NCC course outline - Certified in NeuroCritical Care (ABEM) Updated: 2024 | ||||||||||||||||||||||||||
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Exam Code: NCC Certified in NeuroCritical Care (ABEM) course outline January 2024 by Killexams.com team | ||||||||||||||||||||||||||
NCC Certified in NeuroCritical Care (ABEM) The following are specific diseases, conditions, and clinical syndromes commonly managed by a neurointensivist: A. Cerebrovascular Diseases 1. Infarction and ischemia • Massive hemispheric infarction • Basilar artery occlusion and stenosis • Carotid artery occlusion and stenosis • Crescendo TIAs • Occlusive vasculopathies (Moya-Moya, sickle cell) • Spinal cord infarction 2. Intracerebral hemorrhage • Supratentorial • Cerebellar • Brainstem • Intraventricular 3. Subarachnoid hemorrhage - aneurysmal and other Vascular malformations • Arteriovenous malformations • AV fistulas • Cavernous malformations • Developmental venous anomalies 4. Dural sinus thrombosis 5. Carotid-cavernous fistulae 6. Cervical and cerebral arterial dissections B.Neurotrauma 1. Traumatic brain injury • "Diffuse axonal injury" • Epidural hematoma • Subdural hematoma • Skull fracture • Contusions and lacerations • Penetrating craniocerebral injuries • Traumatic subarachnoid hemorrhage 2. Spinal cord injury • Traumatic injury (transection, contusion, concussion) • Vertebral fracture and ligamentous instability C. Disorders, Diseases, Seizures, and Epilepsy 1 . Seizures and epilepsy • Status epilepticus (SE) Convulsive Non-convulsive (partial-complex and "subtle" secondarily generalized SE) Myoclonic 2. Neuromuscular diseases • Myasthenia gravis • Guillain-Barre syndrome • ALS • Rhabdomyolysis and toxic myopathies • Critical illness myopathy and neuropathy 3. Infections • Encephalitis (viral, bacterial, parasitic) • Meningitis (viral, bacterial, parasitic) • Brain and spinal epidural abscess 4. Toxic-metabolic disorders • Neuroleptic malignant syndrome/malignant hyperthermia • Serotonin syndrome • Drug overdose and withdrawal (e.g., barbiturates, narcotics, alcohol, cocaine, acetaminophen). • Temperature related injuries (hyperthermia, hypothermia) 5. Inflammatory and demyelinating diseases • Multiple sclerosis (Marburg variant, transverse myelitis) • Neurosarcoidosis • Acute disseminated encephalomyelitis (ADEM) • CNS vasculitis • Chemical or sterile meningitis (i.e. posterior fossa syndrome, NSAID induced) • Central pontine myelinolysis • Others 6. Neuroendocrine disorders • Pituitary apoplexy • Diabetes insipidus (including triple phase response) • Panhypopituitarism • Thyroid storm and coma • Myxedema coma • Addisonian crisis D. Neuro-oncology 1 . Brain tumors and metastases 2. Spinal cord tumors and metastases 3. Carcinomatous meningitis 4. Paraneoplastic syndromes E.Encephalopathies 1. Eclampsia, including HELLP Syndrome 2. Hypertensive encephalopathy 3. Hepatic encephalopathy 4. Uremic encephalopathy 5. Hypoxic-ischemic and anoxic encephalopathy 6. MELAS F.Clinical syndromes 1.Coma 2. Herniation syndromes with monitoring & ICP 3. Elevated intracranial pressure and Intracranial hypotension/hypovolemia 4. Hydrocephalus detection & treatment 5. Cord compression 6. Death by neurologic criteria, end of life issues, and organ donation 7. Vegetative state 8. Dysautonomia (cardiovascular instability, central fever, hyperventilation) 9. Reversible posterior leukoencephalopathy 10. Psychiatric emergencies (psychosis) G. Perioperative Neurosurgical Care H.Pharmacotherapeutics II. General Critical Care: Pathology, Pathophysiology, and Therapy A. Cardiovascular Physiology, Pathology, Pathophysiology, and Therapy 1. Shock (hypotension) and its complications (vasodilatory and cardiogenic) 2. Myocardial infarction and unstable coronary syndromes 3. Neurogenic cardiac disturbances (ECG changes, stunned myocardium) 4. Cardiac rhythm and conduction disturbances; use of antiarrhythmic medications; indications for and types of pacemakers 5. Pulmonary embolism 6. Pulmonary edema: cardiogenic versus noncardiogenic (including neurogenic) 7. Acute aortic and peripheral vascular disorders (dissection, pseudoaneurysm) 8. Recognition, evaluation and management of hypertensive emergencies and urgencies 9. Calculation of derived cardiovascular parameters, including systemic and pulmonary vascular resistance, alveolararterial gradients, oxygen transport and consumption B.Respiratory Physiology, Pathology, Pathophysiology and Therapy 1.Acute respiratory failure • Hypoxemic respiratory failure (including ARDS) • Hypercapnic respiratory failure • Neuromuscular respiratory failure 2. Aspiration 3. Bronchopulmonary infections 4. Upper airway obstruction 5. COPD and status asthmaticus, including bronchodilator therapy 6. Neurogenic breathing patterns (central hyperventilation, Cheyne-Stokes respirations) 7. Mechanical ventilation • Positive pressure ventilation (BIPAP) • PEEP, CPAP, inverse ratio ventilation, pressure support ventilation, pressure control, and non- invasive ventilation • Negative pressure ventilation • Barotrauma, airway pressures (including permissive hypercapnia) • Criteria for weaning and weaning techniques 8. Pleural Diseases • Empyema • Massive effusion • Pneumothorax 9. Pulmonary hemorrhage and massive hemoptysis 10. Chest X-ray interpretation 11. End tidal C02 monitoring 12. Sleep apnea 13. Control of breathing C. Renal Physiology,Pathology, Pathophysiology and Therapy 1.Renal regulation of fluid and water balance and electrolytes 2.Renal failure: Prerenal, renal, and postrenal 3.Derangements secondary to alterations in osmolality and electrolytes 4. Acid-base disorders and their management 5.Principles of renal replacement therapy 6. Evaluation of oliguria and polyuria 7.Drug dosing in renal failure 8. Management of rhabdomyolysis 9. Neurogenic disorders of sodium and water regulation (cerebral salt wasting and SIADH). D. Metabolic and Endocrine Effects of Critical Illness 1. Enteral and parenteral nutrition 2. Endocrinology • Disorders of thyroid function (thyroid storm, myxedema coma, sick euthyroid syndrome) • Adrenal crisis • Diabetes mellitus Ketotic and hyperglycemic hyperosmolar coma Hypoglycemia 3. Disorders of calcium and magnesium balance 4. Systemic Inflammatory Response Syndrome (SIRS) 5. Fever, thermoregulation, and cooling techniques E.Infectious Disease Physiology, Pathology, Pathophysiology and Therapy 1. Antibiotics • Antibacterial agents • Antifungal agents • Antituberculosis agents • Antiviral agents • Antiparasitic agents 2. Infection control for special care units • Development of antibiotic resistance • Universal precautions • Isolation and reverse isolation 3. Tetanus and botulism 4. Hospital acquired and opportunistic infections in the critically ill 5. Acquired Immune Deficiency Syndrome (AIDS) 6. Evaluation of fever in the ICU patient 7. Central fever 8. Interpretation of antibiotic concentrations, sensitivities F.Physiology, Pathology, Pathophysiology and therapy of Acute Hematologic Disorders 1 . Acute defects in hemostasis • Thrombocytopenia, thrombocytopathy • Disseminated intravascular coagulation • Acute hemorrhage (GI hemorrhage, retroperitoneal hematoma) • Iatrogenic coagulopathies (warfarin and heparin induced) 2. Anticoagulation and fibrinolytic therapy 3. Principles of blood component therapy (blood, platelets, FFP) 4. Hemostatic therapy (vitamin K, aminocaproic acid, protamine, factor VIla) 5. Prophylaxis against thromboembolic disease 6. Prothrombotic states G. Physiology, Pathology, Pathophysiology and Therapy of Acute Gastrointestinal (GI) and Genitourinary (GU) Disorders 1. Upper and lower gastrointestinal bleeding 2. Acute and fulminant hepatic failure (including drug dosing) 3. Ileus and toxic megacolon 4. Acute perforations of the gastrointestinal tract 5. Acute vascular disorders of the intestine, including mesenteric infarction 6. Acute intestinal obstruction, volvulus 7. Pancreatitis 8. Obstructive uropathy, acute urinary retention 9. Urinary tract bleeding H. Immunology and Transplantation 1. Principles of transplantation (brain death, organ donation, procurement, maintenance of organ donors, implantation) 2. Immunosuppression, especially the neurotoxicity of these agents I. General Trauma and Burns 1. Initial approach to the management of multisystem trauma 2. Skeletal trauma including the spine and pelvis 3. Chest and abdominal trauma - blunt and penetrating 4. Burns and electrical injury J. Monitoring 1. Neuromonitoring 2. Prognostic, disease severity and therapeutic intervention scores 3. Principles of electrocardiographic monitoring 4. Invasive hemodynamic monitoring 5. Noninvasive hemodynamic monitoring 6. Respiratory monitoring (airway pressure, intrathoracic pressure, tidal volume, pulse oximetry, dead space, compliance, resistance, capnography) 7. Metabolic monitoring (oxygen consumption, carbon dioxide production, respiratory