e111CHAPTER 136 Board Review Questions 15 Which of the following symptoms will persist after adminis tration of atropine in a patient with organophosphate poi soning? A Bradycardia B Diarrhea C Muscle[.]
CHAPTER 136 Board Review Questions 15 Which of the following symptoms will persist after administration of atropine in a patient with organophosphate poisoning? A Bradycardia B Diarrhea C Muscle weakness D Salivation Preferred response: C Rationale In both organophosphate and carbamate poisoning, atropine is used as an antidote for muscarinic symptoms (i.e., miosis, excessive salivation, sweating, diarrhea, urination, and bradycardia) Treatment with atropine, however, does not reverse the nicotinic symptoms, which include muscle weakness or respiratory failure Atropine should be administered as quickly as possible and in adequate doses In children older than 12 years, the dosing is to mg intravenously every 10 to 30 minutes In children younger than 12 years, the initial dose is 0.05 mg/kg with maintenance doses of 0.02 to 0.05 mg/kg over 10 to 30 minutes In cases of organophosphate and carbamate poisoning, the atropine dose is to 10 times greater than conventional atropine dosing Atropine should be continued until the muscarinic symptoms begin to abate Signs of atropinization include mydriasis, tachycardia, and xerostomia, which help provide parameters for adequate dosing Atropine should be continued at least 24 hours after severe exposures and then tapered if symptoms are improving 16 Which statement regarding the use of pralidoxime in organophosphate and carbamate poisoning is correct? A Atropine should not be used in association with pralidoxime in organophosphate poisoning B Pralidoxime is not used in carbamate poisoning C Pralidoxime reverses both muscarinic and nicotinic effects of organophosphate poisoning D Pralidoxime is a cholinesterase inhibitor Preferred response: B Rationale Pralidoxime chloride, the only cholinesterase reactivator in the United States, is an antidote for only the nicotinic symptoms of organophosphate poisonings; therefore, atropine must be used concomitantly Pralidoxime chloride does not help in carbamate exposures The dosing for patients older than 12 years is 0.5 to 1.0 g of pralidoxime Pralidoxime should be given intravenously over 15 to 30 minutes If needed, the dose may be repeated every 10 to 12 hours, beginning to hours after the initial dose Chapter 70: Renal Structure and Function In settings of impending shock from dehydration due to diarrhea, angiotensin II helps maintain glomerular filtration rate by: A Expansion of the glomerular basement membrane B Stimulating the production of antidiuretic hormone (ADH) C Vasoconstriction of the efferent arteriole D Vasorelaxation of the afferent arteriole Preferred response: C Rationale Angiotensin II, acting through its receptors on vascular smooth muscle cells, stimulates vasoconstriction of both afferent and efferent arterioles, but with a more intense effect on the efferent e111 vessel, thus maintaining reasonable filtration across the glomerulus even in low flow states Angiotensin II also causes constriction of the glomerular basement membrane which acts to counter higher flow rates and conserve volume Angiotensin II has no direct effect on the stimulation of ADH which is primarily regulated by plasma osmolality Reabsorption of water and solute in the proximal tubule is dependent on generation of electrochemical and concentration gradients In the setting of hypoxic-ischemic injury, the generation of these gradients is negatively impacted by locally decreased activity of: A Aldosterone B Arginine vasopressin C Sodium-potassium adenosine triphosphatase D a-hydroxylase Preferred response: C Rationale Proximal tubule gradients are highly dependent on ATP derived from aerobic metabolism that drives the activity of basolateral sodium-potassium-ATPase In states of low flow and/or oxygen delivery, local ATP generation decreases, the transport capacity of the pump decreases, and the generation and maintenance of gradients falls High activity of the renin-angiotensin system in these settings will stimulate the production of aldosterone and attempt to increase subsequent production of the transporter, but without improvement in ATP content, transformers will not function properly Vasopressin has little effect on proximal tubular gradients, and 1a-hydroxylase catalyzes bioactivation of vitamin D without impact on gradient formation Large volume renal absorption of filtrate sodium occurs in the