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A 12-year-old was playing baseball with friends during inclement weather and was brought to the emergency department after being found unresponsive on the eld. Friends reported a lightning strike near where the child was playing, and observed him to be thrown to the ground at the time of the lightning strike. The child arrives at the emergency department conscious with mild disorientation, and with a cervical collar in place. Super cial thermal burns are observed on his hands and his feet. Skin examination reveals a fern like pattern of erythema along his chest and right arm. Of the following, the BEST next step in management is:
A. evaluate for acute kidney injury
B. evaluate for deep tissue burns
C. perform electrocardiography
D. resuscitate with high-volume (Parkland formula) parenteral fluids
C. ECG
Abnormal changes in the electrocardiogram are common after lightning strike injury; most resolve spontaneously and are not prognostic in children. Deep tissue and internal organ injuries are more likely to occur in high-voltage compared with low voltage electrical injury, but rarely occur with lightning strike injury. In lightning strike injury, keraunoparalysis can cause blue/cyanotic, mottled, and pulseless extremities mimicking compartment syndrome; this condition usually resolves spontaneously, and fasciotomy is rarely indicated
ST elevation, ST and T wave changes, and QT interval prolongation. The most common arrhythmia seen is sinus tachycardia. However, cardiac arrest from asystole is also noted. Troponin/CK-MB elevations may occur but are generally not prognostic
A 7-year-old child with a history of feeding intolerance and severe gastroesophageal re ux disease requiring chronic acid suppression therapy is admitted to the pediatric intensive care unit with severe anemia and altered mental status. The child’s mother reports that they have adopted a diet with no animal products, sh, eggs, or dairy due to his food intolerance. The child’s diet includes white rice, almond milk, many vegetables, and legumes. In the past few weeks the child has become increasingly fatigued and also walks with an unsteady gait. On physical examination, the child has a heart rate of 120 beats/min, but otherwise normal vital signs. There are pale conjunctiva and pale mucous membranes, but no rashes or hepatosplenomegaly. The complete blood count results show severe macrocytic anemia.
Of the following, the MOST likely nutritional de ciency contributing to the abnormal ndings is
A. cobalamin
B. folate
C. niacin
D. thiamin
Answer: A, Vit B12.
Cobalamin de ciency, often resulting from strict vegan diets, results in hematologic ndings, including megaloblastic anemia with clinical symptoms (eg, weakness, impaired cognitive function, and ataxia). Folate deficiency, frequently associated with goat milk intake, can cause megaloblastic anemia, however, diets rich in green vegetables and forti ed cereals are unlikely to be deficient in folate
A 16-year-old su ered a severe traumatic brain injury after being an unrestrained passenger during a high speed motor vehicle collision. In the trauma bay, the patient presents with a Glasgow Coma Scale of 4, and a computed tomography scan of the head shows a large subdural hematoma. They undergo a decompressive hemicraniectomy with placement of an intracranial pressure monitor and ventricular drain. Despite these interventions, the patient develops refractory intracranial hypertension necessitating initiation of burst suppression with a pentobarbital infusion. Twenty-four hours after presentation, intracranial pressure acutely decreases, and urine output increases from 2 cc/kg/hour to 10 cc/kg/hour. A neurologic examination reveals bilaterally xed and dilated pupils, no movement to noxious stimuli, no corneal re exes, and no oculocephalic re exes. Neither cough nor gag are present, and there is no spontaneous respiratory e ort. Urine studies are consistent with a diagnosis of diabetes insipidus. The pentobarbital infusion is stopped. Of the following, the MOST appropriate thing to tell the parents at this time is that the diagnosis of brain death
A. cannot be made until at least 48 hours after presentation
B. cannot be made until sedating medications have cleared
C. has been made based on electrocerebral silence
D. has been made based on neurologic criteria
Answer: B, cannot be made until meds have been cleared
The diagnosis of brain death requires the irreversible cessation of brain function, established based on the following criteria:
1. Absence of confounding factors that might obscure the neurologic examination, including metabolic derangements (e.g. severe hypernatremia or uremia) or drug intoxication (eg, barbiturate coma), hypothermia, or hypotension.