quotient) 8. Use of computers in critical care units for multimodality monitoring K. Administrative and Management Principles and Techniques 1. Organization and staffing of critical care units 2. Collaborative practice principles, including multidisciplinary rounds and management 3. Emergency medical systems in prehospital care 4. Performance improvement, principles and practices 5. Principles of triage and resource allocation, bed management 6. Medical economics: health care reimbursement, budget development L. Ethical and Legal Aspects of Critical Care Medicine 1. Death and dying 2. Forgoing life-sustaining treatment and orders not to resuscitate 3. Rights of patients, the right to refuse treatment 4. Living wills, advance directives; durable power of attorney 5. Terminal extubation and palliative care 6. Rationing and cost containment 7. Emotional management of patients, families and caregivers 8. Futility of care and the family in denial M. Principles of Research in Critical Care 1. Study design 2. Biostatistics 3. Grant funding and protocol writing 4. Manuscript preparation 5. Presentation preparation and skills 6. Institutional Review Boards and HIPAA Ill. Procedural Skills A. General Neuro-Critical Care 1 . Central venous catheter placement; dialysis catheter placement 2. Pulmonary artery catheterization 3. Management of mechanical ventilation, including CPAP/BiPAP ventilation 4. Administration of vasoactive medications (hemodynamic augmentation and hypertension lysis) 5. Maintenance airway and ventilation in nonintubated, unconscious patients 6. Interpretation and performance of bedside pulmonary function tests 7. Direct laryngoscopy 8. Endotracheal intubation 9. Shunt and ventricular drain tap for CSF sampling 10. Performance and interpretation of transcranial Doppler 11. Administration of analgosedative medications, including conscious sedation and barbiturate anesthesia 12. Interpretation of continuous EEG monitoring 13. Interpretation and management of ICP and CPP data 14. Jugular venous bulb catheterization 15. Interpretation of Sjv02 and Pbt02 data 16. Management of external ventricular drains I 7. Management of plasmapheresis and IVIG 18. Administration of intravenous and intraventricular thrombolysis 19. Interpretation of CT and MR standard neuroimaging and perfusion studies and biplane contrast neuraxial angiography 20. Perioperative and postoperative clinical evaluation of neurosurgical and interventional neuroradiology patients 21. Performance of lumbar puncture and interpretation of cerebrospinal fluid results 22. Induction and maintenance of therapeutic coma and hypothermia | ||||||||||||||||||||||||||
Certified in NeuroCritical Care (ABEM) Certification-Board NeuroCritical course outline | ||||||||||||||||||||||||||
Other Certification-Board examsBCBA Board Certification in Business Valuation (BCBA)CDL Commercial Drivers License DMV Driver Motor Vehicle FSOT Foreign Service Officer Test ICTS Illinois Certification Testing System ISEE Independent School Entrance Examination MTEL Massachusetts Tests for Educator Licensure NCE National Counselor SBAC Smarter Balanced Assessment Consortium STAAR State of Texas Assessments ofAcademic Readiness BCB-Analyst Board Certified Behavior Analyst (BCBA) ABCTE American Board for Certification of Teacher Excellence Exam ABFM Family Medicine Board Certification Exam ABPN-VNE American Board of Psychiatry and Neurology - Vascular Neurology Exam CSLE National-Interstate Council Cosmetology Licensing Exam NAB-NHA Nursing Home Administrator (NAB) NCC Certified in NeuroCritical Care (ABEM) NLN-PAX Nursing School Entrance Test NRP Nationally Registered Paramedics (EMT) RACP Royal Australasian College of Physicians exam (FRACP) TCRN Trauma Certified Registered Nurse Exam | ||||||||||||||||||||||||||
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NCC Dumps NCC Braindumps NCC Real Questions NCC Practice Test NCC dumps free Certification-Board NCC Certified in NuroCritical Care (ABEM) http://killexams.com/pass4sure/exam-detail/NCC Question: 710 A 55-year-old man, admitted with a Hunt and Hess grade 4aneurysmal subarachnoid hemorrhage (SAH), is now post bleed day5 with increasing Transcranial Doppler (TCD) velocities. Meanarterial pressure (MAP) is 76 mmHg on norepinephrine 12mcg/min, up from 5 mcg/min 24 hours earlier, intracranial pressure(ICP) is 12 mmHg, and heart rate (HR) is 110/min with sinusvolume control mechanical ventilation receiving 7 mL/kg tidalvolume (TV) with positive end-expiratory pressure (PEEP) of 10White blood cell (WBC) count is 11,000 with a new infiltrate onchest x-ray (CXR); and serum creatinine has increased to 1.5mg/dL. Fluid balance over the past 24 hours is 2 L positive withgood urine output. In addition to sending blood cultures, lactate, andstarting antibiotics, how can volume status be assessed to determinewhether additional fluid is needed for adequate resuscitation? A. Bolus 2 L normal saline (NS) over 2 hours and assess change in B. Perform a straight leg raise and assess for change in cardiac C. Place a Swan-Ganz catheter given the presence of shock and D. Measure inferior vena cava size change during inspiration and E. Insert arterial line and measure pulse pressure or stroke volume G. mmHArterial blood gas (ABG) reveals a PaO2/FiO2 ratio of 250. Answer: B Explanation: Our patient is in septic shock, which requires timely acquisition of cultures, lactic acid, initiating antibiotics, and fluid resuscitation. This question is focused on how to best determine whether a patient in shock has been adequately resuscitateda critical question, since too little fluid leads to inadequate preload, reduced cardiac output (CO) and oxygen delivery, and consequently tissue hypoperfusion. Conversely, excessive volume loading, without further increase in CO, would lead to hemodilution and tissue edema. Fluid overload has been associated with worse outcomes in critically ill patients, and current guidelines recommend frequent assessment for ongoing need for resuscitation prior to fluid administration. Fluid responsiveness can be assessed by several methods. Traditional static measures of cardiac preload, such as central venous pressure (CVP) and pulmonary capillary wedge pressure (PCWP) are unreliable for predicting fluid responsiveness. Dynamic measures of cardiac preload, such as stroke volume variation (SVV) and pulse pressure variability (PPV) require an arterial line, and are excellent measures of volume responsiveness in shock patients - with some notable exceptions: spontaneous respiration; tidal volume (TV) <8 mL/kg; PEEP >5; low lung compliance (i.e., ARDS); and when arrhythmias are present. Our patient was spontaneously breathing, limiting the diagnostic accuracy of SVV/PPV. Variation in inferior vena caval size during mechanical ventilation, as measured by echocardiography, is another means of assessing fluid responsiveness, but seems to be less sensitive and specific than SVV/PPV, with similar limitations. A third technique involves an autotransfusion, by passively raising the legs to 40 degrees in a supine patient, which has been shown to be a sensitive and specific assessment for volume responsiveness, potentially even in spontaneously breathing patients, during low-tidal ventilation, and with cardiac arrhythmia. Question: 711 An 18-year-old man admitted to the hospital with a gunshot woundto the head and intractable intracranial hypertension is being deescalatedfrom hyperosmolar therapy with hypertonic saline andpotassium is 2.0 mEq/L, despite having received approximately 120mEq of potassium chloride in replacement that day, and the urineoutput has been consistently greater than 200 mL/hour. Additionalpertinent labs include Na 153 mEq/L, Mg 1.5 mEq/L, and HCO3 20mEq/L. You notice a change on the telemetry monitor and order aabnormality? A. Acute myocardial infarction (MI) B. Acute pulmonary embolism C. Hypokalemia D. Acidosis E. Hypothermia G. stat ECWhat is the likely cause of this Answer: C Explanation: These ECG changes are typically seen with severe refractory hypokalemia. The earliest ECG changes associated with hypokalemia are a decrease in T-wave amplitude followed by a ST segment depression and T-wave inversions. Subsequently, the PR interval may be prolonged with an increase in amplitude of the P wave. U waves (a positive deflection after the T wave) may be seen and in severe hypokalemia may fuse with the T wave to form giant U waves as seen in the ECG. A pseudo-prolonged QT interval may be seen, which is actually a QU interval in the absence of a T wave. The most common cause of hypokalemia is renal losses after diuretic use (more commonly thiazide than loop or osmotic diuretics), especially if two diuretics acting on different parts of the tubular system are used. Patients who develop secondary hypoaldosteronism from liver disease, congestive heart failure (CHF), or