Lena M. Maynor, PharmD, BCPS

• Clinical Associate Professor and Director of Advanced Pharmacy Practice Experiences, Department of Clinical Pharmacy, School of Pharmacy, West Virginia University, Morgantown, West Virginia

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Lung ultrasonography is limited by the fact that lesions or pathologies surrounded by normally aerated parenchyma will not be seen 5 medications that affect heart rate purchase pristiq 50 mg on line, because air is considered impermeable to ultrasound waves medicine 54 357 order discount pristiq online. Obese patients or those with thick chest walls symptoms stomach flu purchase pristiq mastercard, subcutaneous emphysema symptoms inner ear infection order 100mg pristiq amex, and thoracic wound dressings may have suboptimal images treatment zinc deficiency purchase pristiq toronto. However even interstitial pulmonary edema medications and mothers milk buy generic pristiq canada, pneumothoraces and pulmonary emboli can be diagnosed but require more expertise. Respiratory changes in aortic blood velocity as an indicator of fluid responsiveness in ventilated patients with septic shock. Superior vena caval collapsibility as a gauge of volume status in ventilated septic patients. Pulse pressure variations to predict fluid responsiveness: influence of tidal volume. Respiratory variations of inferior vena cava diameter to predict fluid responsiveness in spontaneously breathing patients with acute circulatory failure: need for a cautious use. Respiratory variation in inferior vena cava diameter: surrogate of central venous pressure or parameter of fluid responsiveness Ultrasound assessment of inferior vena cava collapsibility is not a valid measure of preload changes during triggered positive pressure ventilation: a controlled crossover study. Passive leg raising for predicting fluid responsiveness: importance of the postural change. A 10-second fluid challenge guided by transthoracic echocardiography can predict fluid responsiveness. Changes in aortic blood flow induced by passive leg raising predict fluid responsiveness in critically ill patients. Can dynamic indicators help the prediction of fluid responsiveness in spontaneously breathing critically ill patients Detecting volume responsiveness and unresponsiveness in intensive care unit patients: two different problems, only one solution. International consensus statement on training standards for advanced critical care echocardiography. Guidelines for the Echocardiographic Assessment of the Right Heart in Adults: a Report From the American Right Ventricular Systolic Function endorsed by the European Association of Echocardiography, a registered branch of the European Society of Cardiology, and the Canadian Society of Echocardiography. Guidelines for the Echocardiographic Assessment of the Right Heart in Adults: a Report From the American Society of Echocardiography: Endorsed by the the European Association of Echocardiography, a registered branch of the European Society of Cardiology, and the Canadian Society of Echocardiography. Echocardiographic findings in pulmonary embolism: an important guide for the management of the patient. The use of pointof-care bedside lung ultrasound significantly reduces the number of radiographs and computed tomography scans in critically ill patients. Comparative diagnostic performances of auscultation, chest radiography, and lung ultrasonography in acute respiratory distress syndrome. Bedside ultrasound assessment of positive end-expiratory pressure-induced lung recruitment. On postopeartive day 15, he suddenly develops chest pain, waking him from sleep in the early morning. It is a squeezing, pressure-like sensation in the midline of his chest, without radiation. He has moderate dyspnea and palpitations, which began at the same time as his chest pain. Symptoms do not abate after a few hours, and the patient presents to the emergency department. On further questioning, he admits that he had felt several episodes of mild chest discomfort for the last several months while doing yard work, but it was always mild and transient. Symptoms have been minimal recently, but his physical activity has been markedly reduced because of back pain. He takes low-dose simvastatin for high cholesterol, and his diabetes is diet controlled. He is still having mild-to-moderate chest discomfort on arrival in the emergency department. Angina that is predictable, exertional, and resolves with rest or nitroglycerin is referred to as stable angina. The above patient appears to have a history of stable angina, but is now presenting with unstable angina. This is