thick ascending loop of Henle (TALH) primarily via the activity of which of the following? A Carbonic anhydrase type II B Epithelial sodium channel C Na/H1 antiporter D Na-K-Cl cotransporter (NKCC2) Preferred response: D Rationale The sodium-potassium-chloride cotransporter on the apical surface of cells of the TALH controls sodium reabsorption by moving these ions back from the filtrate in a 1Na:1K:2Cl stoichiometry Na/H1 antiporters are present in the proximal convoluted tubule but are not responsible for high volume sodium reabsorption The epithelial sodium channel is present in the collecting duct and is responsible for the fine-tuning of remaining luminal sodium excretion vs absorption rates Only about 3% of filtered sodium is reabsorbed in the collecting duct Carbonic anhydrase type II catalyzes reactions necessary for bicarbonate reabsorption but has no direct effects on sodium transport In settings of normal blood pressure, loop diuretics, via action in the thick ascending loop of Henle, inhibit sodium and chloride reabsorption resulting in large volumes of urine that are: A Hypertonic to plasma B Hypotonic to plasma C Isotonic to plasma D Unable to predict Preferred response: C e112 S E C T I O N XV Pediatric Critical Care: Board Review Questions Rationale Inhibition of the NaKCC2 transporter by loop diuretics occurs via competitive binding to the chloride binding site This loss of ion transport leads to decreased interstitial hypertonicity and decreased water reabsorption in the TALH along with relative increases in sodium excretion such that filtrate is essentially isotonic Over time, distal responses to higher sodium delivery may counteract the natriuretic and diuretic effects of the drug The macula densa is central to renal secretion of vasoactive mediators that affect both systemic blood pressure and glomerular perfusion pressure primarily by sensing tubular concentration of: A Calcium B Chloride C Magnesium D Phosphate Preferred response: B Rationale Macula densa cells have apical NKCC2 channels through which they sense luminal chloride concentrations Subsequent intracellular signaling pathways, including calcium transients, regulate the secretion of renin and glomerular arteriolar resistance via tightly controlled release of adenosine, prostanoids, nitric oxide, and kinins A newborn infant has a patent ductus arteriosus and is placed on ibuprofen to facilitate closure of the heart defect What is the most obvious sign of the effect on renal perfusion? A Reduction of afferent arterial flow B Reduction in efferent arterial flow C Reduction in medullary blood flow D Reduction in arcuate venous flow Preferred response: A Rationale Ibuprofen is a nonsteroidal antiinflammatory drug (NSAID) that inhibits prostaglandin production Prostaglandins play an important role in maintaining afferent arterial vasodilation with the intent of maintaining the glomerular filtration rate Inhibition of prostaglandin production reduces afferent arterial flow As a result, blood is shunted around the cortex to the medulla and into the venous system of the kidney, hence C and D are incorrect Efferent arterial flow may be reduced somewhat in the context of NSAID use, but the effect is predominantly observed at the afferent arterial system, hence A is the correct response In the early recovery phase of tubular interstitial injury, which of the following would most likely be observed? A Furosemide would be expected to not change tubular flow, and urine output would decrease B Furosemide would be expected to increase tubular flow, and urine output would decrease C Furosemide would be expected to increase tubular flow, and urine output would not change D Furosemide would be expected to not change tubular flow, and urine output would not change Preferred response: D Rationale In the setting of early recovery of tubular interstitial injury, the ability to establish medullary gradients is impaired because the polarization of tubular epithelial cells is perturbed Clinically, this is evident by the polyuric phase of recovery after such injuries happen Furosemide is a loop diuretic that blocks the NKCC2 channel, which is a significant means of establishing medullary gradients As such, the efficacy of furosemide in the setting of recovering tubular injury is reduced or absent Administering furosemide in this setting will have either little or no impact on increasing tubular flow and little or no impact on increasing urine output, which, as noted, may already be in a polyuric state The correct