nephrotic syndrome are also at risk. Antibiotics such as penicillins and aminoglycosides can promote potassium loss. In the neurocritical care setting, patients receiving mannitol or hypertonic saline infusions have been noted to develop hypokalemia because of the diuretic effect and as a consequence of the high-sodium load reaching the collecting ducts. For this reason some centers use potassium-sparing diuretics in conjunction with mannitol to avoid symptomatic hypokalemia in the setting of intracranial pressure (ICP) management. Hypokalemia can be refractory if concomitant hypomagnesaemia is not corrected. The exact etiology of this is not known, but it may be multifactorial. Low intracellular magnesium levels may increase potassium wasting from the collecting tubules, especially in the setting of additional factors such as an increase in distal sodium delivery. ECG changes in hypomagnesemia include an increased PR and QT interval, widened QRS complex, and flattened T wave. The findings can be identical to those seen in hypokalemia; however, in this case, the patients potassium level is much lower than his magnesium level and, given the refractory nature of his disease, hypokalemia is the more likely cause. Hypothermia at 35C (95F) is associated with sinus tachycardia. As the core body temperature drops further (<90F or 32C), sinus bradycardia with prolongation of PR interval, QRS widening, and QT interval are seen. Osborn waves (an upward deflection after the QRS complex) are seen below 86F or 30C. Question: 712 A 44-year-old morbidly obese woman with hypertension anddiabetes is found slumped over in a bathroom stall. At the scene, herblood pressure (BP) is documented at 180/90 with a pulse of 78; herblood sugar is 180 mmol/L. CT scan of the head is shown. What isthe likely cause of this patients findings? A. Hypertensive intracerebral hemorrhage (ICH) B. Embolic stroke with hemorrhagic conversion C. Venous sinus thrombosis D. Aneurysmal subarachnoid hemorrhage (SAH) E. Hemorrhagic encephalitis Answer: D Explanation: This axial CT scan of the head shows an intraparenchymal hemorrhage (IPH) with a sylvian SAH and a small subdural hematoma (SDH), with the outline of an aneurysm visible lateral to the IPH. Approximately 20% of patients with aneurysmal rupture have associated IPH, occurring more commonly in patients with anterior communicating artery (AComm), distal anterior cerebral artery, and distal middle cerebral artery (MCA) aneurysms. These patients present with callosal, interhemispheric, and sylvian/temporal hematomas. In addition, patients may have concurrent intraventricular hemorrhage (IVH) and SDH. Rarely, patients may present with IPH, IVH, or SDH without any evidence of SAH. In these cases, a history of thunderclap headache, absence of risk factors for IPH or IVH, and absence of a history of trauma should raise the suspicion of a saccular aneurysm. Likely causes of the absence of SAH are the location of the dome of the aneurysm close to the ventricular system or brain parenchyma and delayed presentation after the hemorrhage, with radiographic resolution of subarachnoid blood. Another theory is that the IPH/IVH may represent a rebleed after the subarachnoid space has been scarred down by a sentinel hemorrhage. Question: 713 A 29-year-old C5C6 quadriplegic patient is being prepared fortransfer to a rehabilitation facility when you are paged for with thecondition? A. Permanent pacemaker B. PRN intravenous (IV) atropine C. PO albuterol D. PO theophylline E. All of the above G. following findinWhat is an appropriate long-term therapy for this Answer: E Explanation: Patients with acute spinal cord injury suffer a myriad of complications of which pulmonary and cardiac are the most common. Among the cardiac complications, shock and hypotension occur early and are usually the reason for ICU admission in the first week after injury. Sinus bradycardia, dysrhythmia, and cardiac arrest can occur subsequently, usually within the first 14 days after injury. Acute spinal cord injury above T6 can disrupt the descending sympathetic pathways to the intermediolateral cell column in the T1-L2 spinal cord. This results in loss of supraspinal sympathetic control and unopposed parasympathetic activity in the respiratory and cardiac systems in quadriplegic patients, making them prone to prolonged episodes of bradycardia, pauses, and intermittent heart blocks, especially when suctioned or turned. Atropine should be readily available for patients with bradycardia, and 0.5 to 1 mg should be administered when symptomatic or prophylactically before suctioning. Oral albuterol and theophylline can be used to increase resting heart rate, although there are no randomized trials to support this. Some patients with significant heart block or recurrent cardiac arrests may require a permanent pacemaker. Question: 714 Answer: C Explanation: The history of ovarian cancer and the diffuse leptomeningeal enhancement are suggestive of meningeal carcinomatosis. Meningeal carcinomatosis is seen in 1% to 5% of patients with solid tumors (commonly breast, nonsmall-cell lung cancer, and melanoma), 5% to 15% of patients with leukemia/lymphoma (leukemic/lymphomatous meningitis), and 1% to 2% of patients with primary brain tumors. Neurologic symptoms usually localize to several regions of the neuraxis, with those involving the spinal cord and cauda equina being most common, followed by cranial neuropathies and hemispheric dysfunction. Patients often present with signs of hydrocephalus and elevated intracranial pressures (ICP). Diagnosis is made by having a high index of suspicion, meningeal enhancement (often most prominent in the basal meninges, dorsal spinal column, and cauda equina), cerebrospinal fluid (CSF) monocytosis, and isolating tumor cells in CSF on cytology. Although the latter is the gold standard, tumor cells are isolated in only 50% of samples on the first LP, with the yield increasing to 80% on the second puncture. There is no added benefit of subsequent LPs. Treatment is mostly palliative, with median survival of 2 to 3 months. Whole brain radiation therapy and intrathecal chemotherapy are the mainstays of treatment and may prevent further neurologic deterioration and improvement in quality of life. Supportive treatments such as antiepileptic medications, pain medications, and occasionally corticosteroids in patients with concomitant parenchymal disease should be prescribed. Miller Fisher syndrome is a demyelinating cranial and peripheral neuropathy, which is a variant of GuillainBarr syndrome (GBS) and is defined by a triad of areflexia, ophthalmoplegia, and ataxia. Patients classically do not have signs of encephalitis or encephalopathy. Anti-GQ1b antibodies are present in 90% of patients. Bickerstaff brainstem encephalitis presents with ataxia, ophthalmoplegia, hyperreflexia, and alteration of consciousness. Hyperintense lesions are seen in the midbrain, pons, and medulla on MRI. A significant number of patients have evidence of concurrent axonal GBS, suggesting that this may be another variant of the disease. The progression of symptoms and MRI findings preclude pontine infarction, and the EEG does not support a diagnosis of NCSE. Question: 715 A 67-year-old woman was transferred from an outside facility withoutside hospital with complaints of nausea, vomiting, ataxia, andprogressive lethargy. The patient had a history of ovarian cancer inremission for 3 years and was otherwise healthy. CT scan and MRIblood cell (WBC) count of 15 (40% N, 20% L, and 40% M), redblood cell (RBC) count 250, glucose 40, and protein 100. Allbacterial and viral cultures and polymerase chain reactions (PCRs)were negative, and she was empirically treated with acyclovir. Uponyour evaluation, the patient was comatose with sluggish pupillaryresponse, dysconjugate gaze, absent oculocephalic reflexes,extensor posturing bilaterally, and brisk reflexes. She was breathingrepeated and showed WBC 18 (100% M), RBC 50, glucose 28, andprotein 150. Serum glucose was 150 mg/dL. EEG revealedgeneralized delta and theta activity without rhythmicity. Brain MRIwith contrast is shown on the right. What is the most likely cause ofthe patients condition? A. MillerFisher syndrome B. Bickerstaff brainstem encephalitis C. Meningeal carcinomatosis D. Pontine infarction E. Nonconvulsive status epilepticus (NCSE) Answer: C Explanation: The history of ovarian cancer and the diffuse leptomeningeal enhancement are suggestive of meningeal carcinomatosis. Meningeal carcinomatosis is seen in 1% to 5% of patients with solid tumors (commonly breast, nonsmall-cell lung cancer, and melanoma), 5% to 15% of patients with leukemia/lymphoma (leukemic/lymphomatous meningitis), and 1% to 2% of patients with primary brain tumors. Neurologic symptoms usually localize to several regions of the neuraxis, with those involving the spinal cord and cauda equina being