especially common among elderly persons, women, and those with diabetes mellitus, all of whom often experience atypical symptoms including dyspnea, presyncope, fatigue/malaise, or nausea/vomiting. So-called diaphragmatic infarcts of the inferior wall often present with symptoms that, on first glance, appear to be gastrointestinal in nature. Although this can be caused by a number of conditions, it is mostly commonly due to atherosclerotic coronary plaque rupture complicated by acute coronary thrombosis, a process often referred to as atherothrombosis. Using current assays, troponin levels typically become detectable approximately 6 hours after the onset of myocyte necrosis. Waiting for positive biomarkers may lead to unnecessary and costly delays in treatment. Prospective trials consistently show correlation between quantitative troponin levels and shortterm risk. The above case, which is a fairly typical presentation of acute coronary syndrome, is not consistent with demand ischemia. This is frequently seen in conditions of hemodynamic stress resulting from sepsis, hypotension, hypertension, anemia, arrhythmias, postoperative status, or coronary vasospasm. The physical examination should focus on findings such as elevated jugular venous pressure, tachycardia, the presence of an S3, rales, pleural effusions, cool extremities, and lower extremity edema. The goal of risk stratification is to identify patients who are high risk for complications and thus more likely to derive benefit from invasive treatments and more powerful pharmacologic therapies. It includes other factors such as reinfarction, arrhythmia, bleeding, congestive heart failure, stroke, and renal dysfunction. In this case, angiography and revascularization within 24 hours appears to be superior to a delay of 36 hours or more. Newer P2Y-12 inhibitors, such as ticagrelor or prasugrel, have proven more potent and are generally preferred over clopidogrel, assuming there are no contraindications and that the patient will be treated invasively. Maintenance doses higher than 81 mg daily are associated with increased bleeding without an improvement in prevention of ischemia. Three options for P2Y-12 inhibitors are available: clopidogrel, prasugrel, or ticagrelor. Clopidogrel has a robust evidence base, but its major drawback is wide interpatient variability. As a result, as many as 20% of patients may not receive therapeutic platelet inhibition with standard dosing of clopidogrel. This number can be decreased somewhat by giving a loading dose of 600 mg, but unpredictable platelet inhibition may remain. For medically managed patients, clopidogrel is the agent of choice, as it has been shown to outperform prasugrel in this group. It requires only a single-step conversion to its active metabolite, primarily via intestinal esterases. By avoiding hepatic metabolism, it has far less interpatient variability than clopidogrel. Characteristics of Key Antiplatelet Agents Aspirin Route Loading dose Daily dose Prodrug Prasugrel is a very potent antiplatelet agent, but must be used in carefully selected population to minimize serious hemorrhagic events. Ticagrelor is an oral P2Y12 receptor blocker that is not a prodrug and is already in its active form. Compared with clopidogrel and prasugrel, it has a more rapid onset of action and a shorter half-life and is completely independent from hepatic metabolism. This is thought to contribute to pleiotropic effects beyond its simple, reversible platelet inhibition. It is critical that ticagrelor should only be chosen over clopidogrel in patients who are at low risk for bleeding and who can adhere to twice daily dosing. Prasugrel and ticagrelor lead to improvements in ischemic outcomes at the cost of higher bleeding. Large trials in the 1990s demonstrated heterogeneous results, with an unclear effect on mortality. What is the optimal duration of anticoagulation if patients are to be treated conservatively In patients who are medically managed, guidelines suggest that anticoagulation can usually be discontinued after 48 to 72 hours of therapy. There is no firm time at which discontinuing anticoagulation is ideal; however, if there are any concerns for persistent or recurrent ischemia, therapy should be continued. Management of anticoagulation is different in those who undergo angiography and revascularization. In fact, it is likely to be deleterious as patients often receive a number of anticoagulants periprocedure. As such, it is standard practice to discontinue anticoagulation just prior to the revascularization procedure. In addition to dual antiplatelet therapy, you would like to optimize his medical