response is therefore D, as tubular flow and urine output would be expected to either not appreciably change or similarly increase What directly leads to the arterial blood supply to the tubule in an individual nephron? A The arcuate artery B The efferent arteriole C The interlobar arteriole D The afferent arteriole Preferred response: B Rationale The blood supply to the tubule directly arises from the efferent arteriole The arcuate artery feeds the interlobular arteries The renal artery feeds the interlobar arteries There is no structure named the interlobar arteriole The afferent arteriole feeds the glomerulus and efferent arteriole Which of the following explains the polyuric phase of acute tubular injury? A Excessive transport of water into the interstitium by the tubular epithelium B Excessive transport of water into the urinary space by the tubular epithelium C Deficient transport of water into the urinary space by the tubular epithelium D Deficient transport of sodium into the interstitium by the tubular epithelium Preferred response: D Rationale Deficient transport of sodium into the interstitium prevents the establishment of a medullary gradient, which is necessary to draw water out of the tubular lumen in the presence of aquaporin channels Such patients thus have concentrating defects and are polyuric Response A would result in more water leaving the tubular lumen and decreased urine volume Regarding response B, water is not transported into the tubular lumen by tubular epithelium but largely arises through filtration in the glomerulus Although it is true that the urinary space has extra sodium, the sodium arises because of a failure to transport it into the interstitium, not because sodium is actively secreted into the tubular lumen Deficient transport into the urinary space would, in theory, result in lower urinary volume CHAPTER 136 Board Review Questions Chapter 71: Fluid and Electrolyte Issues in Pediatric Critical Illness You are caring for a patient who suffered a traumatic brain injury days ago who has since developed hyponatremia The resident on the team suspects the etiology is either the syndrome of inappropriate antidiuretic hormone (SIADH) secretion or cerebral salt wasting (CSW) What is the primary distinguishing clinical feature between SIADH and CSW? A CSW typically responds to treatment with 1-deamino-8D-arginine vasopressin (DDAVP) whereas SIADH does not B Patients with SIADH are typically normovolemic/hypervolemic, and patients with CSW are typically hypovolemic C Patients with CSW are typically hypervolemic, and patients with SIADH are typically normovolemic D SIADH is typically associated with other electrolyte abnormalities whereas CSW is not Preferred response: B Rationale The primary distinguishing feature between SIADH and CSW is the patient’s fluid balance The physiology of SIADH promotes water retention, therefore promoting euvolemic or mildly hypervolemic Conversely, CSW results in increased natriuresis and urinary fluid losses The relative hypervolemia in SIADH and hypovolemia in CSW may not be readily apparent upon the discovery of hyponatremia SIADH can be treated with salt restriction and fluid restriction CSW is managed with isotonic volume resuscitation/replacement Other electrolyte abnormalities can be seen in CSW secondary to increased urine output An immobile, chronically ill child who was previously lost to follow-up is found to have moderate hypercalcemia on bloodwork What is the first-line acute treatment for this patient? A Activated vitamin D B Correction of hypophosphatemia with IV phosphate supplementation C Intravenous hydration D Osmotic diuresis with mannitol Preferred response: C Rationale Hypercalcemia, though infrequently encountered in the pediatric intensive care unit, can have significant clinical consequences Patients with hypercalcemia are often dehydrated secondary to hypercalciuria-induced polyuria; therefore, intravenous hydration is an appropriate acute treatment for hypercalcemia of any severity Routine use of loop diuretics to enhance renal calcium excretion is not recommended but may have a role among patients who develop edema from rehydration therapy Calcitonin rapidly decreases serum calcium levels by decreasing bone resorption and increasing renal calcium excretion Other adjunctive therapies include bisphosphonates, glucocorticoids, and dialysis A 4-year-old boy presents with significant traumatic brain injury and orthopedic injuries after a motor vehicle accident In the emergency department, he