most common, followed by cranial neuropathies and hemispheric dysfunction. Patients often present with signs of hydrocephalus and elevated intracranial pressures (ICP). Diagnosis is made by having a high index of suspicion, meningeal enhancement (often most prominent in the basal meninges, dorsal spinal column, and cauda equina), cerebrospinal fluid (CSF) monocytosis, and isolating tumor cells in CSF on cytology. Although the latter is the gold standard, tumor cells are isolated in only 50% of samples on the first LP, with the yield increasing to 80% on the second puncture. There is no added benefit of subsequent LPs. Treatment is mostly palliative, with median survival of 2 to 3 months. Whole brain radiation therapy and intrathecal chemotherapy are the mainstays of treatment and may prevent further neurologic deterioration and improvement in quality of life. Supportive treatments such as antiepileptic medications, pain medications, and occasionally corticosteroids in patients with concomitant parenchymal disease should be prescribed. Miller Fisher syndrome is a demyelinating cranial and peripheral neuropathy, which is a variant of GuillainBarr syndrome (GBS) and is defined by a triad of areflexia, ophthalmoplegia, and ataxia. Patients classically do not have signs of encephalitis or encephalopathy. Anti-GQ1b antibodies are present in 90% of patients. Bickerstaff brainstem encephalitis presents with ataxia, ophthalmoplegia, hyperreflexia, and alteration of consciousness. Hyperintense lesions are seen in the midbrain, pons, and medulla on MRI. A significant number of patients have evidence of concurrent axonal GBS, suggesting that this may be another variant of the disease. The progression of symptoms and MRI findings preclude pontine infarction, and the EEG does not support a diagnosis of NCSE. Question: 716 A 60-year-old patient with diabetes and hypertension is transferredto your ICU from another facility, where he was being treated forurosepsis. The patient has been on stable, low-dose vasopressors for4 days, is on antibiotics, and appears adequately volumenot received nutrition since his admission to the hospital 5 days agobecause he was on vasopressors. You would: A. Insert a feeding tube and advance to full dose tube feeds despite B. Order total parenteral nutrition (TPN) C. Order peripheral parenteral nutrition (PPN) D. Start a dextrose solutionit should provide enough calories! E. Start trophic feeds through the gut at 10 to 20 mL/hour while he Answer: A Explanation: Initiation of enteral nutrition (EN) in critically ill patients is not always clear cut. It is preferable to use EN in critically ill patients as it reduces infectious complications, promotes enterocyte health while maintaining a strong mucosal barrier, and has a lesser stress response than parenteral nutrition (PN). However, there is concern that initiating EN in a patient with hemodynamic compromise and possible splanchnic vasoconstriction may promote nonocclusive mucosal ischemia (NOMI) due to increased oxygen demand. Turza et al. recommend a four-stage approach to initiating EN in patients requiring vasopressors: a. Evaluate the patients medical and nutritional history. Patients with multiple vascular risk factors may be predisposed to NOMI, while those with poor nutritional response or high metabolic demand will benefit from early nutrition. b. Evaluate the current physiologic state. Low-dose, nonescalating vasopressors in patients who are volume resuscitated and able to maintain a mean arterial pressure (MAP) greater than 60 should not deter the initiation of EN. Alternately, patients with dropping urine output, worsening lactate levels, and base deficit and those requiring frequent transfusions may not be able to tolerate EN. c. Establish gastrointestinal (GI) access and pick appropriate tube feeds. The use of formulas with lower osmolarity (<700 mOsm) and fiber content and simpler sugars will reduce metabolic demands, improve transit time, and reduce dysmotility, thereby alleviating factors which may result in the bacterial overgrowth that worsens NOMI. d. Postinitiation monitoring includes serial abdominal examinations and gastric residual checks. Laboratory monitoring of lactate, white blood cell counts, and hemoglobin levels or radiologic testing may be performed if there is concern for ileus. At times, a combination of trophic EN and supplemental PN is adopted as an intuitive compromise. This has been shown to increase the risk of nosocomial infections in a retrospective review of trauma patients. Question: 717 A 40-year-old woman is admitted to the hospital after witnessedcardiac arrest for 20 minutes. Bystanders performed CPR untilwas initiated after admission to the hospital, and the patient wasnoted to have frequent myoclonic jerks during rewarming.Brainstem reflexes were intact and the patient had flexor posturingto painful stimulation. MRI brain revealed scattered diffusionweightedimaging changes in the cortex but no damage to the deepstructures. EEG was performed and is shown in the following A. Have a family discussion regarding irreversible brain damage B. Load with an antiepileptic agent until myoclonic jerks stop since C. Continue EEG monitoring and titrate antiepileptic agents until D. Load with antiepileptic drugs until clinical myoclonus stops and E. Recool the patient and rewarm more slowly next time Answer: C Explanation: The EEG is consistent with postanoxic status epilepticus (PSE). Although this diagnosis usually portends a poor prognosis, the administration of therapeutic hypothermia (TH) to postcardiac arrest patients has made the prediction of outcomes based on American Academy of Neurology (AAN) criteria more difficult. In a prospective study by Rossetti et al., three clinical variables were demonstrated to have higher false-positive rates compared to the AAN guidelines: incomplete brainstem reflexes, myoclonus, and absent motor responses to pain. Early lack of reactivity on continuous EEG, prolonged periods of discontinuity, epileptiform discharges or seizures, and absent cortical responses on somatosensory evoked potentials (SSEP) were strongly associated with mortality. PSE is independently associated with a poor outcome after anoxic injury. However, in the presence of brainstem reflexes, SSEP responses, and EEG reactivity can have a favorable outcome if the condition is treated as status epilepticus (SE). Question: 718 A 60-year-old woman with a history of hypertension presented witha cerebellar intraparenchymal hemorrhage (IPH), fourth ventricleintraventricular hemorrhage (IVH), hydrocephalus with partialbrainstem dysfunction, and somnolence on examination. She wasemergently taken for surgical decompression and did well. Aconventional angiogram was subsequently performed and is shownin the following images. Your next steps in management include allof the following, except: A. Wean external ventricular drain (EVD) and tightly control blood B. Use intrathecal tissue plasminogen activator (tPA) to allow quick C. Take a detailed family history D. Send genetic testing E. Continue outpatient, staged management of this condition Answer: B Explanation: The patient has multiple arteriovenous malformations (AVMs) warranting a detailed family history and genetic workup. Intrathecal tPA is contraindicated in this setting. Intracranial vascular malformations include developmental venous anomalies (DVA), capillary telangiectasias, AVM, and cavernous malformations, each of which have different natural histories and treatment options. Capillary telangiectasias are usually angiographically occult lesions, detected incidentally on contrast-enhanced MRI or CT scans, and are rarely symptomatic. They are benign, thin-walled capillaries surrounded by normal brain parenchyma, do not need treatment or follow-up, and account for 4% to 12% of all vascular malformations. De novo development has been reported. DVA also known as venous angiomas are congenitally enlarged, thickened, hyalinized venous vessels draining normal brain tissue. They are the most common intracranial vascular malformation, with a prevalence of 2.5%, discovered mostly incidentally and often associated with cavernous malformations. A causative link between the two has been suggested, with DVAs being a precursor to cavernous malformations. DVAs can be detected on MRI, CT scan, and angiogram as a single dilated vein or caput medusa. They usually have a benign clinical course with low morbidity and mortality and do not warrant treatment. AVMs are a collection of abnormal blood vessels, comprising arteries, veins, and an intervening collection of abnormal vessels called the nidus. They are congenital lesions with an incidence of 1 per 100,000, often presenting as an intracerebral hemorrhage (ICH) in the third to fourth decade. The bleeding risk varies according to size, location, draining pattern, and so on. Magnetic