regimen. The traditionally proposed mechanism is a decrease in heart rate and blood pressure, leading to reduced cardiac oxygen demand, thereby optimizing oxygen balance and potentially reducing infarct size. Generally speaking, -blockers should be considered in patients with a Killip score of 1 or 2, but should be avoided in those with a score of 3 or 4. Statins, particularly in high doses, appear to be beneficial in the setting of acute coronary syndrome. Patients seem to derive benefit whether the statin is started as a new medication or continued prior statin therapy. Although extremes of glycemia appear to be deleterious, so too does attempts at tight glycemic control. Benefits accrued by tight glycemic control may be outweighed by risk of hypoglycemia and a corresponding surge in adrenergic tone, with potentially dangerous effects on the heart. Insulin therapy, when utilized, must be administered prudently to avoid hypoglycemia. Hypoglycemia is associated with increased risk of cardiac death in critically ill patients. This patient is at high risk for ventricular arrhythmias, supraventricular arrhythmias, and bradyarrhythmias. Ischemic and/or scarred myocardium presents an excellent electrical substrate for life-threatening ventricular arrhythmias. In addition to ensuring adequate revascularization, some simple maneuvers can help minimize the risk of ventricular arrhythmias. Second, correction of hypokalemia, hypomagnesemia, hypocalcemia, and acidosis are essential. Any arrhythmogenic inotropes such as catecholamines, dobutamine and milrinone should be stopped as soon as possible. Supraventricular tachycardias, although less dangerous than ventricular arrhythmias, are more common. Advanced age, hypertension, and systolic dysfunction are all thought to be risk factors. Adequate management of electrolytes and acid/base abnormalities will also help to prevent or minimize atrial arrhythmias. They are usually transient, driven by increased vagal tone, and can generally be managed expectantly. Symptomatic sinus bradycardia will often respond to atropine, and if it persists and is associated with hypotension, dopamine can be an effective short-term treatment. Ventricular arrhythmias can be prevented by use of -blockers, correction of electrolyte and acid/base abnormalities, and removal of inotropes. As discussed above, it is essential to assess for recurrent ischemia, correct any electrolyte abnormalities (especially hypokalemia and hypomagnesemia), correct any metabolic acidosis, and remove nonessential inotropes or vasopressors. Rapid revascularization and urgent surgical consultation is usually needed, as medical therapy alone cannot correct the underlying mechanical disorder. It is characterized by a harsh systolic murmur (sometimes with an associated thrill) and shock. Ventricular free wall rupture is a devastating complication that presents suddenly with hemodynamic collapse and pericardial tamponade. Even for those in whom this condition is diagnosed rapidly, mortality rates are quite high. Bedside clues include elevated jugular venous pressure, pulmonary edema, cool extremities, altered mental status, tachycardia, and hypotension. In such situations, new ischemia should be ruled out, and one must consider use of either inotropes or mechanical circulatory support such as intraaortic balloon pump as temporizing measures. A pulmonary artery catheter may be useful in this situation to monitor cardiac output and pulmonary artery oxygenation, and other invasive hemodynamics can be used to monitor response to therapy. However, it is a potentially life-threatening situation, and patients can conceivably exsanguinate into the retroperitoneum if this is unrecognized. Patients may present with little more than mild back pain, termed access site pain. Hypotension may be exacerbated by concurrent vasovagal response, which is a common reaction to access site pain and prolonged compression of the artery. This should be suspected in the setting of concurrent bradycardia and hypotension and may respond to atropine and/or dopamine. Bedside examination to evaluate for groin hematoma is essential, as is serial monitoring of complete blood count. Care is above all supportive, requiring prolonged manual compression of the femoral artery and resuscitation with blood and intravenous fluids. The above conditions can often be rapidly excluded with a keen bedside examination and focused echocardiogram.

Syndromes

• Pregnancy
• Social difficulties related to physical symptoms
• Eat a healthy meal to restore your energy.
• Yawning
• Too much thryoid medication (levothyroxine)
• Avoid arguments during meals.