is hypotensive for age and will require fluid resuscitation Which fluid has been associated with worse outcomes in this clinical situation? A 0.9% Saline B 5% Albumin C Packed red blood cells D Platelets Preferred response: B e113 Rationale The use of colloids in traumatic brain injury was associated with worse outcomes in the original SAFE trial and a subsequent posthoc analysis (SAFE-TBI) A proposed mechanism is that albumin crosses the disrupted blood-brain barrier during the early phase of injury As the blood-brain barrier seals, the translocated albumin creates an oncotic gradient that promotes intracranial hypertension This data supports the use of normal saline fluids over 5% albumin for initial resuscitation in traumatic brain injury In pediatric trauma, blood products should be used for resuscitation when hemorrhagic shock or significant coagulopathy is present A nurse calls you to the bedside of a patient because of changes in the telemetry You observe peaked T waves and a slowing heart rate An electrocardiogram (ECG) confirms your suspicions The nurse says that they began during the nightly total parenteral nutrition (TPN) infusion two hours ago After stopping the TPN infusion, what is the next step in the management of this child? A Bolus intravenous dose of calcium gluconate or calcium chloride B Bolus intravenous dose of sodium bicarbonate C Intravenous phosphate replacement D Intravenous dose of diuretics Preferred response: A Rationale Verification of suspected hyperkalemia would be the first response, unless the ECG complexes were widening, and the ECG was slipping into a sine wave pattern How much the heart rate decreased would be important to know The clinical scenario and ECG changes are most concerning for symptomatic hyperkalemia Treatment is multifactorial Calcium salts help prevent the development of cardiac arrhythmias by stabilizing the cardiomyocyte membranes Additional treatment includes agents that shift serum potassium into the intracellular space such as b-agonists and insulin Glucose is provided in conjunction with insulin to prevent hypoglycemia Sodium bicarbonate may promote cellular uptake of potassium if acidemia is present Elimination of potassium from the body is promoted by potassium wasting diuretics, enteral exchange resins, and hemodialysis; however, these interventions take longer to have an effect An obtunded infant is brought to the PICU from the emergency department just as blood test results are reported as follows: sodium, 116 mEq/L; potassium, 5.9 mEq/L; chloride, 84 mEq/L; bicarbonate, 22 mEq/L; and glucose, 80 mg/dL After attaching monitor leads, the nurse notices the baby exhibiting right-sided tonic-clonic jerking movements, which rapidly become generalized The most appropriate immediate therapy is oxygen plus which of the following? A Administer a bolus of phenobarbital intravenously, 10 mL/kg over minutes B Administer 3% sodium chloride solution intravenously, mL/kg over 15 to 30 minutes C Administer 25% dextrose intravenously, mL/kg D Administer a neuromuscular blocker and perform endotracheal intubation Preferred response: B e114 S E C T I O N XV Pediatric Critical Care: Board Review Questions Rationale This infant has acute hyponatremic cerebral edema and requires a small increase in plasma osmolality to decrease cerebral irritation and seizure activity A slow correction of serum sodium should then follow A neurologically normal 8-month-old, totally breast-fed infant is brought to the PICU with normal blood pressure but is tachypneic with mildly increased work of breathing His wrists are flared, and costochondral junctions are palpable as distinct nodules He has hepatomegaly and cardiomegaly What is the rare but most likely cause of this child’s congestive heart failure? A Carnitine deficiency B Inborn error of metabolism C Increased peripheral vascular resistance D Rachitic hypocalcemic cardiomyopathy Preferred response: D Rationale Prolonged hypocalcemia due to vitamin D deficiency is a rare but recoverable cause of cardiomyopathy Bony changes as described are characteristic of vitamin D deficiency rickets Hyperphosphatemia causes physiologic disturbance mostly because of which of the following conditions? A Acute renal failure B Hypocalcemia C Impaired unloading of oxygen from hemoglobin D Inorganic metabolic acidosis Preferred response: B Rationale Severely elevated blood phosphorus levels cause decreased ionized calcium because of Ca-P binding This phenomenon reduces the free calcium ion available to participate