2. Persistent absence of brain function based on two separate clinical examinations, showing:
a. Unconsciousness without eye opening/ response to pain.
b. Loss of brainstem reflexes, including absent cough, gag, and oculovestibular, corneal, and pupillary light re exes.
3. Absence of spontaneous respirations demonstrated during apnea testing showing no respiratory effort and a terminal PaCO of 60 mm Hg or greater and a change in 20 mm Hg above the baseline PaCO2
Ancillary studies are not required, nor are they a substitute for clinical examinations. They may be used to assist in diagnosis when components of the examination cannot be completed safely or when there is uncertainty about the examination
A previously healthy 2-month-old infant is brought to the emergency department by his mother due to lethargy and tachypnea. He was in his normal state of health 12 hours ago. He has not had fevers, cough, or di culty breathing, and he has been playful, eating well, and having normal bowel movements and urine output. The mother left her child with a caregiver this morning. When she returned from work, the boy was lethargic and breathing fast. The caregiver denied any trauma and stated that these symptoms, as well as vomiting, occurred progressively over the day. In the emergency department, the infant has a temperature of 37 °C, heart rate of 130 beats/min, respiratory rate 60 breaths/min, blood pressure of 91/53 mm Hg, and oxygen saturation of 100% in room air. He appears to be well developed and well nourished. Upon painful stimuli he opens his eyes. There is no nystagmus, and pupils are 3 mm, equal, and sluggish; he cries inconsolably and withdraws non-purposefully. There are no external signs of trauma. The anterior fontanelle is full. He is breathing rapidly and deeply, with good air movement bilaterally and no wheezing or crackles. His abdomen is soft and nontender. Of the following, a computed tomography scan of the head will MOST likely demonstrate
A. epidural hematoma from rupture of the middle meningeal artery
B. ischemic stroke from cerebral venous sinus thrombosis
C. subdural hematoma from shearing of the intracranial bridging
D. thromboembolism of middle cerebral artery
Answer: subdural hematoma from shearing of the intracranial bridging
A subdural hematoma (SDH) is the accumulation of blood between the dura and the arachnoid. Since the dura straddles the sutures but does not cross the hemispheric ssure, computed tomography of the head will show a crescentic pattern of density that crosses suture lines but does not cross the midline. An SDH is caused by shearing of the bridging veins, which drain the brain parenchyma into the dural cerebral venous sinuses. This disruption can be caused by blunt force trauma or acceleration-deceleration forces, either from a coup contrecoup mechanism or from the brain's movement inside the head during shaking. This mechanism causes SDH most commonly in infants because they have less developed neck and trunk muscles to stabilize the head during acceleration and deceleration movement and because the head is larger relative to the rest of the body
A 2-year-old child with sickle cell disease presents with bilateral leg pain. His vital signs are a temperature of 37.1 °C, heart rate of 140 beats/min, blood pressure of 128/64 mm Hg, respiratory rate of 14 breaths/min, and oxygen saturation 99% in room air. He is admitted to the inpatient pediatric unit with vaso-occlusive crisis and started on ibuprofen, a morphine patient-controlled analgesic, and intravenous uids. The following evening, his temperature is 39.2 °C, heart rate is 168 beats/min, blood pressure 124/60 mm Hg, respiratory rate 46 breaths/min, and oxygen saturation 85% in room air. He is placed on 4L nasal cannula and his saturations increase to 88%. He is transferred to the pediatric intensive care unit and intubated. POCUS lungs shows sliding w/o effusion. Laboratory results are: WBC 19, Hb 9.6, HbS 40%
Of the following, the BEST next step in management is to
A. administer intravenous fluid bolus
B. begin exchange transfusion
C. begin packed red blood cell transfusion
D. insert chest tube
Answer: B. begin exchange transfusion
Complications of sickle cell disease include anemia, vaso-occlusive crises, acute chest syndrome, stroke, and venous thromboembolism. Acute chest syndrome is de ned as a new pulmonary in ltrate with fever, chest pain, or respiratory symptoms (eg, cough, tachypnea, dyspnea, hypoxia).