resonance angiography (MRA) and CT angiography (CTA) can both visualize AVMs; however, conventional angiography remains the gold standard for diagnoses, formulation, and implementation of a treatment plan which may include a combination of surgery, embolization, and radiation therapy. Cavernous malformations are acquired or congenital lesions formed by endothelium-lined vascular spaces without intervening brain parenchyma. They can be seen on CT and MRI as popcorn-shaped dystrophic calcifications or hemosiderin deposits from prior hemorrhages. They are angiographically occult and most commonly present with seizures. Treatment is not always warranted, but surgical resection is often necessary if associated with recurrent hemorrhages or intractable epilepsy. Dural arteriovenous fistulas are malformations located in the meninges fed by dural arteries and drained by dural or leptomeningeal venous channels. The most common location is the transverse sinus. They can develop after trauma, venous thrombosis, or spontaneously, and account for 10% to 15% of all cranial malformations. Clinical presentation includes headache, neurologic deficits, bruits, and hemorrhage, with a cortical drainage pattern consistent with more aggressive behavior. Sixvessel cerebral angiogram remains the gold standard in diagnosing a fistula. Treatment includes endovascular or surgical interventions, with surgery being the more definitive approach. Question: 719 A 35-year-old, 2 days postpartum woman had sudden onset of thethe ED was 180/90, and she was somnolent but had a nonfocalneurologic examination. Opening pressure was normal on lumbarpuncture (LP), and cerebrospinal fluid (CSF) was clear with normalchemistries and cell count. Imaging studies are shown in thefollowing images. What is the most likely diagnosis? A. Eclampsia/preeclampsia B. Posterior reversible encephalopathy syndrome (PRES) C. Venous sinus thrombosis D. Reversible cerebral vasoconstriction syndrome (RCVS) E. Sheehans syndrome Answer: D Explanation: RCVS unifies a group of disorders with similar clinical and radiographic characteristics, such as CallFleming syndrome, benign angiopathy of the central nervous system (CNS), migrainous angiitis, drug-induced cerebral angiopathy (selective serotonin reuptake inhibitors [SSRIs], marijuana), and postpartum angiopathy (hormonal changes, serotonergic surge). Typically, patients present with a thunderclap headache with or without focal neurologic signs, normal CSF analysis without evidence of CNS inflammation, exclusion of other causes of sudden severe headache (aneurysm or vascular abnormalities), and presence of segmental cerebral arterial vasoconstriction on catheter, CT, or magnetic resonance angiography (MRA), which resolves within 12 weeks. Cortical (nonaneurysmal) subarachnoid hemorrhage (SAH) is the most common radiographic finding. The gold standard for diagnosis is detecting the presence and subsequent resolution of segmental vasoconstriction on conventional angiography. In most cases the vascular changes resolve without treatment. Calcium channel blockers (nimodipine, verapamil), glucocorticoids, and intravenous (IV) magnesium have been tried with limited success. Although the course is usually benign, severe vasospasm has been reported resulting in transient ischemic attacks (TIAs), seizures, and ischemic and hemorrhagic infarctions. Intraarterial milrinone and verapamil as well as angioplasty have been attempted with some success in severe or refractory cases. Preeclampsia is defined as pregnancy-induced hypertension with proteinuria, but there is no information about urine studies in this case and the condition is not associated with the imaging findings of cerebral vasoconstriction. Eclampsia, a life-threatening condition occurring in pregnancy or early puerperium, is the occurrence of a tonicclonic seizure in the setting of preeclampsia. Treatment includes IV magnesium to a goal of 4 to 7 mEq/L (46 g IV loading dose, then 12 g/hour), BP control with IV hydralazine or labetalol, and emergent termination of pregnancy. If the patient continues to have seizures, the dose of magnesium may be increased (with close observation for respiratory failure or heart block). IV anticonvulsants and mechanical ventilation can be initiated in refractory cases. PRES is characterized by headache, confusion, seizures, and visual loss with acute subcortical and cortical edema on MRI. Although classically seen in the parietooccipital lobes, brainstem, and cerebellum, the edema can extend as far anteriorly as the temporal and frontal lobes. PRES can be seen in the setting of malignant hypertension, eclampsia, hypercalcemia, and due to drugs such as tacrolimus and cyclosporine. Sheehans syndrome, or postpartum pituitary necrosis, is a complication of postpartum hypovolemic shock resulting in panhypopituitarism. The most common presenting symptom is agalactorrhea. Question: 720 An 18-year-old G1P0 woman presented with a severe headachebehind her right ear, followed by a left-sided tingling sensation andmonitoring and treatment while she continues to have frequentcomplex partial seizures. On examination, she is awake, butsomnolent with left-sided hemiparesis. Imaging studies are shown A. Eclampsia/preeclampsia B. Posterior reversible encephalopathy syndrome (PRES) C. Cerebral venous sinus thrombosis (CVST) D. Reversible cerebral vasoconstriction syndrome (RCVS) E. Sheehans syndrome Answer: C Explanation: CVST is a rare disorder affecting 3 to 4 adults per million annually. With the increasing use of oral contraceptives (OCP) in the past few decades, the disease has become more prevalent in adult women of child-bearing age with an almost sixfold increase in the risk of CVST among OCP users. This is followed by patients with inherited thrombophilia, hypercoagulability associated with pregnancy and puerperium, and head and neck infections. Presentation is varied and dependent on the location and extent of venous involvement. Headache is a ubiquitous presenting complaint, accompanied by seizures in 47% and paresis in 43% of patients. The majority of patients have an indolent course with symptoms developing over days to months. Rarely, they may resemble an arterial infarction but with a waxing and waning course. Focal edema and infarctions are often seen when cortical veins are involved. Larger infarctions and hemorrhages are associated with worsening mental status and coma. Abnormal signal change in the venous sinus on MRI with concomitant loss of flow on magnetic resonance venography (MRV) is diagnostic. Treatment includes systemic anticoagulation with weight-based low molecular weight heparin or unfractionated heparin with transition to vitamin K antagonists to a goal International Normalized Ratio (INR) of 2 to 3 for 3 to 6 months. Patients with a history of deep vein thrombosis (DVT) or recurrent CVST will need indefinite treatment. Intraparenchymal hemorrhage (IPH) is not a contraindication to anticoagulation in this population. Local administration of endovascular thrombolysis has been reported, but there is insufficient efficacy or safety data available to justify its utility in patients who are not refractory to systemic anticoagulation. Decompressive hemicraniectomy can be performed in the setting of malignant cerebral edema with reasonable outcomes. Over 80% of the patients have favorable recovery. Mortality of 7% to 13% is seen within the first month, usually due to cerebral edema in the acute phase or due to underlying cause on subsequent follow-up. Question: 721 A 65-year-old alcoholic with traumatic brain injury (TBI), bifrontalcontusions, and right-sided epidural hematoma with midline shiftand uncal herniation is admitted to your ICU. After initialdecompression, intracranial pressure (ICP) remained within normallimits. Four days postoperatively, the patient is now off all sedationwithdraws on the right, and flexes on the left. What is the cause of hispoor mental status? A. Bifrontal injury B. Diffuse axonal injury C. Persistent effects of midline shift after initial injury D. Nonconvulsive status epilepticus (NCSE) E. All of the above Answer: E Explanation: The patient has suffered a severe head injury with multiple contusions, cerebral edema, and herniation. Individually, each of these conditions can result in a persistent comatose state. In addition, the patient is having nonconvulsive focal seizures, which may be contributing to the encephalopathy. The growing recognition of nonconvulsive seizures (NCS) in the critically ill population and the need for treatment has been a subject of debate in latest years. Are these seizures a cause of the encephalopathy or simply a manifestation of the dying brain? Similarly, should they be aggressively treated with the hope of resolution of coma or are they a hallmark of irreversible brain injury and a poor prognostic sign? Although case reports