Enforcing a high-protein diet in ill patients is difficult symptoms of strep throat buy generic pristiq 100mg online, but it is possible if they are fed by enteral tube symptoms queasy stomach purchase pristiq 50mg on line. Demeclocycline is a tetracycline antibiotic that incidentally causes nephrogenic diabetes insipidus in about 70% of patients 911 treatment center buy cheap pristiq 50 mg line, increasing electrolyte-free water excretion by inhibiting vasopressinmediated water reabsorption in the collecting duct medicine kit cheap 50mg pristiq overnight delivery. Demeclocycline is contraindicated in patients with renal disease medicine 44 159 order pristiq without a prescription, hepatic cirrhosis treatment 5ths disease effective 50 mg pristiq, or congestive heart failure because drug-related renal insufficiency has been described in these situations. According to the family, she was taking insulin, amlodipine, and lithium carbonate. Water ingestion can defend against the development of hypernatremia even when water losses are prodigious. For that reason, hypernatremia occurs most commonly in patients who are incapacitated: those who have impaired thirst sensation, who cannot access water, or who cannot express their need for water (eg, infants and patients with neurologic impairments). Thus, the development of hypernatremia in hospitalized patients is considered to be iatrogenic, reflecting an incomplete understanding of the factors that lead to hypernatremia. Euvolemic Hypernatremia Hypernatremic patients who appear euvolemic most likely have pure, solute-free, water loss as an explanation for their hypernatremia. This is because the water is lost from all body compartments proportionately; only one-twelfth of the water loss is intravascular. Insensible losses amount to about 10 mL per kilogram body weight per day under normal environmental conditions in an afebrile individual with a normal respiratory rate. About a week later, an antidiuretic phase ensues, characterized by urinary concentration and water retention with a tendency toward hyponatremia, lasting 2 to 14 days. They develop hypernatremia only with water deprivation, due to mental or physical incapacity, and/or neglect. Hypovolemic Hypernatremia the loss of salt and water, with the water loss greater than the sodium loss, will lead to hypernatremia and volume depletion, manifested by orthostatic or persistent hypotension and tachycardia, and evidence of organ underperfusion (eg, acute renal failure, lactic acidosis). Most gastrointestinal fluids have an electrolyte concentration below that of plasma: the concentration of sodium plus potassium in stool is roughly constant at 110 to 120 mmol/L over a wide range of stool volume. The loss of sweat, which contains some sodium, can cause hypovolemic hypernatremia in individuals who exercise vigorously in a hot environment. Hypervolemic Hypernatremia Hypervolemic hypernatremia is relatively uncommon and often results from the administration of hypertonic sodium salts to patients without free access to water. Patients show signs of extracellular volume expansion (eg, hypertension, edema, congestive heart failure, and pulmonary edema). In infants, this syndrome has been caused by erroneous preparation of dietary formula using salt instead of sugar; in adult outpatients, it may be caused by ingestion of a concentrated salt solution, usually for its emetic effect. In patients with neurosurgical disease, it is often caused by parenteral administration of hypertonic saline solutions to reduce intracranial pressure and possibly decrease inflammation. The patient therefore appears euvolemic, so the most likely explanation for her hypernatremia is pure, electrolyte-free, water loss. This would be unlikely to cause significant fluid overload in a patient with normal heart and kidney function, although it exacerbated her hypernatremia. A high Uosm would be consistent with appropriate urinary concentration in the face of extrarenal water loss. To counteract cellular volume contraction, cells begin to adapt within minutes by allowing the influx of electrolytes, thus mitigating cell shrinkage. When hypernatremia lasts more than a few hours, brain cells generate new organic osmolytes. This leads to further water movement back into brain cells, restoring cell volume nearly to normal after about 3 days. Patients with hypernatremia tend to present with weakness, lethargy, and confusion. Acute severe hypernatremia in infants and small children is associated with intracranial bleeding,69 presumably caused by brain shrinkage and traction on the penetrating vessels. There is some controversy, however, as to whether the hypernatremia in that situation is the cause or the effect of the intracranial hemorrhage. For patients with pure water losses (euvolemic), therapy has two goals: (1) reduction and/or replacement of ongoing water losses and (2) replacement of the existing water deficit. This formula provides only a rough estimate