According to the American Society of Hematology 2020 guidelines for sickle cell disease, they recommend red cell exchange transfusion over simple packed red blood cell transfusion in severe disease. Exchange transfusion should be performed to decrease the hemoglobin S level to less than 30%. A simple packed red blood transfusion would be appropriate in mild acute chest syndrome, but not to exceed a hemoglobin concentration of 11 g/dL (110 g/L).
A 2-year-old child with sickle cell disease presents with bilateral leg pain. His vital signs are a temperature of 37.1 °C, heart rate of 140 beats/min, blood pressure of 128/64 mm Hg, respiratory rate of 14 breaths/min, and oxygen saturation 99% in room air. He is admitted to the inpatient pediatric unit with vaso-occlusive crisis and started on ibuprofen, a morphine patient-controlled analgesic, and intravenous uids. The following evening, his temperature is 39.2 °C, heart rate is 168 beats/min, blood pressure 124/60 mm Hg, respiratory rate 46 breaths/min, and oxygen saturation 85% in room air. He is placed on 4L nasal cannula and his saturations increase to 88%. He is transferred to the pediatric intensive care unit and intubated. POCUS lungs shows sliding. Laboratory results are: WBC 19, Hb 9.6, HbS 40%
Of the following, the BEST next step in management is to
A. administer intravenous uid bolus
B. begin exchange transfusion
C. begin packed red blood cell transfusion
D. insert chest tube
Answer: B. begin exchange transfusion
Complications of sickle cell disease include anemia, vaso-occlusive crises, acute chest syndrome, stroke, and venous thromboembolism. Acute chest syndrome is de ned as a new pulmonary in ltrate with fever, chest pain, or respiratory symptoms (eg, cough, tachypnea, dyspnea, hypoxia)
According to the American Society of Hematology 2020 guidelines for sickle cell disease, they recommend red cell exchange transfusion over simple packed red blood cell transfusion in severe disease. Exchange transfusion should be performed to decrease the hemoglobin S level to less than 30%. A simple packed red blood transfusion would be appropriate in mild acute chest syndrome, but not to exceed a hemoglobin concentration of 11 g/dL (110 g/L).
A 2-day-old neonate is sent to the emergency department by her primary care doctor because of a murmur. The child was born at a local birthing center at term to a 27-year-old mother via normal spontaneous vaginal delivery with APGAR scores of 8 at 1 minute and 10 at 10 minutes, respectively. The mother received no prenatal care. The baby appears to be in no distress. Her heart rate is 150 beats/min, respiratory rate is 40 breaths/min, blood pressure is 75/45 mm Hg, and oxygen saturation is 95% in room air. She is breathing comfortably, aerating well, and is warm and well perfused. Her liver is palpable 3 cm below the right costal margin. There is a normal S1 and S2 with a 3/6 harsh systolic murmur heard best at the left upper sternal border. Echocardiography demonstrates severe pulmonary stenosis. Of the following, the BEST next step in management is
A. initiation of a milrinone infusion
B. observation with cardiorespiratory monitoring
C. referral for a cardiology evaluation upon discharge
D. urgent referral to cardiology for cardiac catheterization
E. immediate initiation of prostaglandin infusion
Answer: D, urgent cardiac cath
With severe pulmonary stenosis, the right ventricle can ultimately fail because of the increased work needed for pulmonary blood flow in the physiological context of a high-pressure gradient.
This neonate’s oxygen saturations are normal, which is not consistent with critical pulmonary stenosis implying a patent ductus is present. If the infant was hypoxic or cyanotic, signifying critical pulmonary stenosis, it would be necessary to initiate prostaglandin infusion to maintain a patent ductus arteriosus.