supporting both arguments exist, these questions are yet to be answered in a randomized controlled trial. Additionally, many reports of NCSE lump together patients who are delirious with patients who are deeply comatose in the setting of NCS, making it all the more difficult to establish prognosis. Until the availability of further evidence, the best way to approach these situations is to look at the entire clinical picture. Aggressive treatment, with its risks, may be warranted if the clinical picture looks worse than can be explained by the level of injury. Similarly, in the setting of a devastating injury, administration of further sedatives to treat focal NCSE may not be worthwhile. Question: 722 A 46-year-old man is admitted to your ICU after facial assault witha penetrating object through his orbit. You are called to the bedsideon postop day 1 after removal of the object because the patient is insevere pain. Upon your examination, the eye is swollen, injected,movements are difficult to assess because of pain. He has lightperception on visual acuity, which is unchanged from the time ofpresentation. What is the most likely diagnosis? A. Orbital cellulitis B. Orbital hematoma C. Cavernous sinus thrombosis D. Carotid-cavernous fistula (CCF) E. Orbital compartment syndrome G. and pulsatinThe pupil is minimally reactive and extraocular Answer: D Explanation: The patient has a CCF, which is an abnormal communication between the arterial and venous blood within the cavernous sinus and is characterized by pain, chemosis, pulsatile proptosis, ocular bruit, and progressive vision loss. The most common form of CCF is a direct communication between the internal carotid artery (ICA) and cavernous sinus (type A) usually as a result of trauma (young males) or aneurysm rupture (older women). Traumatic CCFs are the most common type, accounting for 75% of all CCFs, and occur in 0.2% of all head trauma and 4% of basilar skull fractures. Conventional angiogram is the gold standard for diagnosis. Endovascular transvenous embolization of the fistula while maintaining patency of the ICA is the mainstay of treatment, with greater than 80% cure rates at 1 year. Symptoms of chemosis and proptosis usually resolve within hours to days of intervention, while cranial nerve (CN) palsies may persist for a few weeks. Visual loss may or may not be reversed depending on the degree of blindness at presentation and the underlying cause. Cavernous sinus thrombosis is a close differential diagnosis and usually presents with ptosis, chemosis, proptosis, CN palsies, vision loss, and a dilated, sluggishly reactive pupil. The most common etiology is infectious with direct spread from the nose, sinuses, or teeth. Diagnosis is made by clinical findings, MRI, and magnetic resonance venography (MRV), and treatment includes intravenous (IV) antibiotics and close monitoring for complications such as meningitis, vision loss, sepsis, or septic emboli. Orbital cellulitis is a bacterial infection of the tissues surrounding the eye, including eyelids, eyebrows, and cheeks, resulting in swelling of the eyelids, pain with eye movements, fever, and decreased vision if not treated promptly. Orbital hematomas can be preseptal or postseptal. Preseptal hemorrhages are usually posttraumatic and benign, resulting in extensive ecchymoses of the eyelids. Postseptal hemorrhages may occur due to trauma, surgical intervention, arteriovenous malformations, or bleeding diathesis, among other causes, and can lead to orbital compartment syndrome with increase in intraocular pressures and vision loss from orbital nerve compression. Question: 723 A 78-year-old man with a history of hypertension, hyperlipidemia,and mild hearing loss is brought to the hospital by ambulance after amotor vehicle accident. He is intubated in the ED for airwayprotection and undergoes massive blood transfusion forhemorrhagic shock. He is admitted to the ICU. Which of thefollowing reduces the risk of delirium in the ICU? A. Benzodiazepine-induced coma B. Mechanical ventilation C. Polytrauma D. Metabolic acidosis E. Sedation with dexmedetomidine Answer: E Explanation: A systematic review identified eleven risk factors for developing delirium in the ICU. These included age, dementia, hypertension, poly-trauma, emergency surgery prior to ICU admission, sedative-induced coma, delirium on the day prior, use of mechanical ventilation, metabolic acidosis, multi-organ failure and APACHE II score. Factors that were clearly associated with reduction in delirium were dexmedetomidine. It is unclear if this was a physiological effect of the drugs itself or because dexmedetomidine use was associated with less benzodiazepine use. Question: 724 A 65-year-old man with a history of hypertension andhyperlipidemia is found down at home by his son at 6 p.m. after hedoes not show up at his granddaughters birthday. He was last seenvital signs are blood pressure (BP) 178/92 mmHg, heart rate (HR)examination, the HR is irregularly irregular. He is awake butaphasic with right lower facial droop and flaccid right arm. Hisinitial National Institutes of Health Stroke Scale (NIHSS) score is18. A noncontrast CT scan of the brain shows loss of grey-whitematter differentiation in the left frontal lobe and hypoattenuation ofCT angiogram of the head shows an occlusion of the first segmentof the middle cerebral artery (MCA); and perfusion CT estimates aninfarct size of 28 mL. At baseline, the patient is independent withnext step in management? A. Start aspirin 325 mg. Patient is not eligible for either intravenous B. Initiate IV thrombolysis with alteplase based on neuroimaging C. Proceed with endovascular thrombectomy based on mismatch D. Initiate IV thrombolysis with alteplase followed by endovascular E. Need to calculate the ratio of the volume of ischemic tissues on Answer: C Explanation: The patient is out of 4.5-hour time window for IV thrombolysis. However, he is a candidate for endovascular thrombectomy based on the latest DWI or CTP Assessment with Clinical Mismatch in the Triage of Wake-Up and Late Presenting Strokes Undergoing Neurointervention with Trevo (DAWN) trial. In this trial, patients with occlusion of the intracranial internal carotid artery (ICA) or proximal middle cerebral artery (MCA) who had last been known to be well 6 to 24 hours earlier and showed evidence of salvageable brain tissue were randomly assigned to thrombectomy plus standard care (the thrombectomy group) or to standard care alone (the control group). Enrolled patients had good premorbid baseline defined as modified Rankin scale (mRS), 0 to 1. Infarct volume was assessed on diffusion-weighted imaging (DWI) sequence of brain MRI or perfusion CT scan using the automated RAPID software. Presence of salvageable brain tissue was based on a mismatch between severity of their neurological deficits and the volume of infarcted brain, and not the ratio of the volume of ischemic tissue at risk to infarct volume: DAWN trial measured utility-weighted mRS at 90 days as the primary outcome. In contrast to mRS, a lower score in utilityweighted mRS indicates a better outcome (ranges from 0 = death to 10 = no deficits). At 90 days, the utility-weighted mRS was 5.5 for the thrombectomy group compared to 3.4 in the control group, and 49% of patients in the thrombectomy group achieved functional independence versus only 13% in the control group. These translate to number-to-treat (NTT) of 2 and 2.8 for less disability and functional independence at 90 days, respectively. Rate of procedurerelated complications was very low. Serious adverse events including mortality and stroke-related death at 90 days as well as and symptomatic intracerebral hemorrhage (ICH) were similar between the two groups. Question: 725 A 72-year-old woman with a past medical history of diabetes,hypertension, hyperlipidemia, and atrial fibrillation on warfarinpresents to the ED with a new severe dysarthria, left-sidedweakness, and neglect (National Institutes of Health Stroke Scale[NIHSS] score 17). Her vital signs are blood pressure (BP) 169/83mmHg, heart rate (HR) 87/min, respiratory rate (RR) 18/min, and1.3. She was last seen 12 hours prior to presentation. MRI of thebrain shows an acute stroke in the territory of the right middlecerebral artery (MCA) without evidence of intracranial hemorrhage.Infarct volume on diffusion-weighted imaging (DWI) is measured48 mL; and volume of ischemic tissue on MRI perfusion scan iscalculated as 110 mL. Magnetic resonance angiography (MRA)treatment for her stroke? A. Start intravenous (IV) alteplase infusion based on clear evidence B. Start heparin drip with a goal partial thromboplastin time (PTT) C. Start warfarin for secondary stroke prevention D. Immediate endovascular thrombectomy E. Start aspirin 325 mg Answer: D Explanation: The patient is not a candidate for IV alteplase as she presents out of 4.5-hour treatment time