of the water deficit, and tends to underestimate the water deficit in patients who have loss of both salt and water (hyponatric fluid loss). In that setting, one should aim to correct half the water deficit in the first 24 hours and the remainder over the next 24 to 48 hours. If that route is unavailable, 5% dextrose in water (D5W) may be used, with the understanding that the capacity to metabolize glucose is limited to about 15 g/h in a critically ill adult. The hyperglycemia will exacerbate urinary water losses by causing an osmotic diuresis. For the hypernatremic patient who presents with obvious volume depletion-manifested by hypotension, tachycardia, and evidence of impaired tissue perfusion-normal (0. This is consistent with the first principles of emergency and critical care, prioritizing the adequacy of the circulation. Only after addressing the extracellular volume deficit may the clinician direct his or her attention to the total body water deficit (see above). Patients with hypervolemic hypernatremia need reduction in their extracellular and intravascular volume before their water deficit can be corrected. For patients with adequate renal function, this may be accomplished with the use of diuretic drugs. Loop diuretics tend to cause the excretion of an isotonic urine with about half the electrolyte concentration of plasma. Replacement of that urine volume with pure water will allow correction of the hypervolemia and the hypernatremia simultaneously. Because of the imprecision of the estimation formulas and the failure of the foregoing analysis to take account of other fluids and electrolytes both administered and lost, it is imperative that the plasma electrolytes be monitored every 4 to 6 hours during the correction of hypernatremia, because of the risk of cerebral edema with overlyrapid correction. Hyponatremia itself is important only when it is associated with a low Posm, because it can cause cerebral edema. Severe hyponatremia due to hypopituitarism with adrenal insufficiency: report on 28 cases. A method to estimate urinary electrolyte excretion in patients at risk for developing cerebral salt wasting. Antidiuretic effect of hydrochlorothiazide in lithium-induced nephrogenic diabetes insipidus is associated with upregulation of aquaporin-2, Na-Cl co-transporter, and epithelial sodium channel. Pathogenesis and management of sodium and water retention in cardiac failure and cirrhosis. Hyponatremia with hypoxia: effects on brain adaptation, perfusion, and histology in rodents. Hyponatremia and cerebral infarction in patients with ruptured intracranial aneurysms: is fluid restriction harmful Efficacy and safety of oral conivaptan: a V1A/V2 vasopressin receptor antagonist, assessed in a randomized, placebo-controlled trial in patients with euvolemic or hypervolemic hyponatremia. Rapid correction of hyponatremia causes demyelination: relation to central pontine myelinolysis. Long-term treatment of patients with inappropriate secretion of antidiuretic hormone by the vasopressin receptor antagonist conivaptan, urea, or furosemide. Hypernatremia and subdural hematoma in the pediatric age group: is there a causal relationship The patient and his family deny any other symptoms including fevers, shortness of breath, slurring of speech, or seizures. Vascular injury, tissue ischemia, and the release of vasoconstrictive mediators worsen the condition. Flair imaging is the most sensitive sequence with which to detect areas of cerebral edema. The lesions are hyperintense on T2-weighted imaging and flair, and iso- to hypo-intense on T1-weighted imaging. Small renal artery with severe mucinoid intimal inflammation and pinpoint lumen consistent with hypertensive emergency. This is seen most commonly with at least some calcium antagonists and hydralazine. Apart from this example, it is uncertain if there is a class-specific beneficial pharmacologic effect of antihypertensive drugs directly on the cerebral circulation. Intimal fibroelastic findings associated with chronic hypertension leading to a 70% lumen narrowing. The development of uncontrolled hypertension associated with sudden discontinuation of antihypertensive medications has been described frequently in the medical literature and is referred to as discontinuation syndrome, acute post treatment syndrome, acute withdrawal syndrome, and rebound hypertension. Clonidine is a widely used antihypertensive drug that suppresses the sympathetic nervous system via a central mechanism by agonism of inhibitory receptors. Sudden discontinuation of clonidine leads to rebound hypertension due to secretion of stored norepinephrine. Hypertension is associated with impaired cognition, particularly executive functions, and is believed to play a causal role in cognitive decline above and beyond its relationship to stroke. This case emphasizes the importance of educating patients about the adverse effects of abrupt discontinuation of antihypertensive agents, particularly