A 14-year-old adolescent with a history of chronic lung disease, heart failure, and chronic renal insu ciency is admitted to the pediatric intensive care unit for exacerbation of heart failure. He has an extensive medical history and con rmed severe allergic reactions to morphine, vancomycin, and sulfamethoxazole trimethoprim. He has a heart rate of 100 beats/min, respiratory rate of 20 breaths/min, blood pressure of 145/85 mm Hg, and oxygen saturation of 95% on 3 L/min of oxygen. Physical examination ndings are signi cant for signs of plethora with facial and eyelid edema, di use ne crackles in his lungs, and a S gallop. Chest radiography shows cardiomegaly and di use interstitial edema with small bilateral pleural e usions. He is given medication to help with his condition, and within 30 minutes he develops di use urticaria, wheezing, hypotension, and respiratory distress. Of the following, the medication that was MOST likely administered is
A. digoxin
B. enalapril
C. furosemide
D. spironolactone
Answer: furosemide
Furosemide is a sulfonamide; it should be avoided in patients with sulfa allergy. Loop diuretic therapy can result in clinically signi cant electrolyte abnormalities, including hypokalemia, hypomagnesemia, hypocalcemia, and hyponatremia. Loop diuretic–induced ototoxicity is a function of serum concentration and rate of drug administration
A 2-year-old patient is admitted to the pediatric intensive care unit with acute respiratory failure in the setting of an adenovirus infection. The child is intubated and mechanically ventilated and is receiving continuous infusions of dexmedetomidine and fentanyl. Despite increasing doses of these medications, the patient is agitated, making him di cult to ventilate; he is in danger of unplanned extubation. The patient is prescribed intermittent lorazepam (0.1 mg/kg) every one hour as needed. Due to the ongoing agitation, the patient is receiving the as-needed lorazepam every hour. On routine serum blood gas monitoring, the patient is noted to have a worsening metabolic acidosis. Of the following, the additional laboratory study that should be monitored is
A. serum alanine transferase
B. serum creatinine
C. serum osmolality
D. serum procalcitonin
Answer: serum osmolality
Propylene glycol, an additive in lorazepam formulation and other medications, can cause an elevated osmolar gap. Patients receiving continuous lorazepam or frequent lorazepam dosing should be monitored for accumulation of propylene glycol and subsequent osmolar gap; midazolam is a better choice for continuous administration. Discontinuation of lorazepam will usually resolve the toxicity although hemodialysis has been described. Propylene glycol is metabolized to lactate, another laboratory value to assess in patients receiving repeated doses of lorazepam.
A pediatrician is called to the emergency department to assess a 12-year-old child in respiratory distress. The child presents with several hours of fatigue and progressively worsening dyspnea, which was preceded by 1 day of nonspeci c upper respiratory tract infection symptoms. On arrival, the patient is alert but answers questions in brief, 4- to 5-word replies. On auscultation, he has poor air movement with faint end-expiratory wheezing and demonstrates signi cant accessory muscle use. His vital signs are a heart rate of 122 beats/min, blood pressure of 110/54 mm Hg, respiratory rate of 34 breaths/min, and SpO is 92% while receiving inhaled ꞵ-agonist therapy. Of the following, the pharmacotherapy of this agent works by
A. agonizing the Gq subunit, with increased inositol triphosphate and increased intracellular calcium
B. agonizing the Gs subunit, increasing adenylate cyclase and cyclic adenosine monophosphate
C. agonizing the Gi subunit, reducing adenylate cyclase and cyclic adenosine monophosphate
D. antagonizing the Gs subunit, reducing adenylate cyclase and cyclic adenosine monophosphate
The autonomic nervous system is delineated into the sympathetic and parasympathetic systems. The sympathetic nervous system has 4 receptor phenotypes, all of which utilize secondary-messenger cascades. Inhaled and/or intravenous ꞵ agonists are sympathomimetic agents that function at the ꞵ-2 receptor by Gs stimulation, thereby promoting smooth muscle relaxation.