in transmembrane Ca11 events critical to the function of neurons, myocytes, and the myocardium In a critically ill child, which of the following would be expected to increase ionized calcium (Ca11)? A Acidosis B Diffuse capillary leak C IL-6 1000 pg/mL D Packed red blood cell transfusion Preferred response: A Rationale Acidosis will decrease binding sites on plasma proteins and hence increase Ca11 Citrate anticoagulant will bind calcium and decrease Ca11 Renal failure will result in abnormal vitamin metabolism, and reclamation of calcium in the filtrate also may be impaired, both resulting in decreased Ca11 Increased free and bound calcium will be lost into the interstitium in the setting of diffuse capillary leak and may result in decreased Ca11 Systemic inflammatory response (IL-6 1000 pg/mL) is associated with hypocalcemia, perhaps via decreased parathyroid hormone levels Chapter 72: Acid-Base Balance in Critical Illness A 2-month-old patient is brought to the intensive care unit with fever and increased work of breathing Serum blood tests reveal pH, 7.18; Paco2, 38 mm Hg; serum bicarbonate level, 14 mEq/L; albumin, 2.0 g/dL How would the albumin level affect her anion gap? A Decreases the anion gap B Does not affect the anion gap C Elevates the anion gap D Unable to be assessed without calculating a delta/delta ratio Preferred response: A Rationale Hypoalbuminemia leads to a decrease in the anion gap Albumin is a negatively charged molecule (anion), and a decrease in albumin for any reason results in an increase in other anions such as Cl2 and HCO23 to maintain electroneutrality As both HCO23 and Cl2 are included in the anion gap calculation, this would lead to a decrease in the anion gap, even if an anion gap acidosis (e.g., diabetic ketoacidosis) occurs Anion gap should be corrected (AGcorr) in the setting of significant hypoalbuminemia AGcorr AG 2.5 (4 albumin level) A 17-year-old girl presents with vomiting, abdominal pain, and decreased oral intake for the last several days She has no significant past medical history, does not take any prescription medications, and she denies any exposure to medications or toxins Her physical exam is notable for a disoriented teenager without any focal findings Her laboratory results reveal serum sodium, 131 mEq/L; potassium, 3.8 mEq/L; chloride, 88 mEq/L; bicarbonate, 10 mEq/L Kidney function assessment reveals blood urea nitrogen (BUN), 37 mg/dL; serum creatinine, 2.1 mg/dL Her blood glucose is 383 mg/dL and arterial blood gas shows a pH of 7.01, Paco2 of 32 mm Hg and Pao2 of 92 mm Hg What is the most likely acid-base disturbance? A Anion gap metabolic acidosis B Hyperchloremic metabolic acidosis C Normal anion gap metabolic acidosis D Respiratory acidosis Preferred response: A Rationale This patient has acidemia, given blood gas findings an arterial pH of 7.01 In evaluating the low bicarbonate level, this is most consistent with a primary metabolic acidosis Calculation of the anion gap, which is the difference between the measured cations and anions in the blood, is consistent with an elevated anion gap metabolic acidosis Common causes of anion gap metabolic acidosis can be remembered by the mnemonic GOLDMARK, and include lactic acidosis, ketoacidosis, and ingested toxic alcohols, among others This patient has a partially compensated metabolic acidosis with an elevated anion gap, which when considered with her elevated serum glucose level is consistent with a diagnosis of diabetic ketoacidosis CHAPTER 136 Board Review Questions A 3-year-old boy is transferred to the ICU from an outside emergency department after being found by his parents unconscious at home with increased work of breathing On examination immediately after arrival, he is hemodynamically stable and is febrile to 39.4°C He is minimally responsive and tachypneic, without other focal findings An arterial blood gas is obtained which reveals pH, 7.38; Pco2, 28 mm Hg; serum bicarbonate, 14 meq/L What is the most likely etiology of this acid-base disturbance? A Diabetic ketoacidosis B Ethylene glycol ingestion C Renal tubular acidosis D Salicylate ingestion Preferred answer: D Rationale The clinical picture in this question stem and laboratory findings are most consistent with salicylate ingestion Initially following ingestion, salicylates result in central hyperventilation and respiratory alkalosis As time progresses and as ketoacids accumulate metabolic acidosis results This mixed acid-base disturbance results in a sometimes normal pH despite two primary