clonidine. Consider now if this extremely hypertensive patient presented with a nonhemorrhagic or hemorrhagic stroke. Typical examples of end-organ damage include hypertensive encephalopathy, aortic dissection, acute renal failure, acute pulmonary edema, or acute myocardial infarction. They are also independently associated with increased risk of stroke in elderly hypertensive subjects. Volume expansion, with the goal of improving cerebral perfusion, does not have a role, unless polycythemia is present. Apart from volume depletion, other causes of hypotension one should consider include arrhythmias, sepsis, or aortic dissection. Autonomic dysreflexia describes the phenomenon of vasoconstriction that occurs in spinal cord injuries above the level of T5. Specifically, a peripheral stimulus initiates a strong sympathetic nervous system discharge. Mechanisms include excess sympathetic drive, renal vasoconstriction, and an inability to dilate the splanchnic vessels. Because of excess parasympathetic activity above the spinal lesion, mediated by carotid baroreceptors, flushing and bradycardia are frequent. Nifedipine has been shown to be effective in treating and preventing the hypertension of autonomic dysreflexia. Clinical assessment and evidence of abnormal tissue perfusion, especially underperfusion, should ultimately guide therapy. A study of regional autoregulation in the cerebral circulation to increased perfusion pressure in normocapnia and hypercapnia. Role of perivascular sympathetic nerves in autoregulation of cerebral blood flow and in blood-brain barrier functions. Magnetic resonance imaging demonstration of reversible cortical and white matter lesions. Cerebral cortical changes in acute experimental hypertension: an ultrastructural study. Cerebrovascular, neuronal, and behavioral effects of long-term Ca2+ channel blockade in aging normotensive and hypertensive rat strains. Drug withdrawal and rebound hypertension: differential action of the central antihypertensive drugs moxonidine and clonidine. Consequences of the discontinuation of antihypertensive treatment in successfully treated patients. Comparison of withdrawing antihypertensive therapy between diuretics and angiotensin converting enzyme inhibitors in essential hypertensives. Beta-adrenergic blocker withdrawal syndromes in hypertension and other cardiovascular diseases. Abrupt cessation of treatment in hypertension: consideration of clinical features, mechanisms, prevention and management of the discontinuation syndrome. Discontinuation syndrome following cessation of treatment with clonidine and other antihypertensive agents. Blood pressure and blood pressure variability following withdrawal of propranolol and clonidine. High blood pressure as risk factor and prognostic predictor in acute ischaemic stroke: when and how to treat it Guidelines for the early management of adults with ischemic stroke: a guideline from the American Heart Association/American Stroke Association Stroke Council, Clinical Cardiology Council, Cardiovascular Radiology and Intervention Council, and the Atherosclerotic Peripheral Vascular Disease and Quality of Care Outcomes in Research Interdisciplinary Working Groups: the American Academy of Neurology affirms the value of this guideline as an educational tool for neurologists. Intracranial pressure changes induced by sodium nitroprusside in patients with intracranial mass lesions. Effect of intravenous nimodipine on blood pressure and outcome after acute stroke. Effects of blood pressure lowering in the acute phase of total anterior circulation infarcts and other stroke subtypes. New-onset hypertension and inflammatory response/poor outcome in acute ischemic stroke. Significance of elevated blood pressure and its management on the short-term outcome of patients with acute ischemic stroke. No evidence for an ischemic penumbra in massive experimental intracerebral hemorrhage. Treatment of acute hypertension in patients with intracerebral hemorrhage using American Heart Association guidelines. Autonomic dysfunction in spinal cord injury: clinical presentation of symptoms and signs. A comparison of the efficacy of an alpha-I-adrenergic blocker in the slow calcium channel blocker in the control of autonomic dysreflexia. Risk factors for hypertensive crisis: importance of out-patient blood pressure control. The differential diagnosis includes the following: thrombotic thrombocytopenic purpura, idiopathic thrombocytopenic purpura, disseminated intravascular coagulation, and heparininduced thrombocytopenia. It is an acquired state that occurs as a result of a number of underlying conditions (Table 51-1). Fibrin deposition leads to thrombosis and occlusion of small vessels, with subsequent end-organ damage. At the same time, depletion of platelets and clotting factors can also lead to bleeding. The brain has a high concentration of tissue thromboplastin, which has a tendency to become prothrombotic when released into systemic circulation.