This secondary messenger confers its biological e ect of smooth muscle relaxation by activating phosphokinase A, which phosphorylates proteins associated with calcium channels. Phosphokinase A activation also promotes modulating of intracellular calcium. The net e ect is calcium sequestration and smooth muscle relaxation
A 10-year-old child is an unrestrained passenger in a motor vehicle collision. She lost consciousness at the scene, but when emergency medical services arrived, she was crying and moving all extremities Her pupils are equally round and reactive to light. She is placed in a cervical collar and transported to a local hospital. Head computed tomography demonstrates a 1 cm left-sided subdural hematoma with no midline shift. En-route to the trauma center she becomes more somnolent. She is unarousable to painful stimulation and is placed on a nonrebreather mask. On arrival she has a respiratory rate of 14 breaths/min and oxygen saturation of 88%. She is immediately intubated with the aid of neuromuscular blockade. A neurosurgeon evaluates the patient within 10 minutes of the intubation and requests a train-of-four stimulation. Surface electrodes are placed along the ulnar nerve. Four stimuli are delivered with a frequency of 2 Hz, each separated by 0.5 seconds. Four equal, faint, low amplitude twitches are visualized. Of the following, the neuromuscular blocking agent MOST likely administered for intubation was
A. cisatracurium
B. rocuronium
C. succinylcholine
D. vecuronium
Answer: Succinylcholine
Train-of-four stimulation can be used to monitor the degree of neuromuscular blockade. With train-of-four stimulation, non-depolarizing muscle relaxants exhibit fade, a progressive reduction in the amplitude of the muscle contraction. These drugs not only block postsynaptic nicotinic receptors at the motor end plate, but also block presynaptic nicotinic receptors that normally facilitate mobilization of ACh during repetitive stimulation. (so less and less ACh released with each trigger)
With train-of-four stimulation, depolarizing neuromuscular blockade results in equal contractions of lower amplitude than baseline contractions. It does not impair the presynaptic mechanisms needed for sustained ACh release.
A 7-year-old child is awaiting a liver transplant in the pediatric intensive care unit. He is intubated and sedated after recovering from an episode of spontaneous bacterial peritonitis. He requires an FiO of 1.0 to keep his saturations >92% and has developed notably worsened abdominal distension alongside generalized edema, with urine output of only 0.2 mL/kg/hr in the past 24 hours. Bladder pressure was assessed and noted to be 10 cm H O. His most recent laboratory values are shown: ALT/AST in thousands, low albumin, high bilirubin, high creatinine. Of the following, the definitive treatment for this patient’s condition is
A. orthotopic liver transplantation
B. renal replacement therapy
C. serial infusions of albumin and antibiotics
D. terlipressin
Answer: A, orthotopic liver transplant
Hepatorenal syndrome is the development of renal failure in the setting of chronic liver failure; it is a very rare complication, but one with high mortality. Liver transplantation is the definitive treatment for hepatorenal syndrome.
In hepatorenal syndrome, portal hypertension causes stasis and release of vasodilatory mediators, leading to splanchnic vasodilatation. This low vascular resistance then activates compensatory systems, including the renin angiotensin aldosterone system and the sympathetic nervous system. The activation subsequently leads to renal vasoconstriction, which contributes to the AKI. The persistent hypotension and low resistance also result in hyperdynamic circulation as compensation, building cardiac debt. If these conditions persist, they may lead to cardiac and renal dysfunction.
The diagnosis of HRS is based on the International Club of Ascites (ICA) criteria. In the past, two types of HRS have been described, with type 1 HRS characterized by rapid worsening of kidney function usually with a precipitating event, and type 2 by a slow, progressive form of kidney failure.
Optimizing kidney function should be a pretransplant goal, as it is a predictive factor for postoperative survival.