window. However, she is a candidate for endovascular thrombectomy. In DEFUSE 3 trial, patients 6 to 16 hours after they were last known to be well who had a proximal MCA or internal carotid artery (ICA) occlusion, an initial infarct size of less than 70 mL, and a ratio of the volume of ischemic tissue on perfusion imaging to infarct volume of 1.8 or more were randomly assigned to thrombectomy plus standard medical therapy (thrombectomy group) or standard medical therapy alone (control group). Thrombectomy was associated with better functional outcomes (odds ratio, 2.77) and lower mortality (14% vs. 26% in the control group) without a difference in symptomatic intracranial hemorrhage or serious adverse events. Question: 726 A 70-year-old man is admitted to the neurointensive care unit foraneurysmal subarachnoid hemorrhage (SAH). He is intubated onmechanical ventilation. On day 3 of admission, he develops septicshock. He is fluid resuscitated and broad-spectrum antibiotics withearly and aggressive treatment, 12 hours later, he remainshemodynamically unstable necessitating escalating doses ofnorepinephrine (>1 mg per hour) to maintain a systolic blooddecrease vasopressor requirement and mortality in septic shock? A. Switch antibiotics to linezolid plus meropenem B. Add vasopressin infusion C. Add intravenous (IV) infusion of hydrocortisone 200 mg per day D. Add oral fludrocortisone 50 mcg daily E. Add IV hydrocortisone 50 mg 4 times a day plus fludrocortisone G. pressure (SBP) >90 mmHWhich intervention has been shown to Answer: E Explanation: Two latest trials (ADRENAL and APROCCHSS) studied the effects of adjunctive glucocorticoid therapy and glucocorticoid + mineralocorticoid therapy in patients with septic shock. In the former study, 3,800 patients with septic shock who were undergoing mechanical ventilation were randomized to receive hydrocortisone (at a dose of 200 mg per day) or placebo for 7 days (or until death or discharge from the ICU). Although patients in the hydrocortisone group had faster resolution of shock (3 days vs. 4 days in the control group), no significant between-group difference was found in mortality. In APROCCHSS, the effect of hydrocortisone plus fludrocortisone in patients with septic shock was compared to the placebo. Mortality was significantly lower in the hydrocortisone-plus-fludrocortisone group than in the placebo group at ICU and hospital discharge, and at 90 and 180 days. In addition, hydrocortisone plus fludrocortisone therapy increased the number of vasopressorfree and organ-failure-free days without increasing the rate of serious adverse events except for hyperglycemia. For More exams visit https://killexams.com/vendors-exam-list Kill your exam at First Attempt....Guaranteed! | ||||||||||||||||||||||||||
Should I take EDCI 5515 or EDCI 5959 credits? EDCI 5515 credits should be taken if you want to use the National Board Certification toward your Master's degree in Curriculum & Instruction. EDCI 5959 credits are for continuing education only and will NOT be accepted on your Program of Study for the Master's degree in C&I. Will there be classes offered to help me proceed through the National Board Certification process? Yes, a series of seminars and workshops are offered through the Wyoming National Board Certification Initiative each semester. Information about these seminars and workshops is posted and updated on the Wyoming NBC website. Graduate level Curriculum and Instruction credit is available for these seminars (courses listed as EDCI 5515). These courses are designed to support teachers as they grow as professionals and simultaneously proceed through the Board Certification process and the UW Master’s program. Where will the classes be offered? The classes are offered around the state of Wyoming to allow participation across the state. Dates and locations for upcoming seminars and workshops can be found on the Wyoming NBC website. Participants enroll in the courses through UW Outreach Credit Programs (toll free phone number: 1-800-448-7801). Up to 9 total credit hours of the seminars can be taken by enrolled graduate students. Up to 9 total seminar/workshop credit hours may be applied as electives in the Curriculum and Instruction Master’s program. Who will teach these classes? The seminars are taught by Barbara Maguire, a Nationally Board Certified teacher and expert in the NBC process. How many times can I take the NBC class? Graduate students/National Board Candidates can enroll in the seminars as many times as necessary/desired. For those seeking graduate degrees, up to 9 credits can be applied to the Curriculum and Instruction Master’s degree program as elective hours dependent upon the student’s committee approval. What about tuition? Students will pay regular graduate tuition for the seminar classes. View the current UW fee schedule. Will I need to complete a Thesis or Plan B paper to finish my C&I degree? No, the NBC Portfolios will be accepted in Lieu of a Plan B Paper for teachers pursuing NBC Certification and a UW Master’s degree simultaneously. This acceptance is dependent upon committee approval (not acceptance by the National Board). An agreement to utilize this procedure and maintain portfolio confidentiality has been reached between UW and the NBPTS (National Board for Professional Teaching Standards). The NBC portfolio must be submitted and defended (in a meeting with the student’s graduate committee) prior to initial submission to the NBPTS. The committee’s portfolio copies will be destroyed after the defense. Note: The Rubric for Assessment of the presentation is provided below. If I am already a National Board Certified teacher, can I apply my NBC work retroactively to a graduate degree? No, the program is designed for those working on National Board Certification and a C&I Master’s degree simultaneously. How do I apply for a UW Curriculum and Instruction Graduate Program? The graduate application and other information can be found here. What if I have Additional Questions? If you have additional questions, please contact the UW Department of Curriculum and Instruction (curriculum@uwyo.edu; 307-766-6371). Assessment Checklist for National Board Certification (NBC)Portfolio & Presentation Committee members will evaluate the following areas and will determine if the student/NBC candidate accomplished each of these aims/activities at a level sufficient to warrant the substitution of the NBC portfolio and presentation for the Plan B requirement. S/U (Satisfactory/Unsatisfactory) will be assigned for each area, and an overall evaluation of “S” must be achieved for portfolio to serve in lieu of the Plan B paper. ______ Overall evaluation of the portfolio and presentation as suitable substitutes for Plan B paper/project and defense Presentation of NBC Portfolio to Master’s Committee: ______Student provides a brief overview of National Board Certification process and portfolio ______Student describes process of working on the portfolio (including connections to C&I courses taken, time commitment, assessments and data analysis, and reflections) ______ Student presents at least one explicit connection between the portfolio documentation and his/her C&I Master’s Degree coursework (e.g. assessment strategy learned in literacy specific course was used to evaluate student work included in NBC portfolio), and explains ways processes informed each other _____ Student describes challenges, pleasures, difficulties associated with the NBC process _____Student summarizes learning derived from portfolio process and completion More information on National Board Certification:Visit our Course Schedule page to view projected MA core and emphasis course offerings
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Quick Facts | |
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Online | Yes |
Format | Instructor-led (Asynchronous) |
Course Fee | $1,795 |
CEUs | 2.1 |
Course Availability | 4 times per year |
Time to Complete | 5 weeks |
Prerequisites | None |
The five-week Purdue Agile Certificate Online Course is a deep dive into the core principles and frameworks of the project management methodology.
Developed by subject matter experts in project management and aligned with the Agile Practice Guide of the Project Management Institute, this standalone course equips learners with the latest Agile tools and methods, enhancing their ability to drive project success and Strengthen customer satisfaction.
In this asynchronous program, learners view on-demand lecture videos and complete practical assignments that will deepen their understanding of Agile concepts and tools. They’ll have the opportunity to engage with their instructor and peers through discussion boards. The program is supplemented by two key textbooks: Agile Practice Guide from the Project Management Institute and Agile Project Management: 2 Books in 1 by Sam Ryan.
