypnea, diaphoresis, and uncoupling of oxidative phosphorylation. Thus, careful attention should be paid to volume status and early volume resuscitation in the significantly poisoned patient. Signs of severe salicylate toxicity include hyperthermia, coma, and seizures. Chronic salicylism can have a more insidious presentation, and patients can show marked toxicity at significantly lower salicylate levels than in acute toxicity. The classic blood gas of salicylate toxicity reveals a primary respiratory alkalosis and a primary, anion gap, metabolic acidosis. Hyperglycemia (early) and hypoglycemia (late) have been described. Abnormal coagulation studies, clinically manifested as bleeding and easy bruising, also may be seen. (See Chapter 58, page 260.) 22. A 2 yr old boy is noted to be drinking from a container filled with kerosene. He immediately coughs, becomes tachypneic, and is brought to the hospital. The best approach to his treatment is to: □Induce emesis □Perform nasogastric tube lavage □Instill mineral oil □Administer steroids ■ None of the above description The most important manifestation of hydrocarbon toxicity is aspiration pneumonitis. Aspiration usually occurs during coughing and gagging at the time of ingestion or vomiting after the ingestion. The propensity of a hydrocarbon to cause aspiration pneumonitis is inversely proportional to its viscosity. Compounds with low viscosity, such as mineral spirits, naphtha, kerosene, gasoline, and lamp oil, spread rapidly across surfaces and cover large areas of the lungs when aspirated. Only small quantities (<1 mL) of low-viscosity hydrocarbons need be aspirated to produce significant injury. Respiratory symptoms can remain mild or progress rapidly to acute respiratory distress syndrome (ARDS) and respiratory failure. Emesis and lavage are contraindicated given the risk of aspiration. Activated charcoal is not useful because it does not bind the common hydrocarbons and can also induce vomiting. If hydrocarbon -induced pneumonitis develops, respiratory treatment is supportive. Neither corticosteroids nor prophylactic antibiotics have shown any clear benefit. (See Chapter 58, page 267.) 23. A 2 yr old child is found playing with a can of crystalline drain cleaner. The child's mother telephones you for help. There are several crystals in the mouth, which you have the mother wash out. The next step in treatment should be to: □Have the mother administer lemon juice or orange juice to neutralize the alkaline crystals and come to your office □Have the mother administer water or milk and call you back in 2 hr ■ Have the mother administer water or milk and bring the child in for esophagoscopy □Simply observe the child because the crystals are so bitter that the child was trying to spit them out when the mother called, and therefore no problems should occur □Administer ipecac at home and bring the child in to see you description Alkalis produce a liquefaction necrosis, allowing further tissue penetration of the toxin and setting the stage for possible perforation. Ingestion of caustic materials can produce injury to the oral mucosa, esophagus, and stomach. Patients can have significant esophageal injury even in the absence of visible oral burns. Symptoms include pain, drooling, vomiting, abdominal pain, and difficulty swallowing or refusal to swallow. Laryngeal injury can manifest as stridor and respiratory distress, necessitating intubation. In the most severe cases, patients can present in shock after perforation of a hollow viscus. Initial treatment of caustic exposures includes thorough removal of the product from the skin or eye by flushing with water. Emesis and lavage are contraindicated. Activated charcoal should not be used because it does not bind these agents and can predispose the patient to vomiting and subsequent aspiration. Endoscopy should be performed within 12-24 hr of ingestion in symptomatic patients or those in whom injury is suspected on the basis of history and known characteristics of the ingested product. (See Chapter 58, page 266.) 24. A 16 yr old, 165-lb patient reports consuming 20-40 325-mg capsules containing acetaminophen 1 hr ago. The most appropriate approach to treatment is to: □Measure the plasma level and determine potential toxicity from the level on the nomogram □Wait until 4 hr after ingestion to measure the plasma level and do nothing else ■ Administer activated charcoal immediately and measure the plasma level of acetaminophen 4 hr after ingestion □Send the patient home because an ingestion of this magnitude is not toxic □Administer N-acetylcysteine at a dose of 140 mg/kg description Initial treatment should focus on the ABCs and consideration of decontamination with activated charcoal in patients who present within 1-2 hr of ingestion. The antidote for acetaminophen poisoning is NAC, which works primarily via replenishing hepatic glutathione stores. NAC therapy is most effective when initiated within 8 hr of ingestion. However, there is no demonstrated benefit to giving NAC before the 4 hr postingestion mark. Thus, patients who present early after ingestion should have a 4-hr level drawn and decision to initiate NAC should be based on this level. (See Chapter 58, page 259.) 