acid-base disturbances A 6-year-old boy is admitted with upper respiratory tract infection with fever, cough, congestion, and rhinorrhea His fever has been treated with a medication that the family purchased overseas, and they not know what it is called His vital signs are as follows: temperature, 37°C; heart rate, 110 beats per minute; blood pressure, 98/60 mm Hg; respiratory rate, 22 breaths/minute His examination is notable for rhinorrhea and bilateral otitis media His neurologic examination demonstrates agitation, decreased responsiveness, and poor strength Laboratory results reveal serum sodium, 134 mEq/L; potassium, 6.1 mEq/L; chloride, 98 mEq/L; bicarbonate, 15 mEq/L; blood urea nitrogen, 86 mg/dL; creatinine, 1.6 mg/dL; glucose, 140 mg/dL Measured plasma osmolarity is 355 mOsm/ kg Arterial blood gas reveals pH, 7.24; Pco2, 26 mm Hg; bicarbonate, 12 mEq/L Which is the most likely diagnosis? A Acute on chronic kidney disease B Ethylene glycol ingestion C Salicylate intoxication D Sepsis Preferred response: B Rationale This patient has a metabolic acidosis with an elevated anion gap (134 – (98 15) 21 mEq/L) consistent with an anion gap metabolic acidosis In an anion gap acidosis, the next step is to evaluate whether a plasma osmolar gap is present The calculated osmolality is 2(134) 140/18 86/2.8 303.5 mOsm/kg, and the osmolar gap is 355 303.5 51.5 mOsm/kg An elevated osmolar gap usually indicates a toxic alcohol poisoning, such as methanol, ethylene glycol, or diethylene glycol This patient likely was given a cough remedy which contained diethylene glycol, resulting in this acid-base disturbance e115 Two days following admission for new onset diabetes mellitus, diabetic ketoacidosis, and clinically suspected cerebral edema, a 3-year-old is being transitioned to subcutaneous insulin but is found to have a persistent metabolic acidosis, despite normalization of blood glucose for approximately 12 hours What is the most likely cause of the metabolic acidosis? A b-hydroxybutyrate B Gastric acid production C Hyperchloremia D Lactic acid E Metformin toxicity Preferred response: C Rationale Because of concern for cerebral edema, this child was likely administered normal saline for replacement and maintenance fluid Because sodium and chloride are both strong ions, IV administration of 0.9% NaCl necessarily will decrease plasma strong ion difference, creating a strong ion acidosis, as long as such an infusion does not cause a change in Pco2 or albumin or phosphate concentrations Lactate and b-hydroxybutyrate should be normal in this patient It is not likely that metformin was utilized in the treatment plan for DKA Increased gastric acid production is not a cause of systemic metabolic acidosis A toddler with septic shock is initiated on an infusion of epinephrine, and serum lactate is noted to increase from 2.5 mmol/L to 3.5 mmol/L at a time when the blood pressure is 110/40 mm Hg, and qualitative cardiac function by ultrasonography is hyperdynamic Which of the following is the most likely cause of this observation? A Aerobic glycolysis B Cellular lysis C Oxygen debt D Mitochondrial dysoxia E Tissue hypoxia Preferred response: A Rationale Evidence now supports the view that sepsis-associated hyperlactatemia is not due only to tissue hypoxia or anaerobic glycolysis and that this response may actually facilitate bioenergetic efficiency through an increase in lactate oxidation In this sense, the characteristics of lactate production best fit the notion of an adaptive survival response that increases in intensity as disease severity increases Skeletal muscle appears to be a leading source of lactate formation as a result of exaggerated aerobic glycolysis through Na1K1ATPase stimulation by circulating epinephrine, both endogenous and exogenous Increased lactate as a result of hypoxia or dysoxia may be more the exception than the rule, at least in the hyperdynamic, hypermetabolic phase of sepsis ... work of breathing His wrists are flared, and costochondral junctions are palpable as distinct nodules He has hepatomegaly and cardiomegaly What is the rare but most likely cause of this child’s... acidosis Preferred response: A Rationale This patient has acidemia, given blood gas findings an arterial pH of 7.01 In evaluating the low bicarbonate level, this is most consistent with a primary... etiology of this acid-base disturbance? A Diabetic ketoacidosis B Ethylene glycol ingestion C Renal tubular acidosis D Salicylate ingestion Preferred answer: D Rationale The clinical picture in this