To learn more about Purdue University’s online Agile Certificate Online Course and , fill out this form. You can also call (888) 390-0499 to speak to one of their program advisors.
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“In designing the Agile Certificate Online Course, they made sure to closely follow the Project Management Institute (PMI) global standards. Learners can use this content to prepare for their certifications, and it ensures that they’re up on the latest and greatest tools and techniques.”
Rachel Lamb, Agile Instructor
The 100% online, instructor-led Agile Certificate Online Course is conducted in the Brightspace online environment. Learners will complete two to three modules per week, for a total of 12 modules.
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Learners can expect to spend an average of four to five hours each week on assignments, depending on prior knowledge and experience. Most course materials will be provided in Brightspace, but learners are responsible for purchasing their textbooks.
Agile projects have a 64% success rate, compared to a 49% success rate for waterfall.
Zippia, Agile Statistics
Upon completion of the program, learners will be able to:
The Agile Certificate Online Course is advantageous to anyone who manages projects, regardless of industry. Current project managers, those interested in moving into a project management position and individuals who require Agile knowledge in their roles — including business analysts, marketing strategists and software engineers — will all benefit from this program.
After completing this course, some learners go on to pursue their Agile Certified Practitioner (PMI-ACP)® certification through the Project Management Institute (PMI). Others choose to build on their skills with Purdue’s Project Management Essentials and PMP® exam Preparation courses, with the goal to sit for the Project Management Professional (PMP)® certification exam.
Learners who are already PMI-ACP certified earn 2.1 continuing education units, which they can apply toward maintaining certification.
One career option for course completers is Scrum master. These individuals are part of a Scrum team working to meet sprint goals and are well versed in Agile methodology and the Scrum approach. The average annual salary for Scrum masters is upwards of $107,000.
Agile methodology is an adaptable type of project management. It has many frameworks for implementation, but at its core, it is about being flexible, collaborative and efficient. Teams work in short cycles, or iterations, to develop small parts of a project over time. This approach allows teams to respond quickly to changes and continuously Strengthen the product based on feedback. Agile works best for projects with shifting requirements and for those where not all requirements are known.
The Purdue Agile Certificate Online Course is an instructor-led program, meaning you’ll benefit from having a subject matter expert available for guidance whenever you have a question or need further examples to aid in your comprehension.
Additionally, the Agile program is a paced program, with assignments due on a weekly basis to keep you on track.
The Project Management Institute (PMI) offers an Agile Certified Practitioner (PMI-ACP)® certification. The PMI-ACP® is the PMI’s fastest-growing certification and demonstrates your mastery of Agile practices and principles to employers. Obtaining this certification can lead to a 33% increase in median salary.
The Purdue Agile Certificate Online Course meets the PMI-ACP® exam prerequisite for 21 contact hours of training in Agile practices. Because the course focuses on the PMI’s Agile Project Guide, it also prepares you for the content you will find on the exam.
For more details about how to get Agile certified, including Agile certification cost, visit the PMI website.
Completing the Agile Certificate Online Course is valuable in preparing for the Project Management Professional (PMP)® exam through the PMI. According to the PMI, half of the questions on the PMP exam focus on Agile or hybrid project management approaches.
Find more answers on their full project management FAQs page, or contact a program advisor at PMonline@purdue.edu or (888) 390-0499.
Rachel Lamb is the designer and instructor for the Agile Certificate Online Course. Both PMP® and Lean Six Sigma Black Belt certified, Rachel’s focus throughout her career has been on process improvement and project management. She is available to assist learners with questions throughout the program. Visit their instructors page to learn more about Rachel.
Dec. 13—During their first time meeting as a group Wednesday, members of a newly formed state police board revoked the certification of six officers — and one law enforcement communication worker — from around the state.
The board also issued certification suspensions — from 30 hours to 180 days — to eight officers or dispatchers and dismissed four disciplinary cases.
They were the first steps in a process that could shape law enforcement statewide for years to come — changes that could include the overhaul of rules that govern law enforcement policies, discipline and training.
In the short term, Wednesday's moves cut down some of the backlog in disciplinary cases for the Law Enforcement Certification Board, a product of state legislation earlier this year that split the former Law Enforcement Academy Board into two different groups that each oversee different functions of the state's police academy program.
The other newly formed body — the Standards and Training Council — met in latest weeks to begin its review of police training around the state.
One of the actions the board took Wednesday was a temporary suspension of certification for Brad Lunsford, a Las Cruces police officer who recently was indicted on a voluntary manslaughter charge after he was accused of shooting and killing a man.
The board requested the academy's staff to expedite an investigation into Lunsford's disciplinary case.
Board members voted on the disciplinary cases after spending more than three hours in private discussions. The closed session also included discussion of four pending court appeals challenging suspensions or revocations by the former board, as well as one pending lawsuit from an Albuquerque Police Department officer whose certification-by-waiver was rejected by the former board in latest years.
The new certification board is made up of sheriffs and police chiefs from around the state as well as civil rights attorneys and academics.
Board member and attorney Joseph Walsh called the new board structure "effectively a new paradigm that's trying to be implemented to hopefully be a model for law enforcement."
He added the new board structure can bring "true accountability."
The board began a process to hire a CEO for the academy Wednesday with the approval of a job description to be posted for recruiting. Members expressed hope the position would be filled in six months to a year.
A CEO will act as the "enforcement mechanism" of the board's directives at the academy, Walsh said, and make business decisions such as hiring and firing.
Until the position is filled, the board authorized academy director Sonya Chavez to make decisions.
Chavez, who began in the position Oct. 30, previously served as the U.S. Marshal of New Mexico. Before that, she worked as a special agent in the FBI.
"What we're involved in I think is going to be monumental for law enforcement in New Mexico," Chavez told the board Wednesday.
The board's misconduct investigations and hearings are still conducted according to administrative rules set decades ago for the former board, which was for years led by the state Attorney General.
On Wednesday, board members voted to form a four-member working group to draft changes to the rules.
The two members tasked with drafting changes to the rules for the board's disciplinary actions are public defender Julie Ball and Cody Rogers, a Las Cruces-based attorney. Rule changes pertaining to certification qualifications were assigned to be reviewed and redrafted by John Soloman, a criminal justice program director at Central New Mexico Community College, and Carly Lea Huffman, a training coordinator at the Bernalillo County Emergency Communications Center.
The rulemaking process is expected to generate new administrative rules for the board to be in place by the end of 2024.
The goal of this program is to establish an online flagger certification program for those working as flaggers in Wyoming. This online certification program will be replacing the current Flagger Traffic Control Certification conducted through AGC of Wyoming. There has been an increase in roadwork projects over the years, which has led to an increase in motorists encountering highway work zones. Therefore there is a need for a user-friendly and online training and certification program for Wyoming Flagger Traffic Control personnel. This course will help prepare each worker to handle the responsibilities and understand their requirements for traffic control in Wyoming.
The course has been approved by a certification board made up of members from the Wyoming Department of Transportation (WYDOT) and the Association of General Contractors of Wyoming (AGC). All course and examination materials have been established and approved by the certification board.
Codes expire on December 31, 2023 but remaining useage will roll-over to the next years code.
If you want to purchase bulk registrations or need your AGC registration code, please contact their office at WYT2C@uwyo.edu or call 307.766.6743
WYDOT and AGC of Wyoming have updated the Flagging Traffic Control Manual for the course. Click on the link to download the Manual.
Wyoming Flagger Traffic Control Manual
In order to earn your certification, you must earn 80% or higher on your Certification Exam. You are allowed 3 attempts on the exam. A certificate will be emailed to participants upon achieving the desired score on the exam. They will no longer be using certification cards and assigning certification numbers. Your proof of completion will be the certificate and they will be publishing a list of certified people each week. You can find the Certification list below.
Each course participant needs to use a personal email address.
PDF with screenshots showing how to register and navigate the course.
If you need assistants please contact their office at WYT2C@uwyo.edu or call us at 307-766-6743. Our office is open from 8 am to 4 pm Mon-Fri except for holidays.
The Wyoming Flaggers Traffic Control Certification list will be updated weekly. Last Update: 12/18/2023.
The certification list is organized alphabetically by employers, then by last names.
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