25. A 2 yr old child presents in the emergency department after the reported ingestion of a mouthful of lamp oil. The child reportedly vomited once at home. The child has a heart rate of 160 beats/min, a respiratory rate of 48 breaths/min, and a temperature of 37.2°C. A chest film is read as normal. The most appropriate therapy for this child is to: □Administer syrup of ipecac □Administer activated charcoal □Remove any ingested lamp oil by gastric lavage ■ Admit the child for observation and supportive care □Discharge the child home with a follow -up office visit in the morning description The most important manifestation of hydrocarbon toxicity is aspiration pneumonitis. Aspiration usually occurs during coughing and gagging at the time of ingestion or vomiting after the ingestion. The propensity of a hydrocarbon to cause aspiration pneumonitis is inversely proportional to its viscosity. Compounds with low viscosity, such as mineral spirits, naphtha, kerosene, gasoline, and lamp oil, spread rapidly across surfaces and cover large areas of the lungs when aspirated. Only small quantities (<1 mL) of low-viscosity hydrocarbons need be aspirated to produce significant injury. Chest radiographs may initially be normal, but they often show abnormalities within 6 hr of exposure in patients who have aspirated. Respiratory symptoms can remain mild or progress rapidly to acute respiratory distress syndrome (ARDS) and respiratory failure. Emesis and lavage are contraindicated given the risk of aspiration. Activated charcoal is not useful because it does not bind the common hydrocarbons and can also induce vomiting. If hydrocarbon -induced pneumonitis develops, respiratory treatment is supportive. (See Chapter 58, page 267.) 26. A teenage girl presents in the emergency department with the story that she got upset with her boyfriend and swallowed a "handful of aspirin" about 4 hr previously. One hour afterward, after she began vomiting, she confessed to her mother what she had done. On examination the patient has normal vital signs and is asympto matic except for the complaint of nausea. A serum salicylate level is ordered, but the laboratory reports no salicylates in her blood. The most appropriate next step in management is to: □Discharge the patient home ■ Order an acetaminophen level □Request a psychiatric consultation □Send a second sample for salicylate determination □Order an abdominal radiograph to look for pills in the stomach description Acetaminophen is a widely available medication and a commonly detected co-ingestant with the potential for severe toxicity. Given that patients might initially be asymptomatic and might not report acetaminophen as a co-ingestant, an acetaminophen level should be checked in all patients who present after an intentional exposure or ingestion. (See Chapter 58, page 253.) 27. Brain perfusion pressure generally equals: ■ Mean arterial pressure minus intracranial pressure □Diastolic blood pressure minus intracranial pressure □Intracranial blood pressure minus systolic blood pressure □Systolic blood pressure minus diastolic blood pressure description The perfusion pressure of the brain (cerebral perfusion pressure [CPP]) is equal to the pressure of blood entering the cranium (mean arterial pressure [MAP]) minus the ICP, in most cases. (See Chapter 63, page 296.) 28. Severe traumatic brain injury is characterized by a Glasgow Coma Score (GCS) of: □0 □1-3 ■ 3-8 □9-12 description The hallmark of severe TBI is coma (GCS score 3-8). Often, coma is seen immediately after the injury and is sustained. In some cases, such as with an epidural hematoma, a child may be alert at presentation but the condition may deteriorate after a period of hours. A similar picture can be seen in children with diffuse swelling, in whom a talk-and-die scenario has been described. Clinicians also should not be lulled into underappreciating the potential for deterioration of a child with moderate TBI (GCS score 9-12) with a significant contusion, because progressive swelling can potentially lead to devastating complications. In the comatose child with severe TBI, the second key clinical manifestation is the development of intracranial hypertension. Increased ICP can be appropriately managed only with continuous ICP monitoring. The development of brain swelling is progressive. Significantly raised ICP (>20 mm Hg) can occur early after severe TBI, but peak ICP generally is seen at 48 -72 hr. Need for ICP -directed therapy may persist for longer than a week. A few children have coma without increased ICP, resulting from axonal injury or brainstem injury. (See Chapter 63, page 298.)