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The outcome of therapies in refractory and super-refractory convulsive status epilepticus and recommendations for therapy symptoms enlarged spleen 50mg pristiq. Intravenous lacosamide as successful treatment for nonconvulsive status epilepticus after failure of first-line therapy symptoms syphilis generic 100 mg pristiq overnight delivery. N-methyl-daspartate receptor antagonists abolish the maintenance phase of self-sustaining status epilepticus in rat treatment 4 sore throat discount pristiq 100mg with visa. A combination of ketamine and diazepam synergistically controls refractory status epilepticus induced by cholinergic stimulation treatment jalapeno skin burn purchase 50mg pristiq with amex. Intravenous ketamine for the treatment of refractory status epilepticus: a retrospective multicenter study medicine on airplane pristiq 50 mg otc. Generalized status myoclonicus in acute anoxic and toxicmetabolic encephalopathies harrison internal medicine purchase 100 mg pristiq. Prognostic value of electrographic postanoxic status epilepticus in comatose cardiacarrest survivors in the therapeutic hypothermia era. Resective surgery to treat refractory status epilepticus in children with focal epileptogenesis. Generalized periodic discharges in the critically ill: a case-control study of 200 patients. Digital videoelectroencephalographic monitoring in the neurological-neurosurgical intensive care unit: clinical features and outcome. Oddo M, Carrera E, Claassen J, et al Continuous electroencephalography in the medical intensive care unit. Epilepsia partialis continua associated with nonketotic hyperglycemia: 79 clinical and biochemical profile of 21 patients. There has been a loss of consciousness immediately after the fall, and he remains in obtunded mental status. Its proximity to the bony structures makes it a frequent location in the brain to be contused in trauma. The aim of all good early resuscitation efforts is to begin as early as possible, with many efforts beginning in the prehospital setting, with an attention to airway, breathing, and circulation. Aggressive volume resuscitation for hypotension and adequate ventilation are the primary focus of initial resuscitation efforts. Therefore, the administration of isotonic crystalloids is the preferred method by which to volume resuscitate. The results of his neurologic examination remain poor, and he is only partially responsive to painful stimulation. The majority of early posttraumatic seizures occur within the initial 48 hours of injury. Effective prophylaxis of early posttraumatic seizures reduces brain metabolic demands, thereby reducing intracranial pressure and neurotransmitter release. Furthermore, anticonvulsant treatment can minimize cognitive and behavioral sequelae. However, existing studies of levetiracetam regarding the safety and efficacy are not definitive and do not provide enough evidence that levetiracetam has better short- and long-term outcomes when compared with phenytoin. High doses of steroids are greatly beneficial in experimental models, reducing lipid peroxidation and improving tissue recovery. The first choice for monitoring should always be an external ventricular drain because it can be recalibrated after placement and also offers therapy in the form of cerebrospinal fluid diversion. However, many questions regarding the utility of this monitoring technique have yet to be answered, such as timing, location, and pertinent treatment thresholds. Until such data become available, it is important to remember that the Pbto2 value is a composite of various components of the content of oxygen in the arteries as well as an unknown quantity of passive diffusion. This value is also a very focal/regional measure and should be put into context of the entire clinical picture prior to embarking on therapeutic interventions. There are sufficient data to support the use of periprocedural antibiotics, but the infusion must begin prior to the skin incision. The continued use of antibiotics for prophylaxis is controversial and has not been proven to reduce the rate of ventriculitis and may increase the incidence of drug-resistant bacterial infections. The risk for infectious complications with therapeutic hypothermia is duration dependent, with the rate of infectious complications rising sharply at greater than 72 hours. As a result of reduced metabolic activity, there is decreased production of carbon dioxide at lower body temperatures. If mechanical ventilation parameters are left unchanged during cooling, hyperventilation will occur, which may cause cerebral vasoconstriction and reduced cerebral blood flow. This method of blood gas management may lead to hyperventilation as a result of the overestimation of Pco2. This poses the risk for inducing hypercapnia, which may result in cerebral vasodilation and increased intracranial pressure. The patient is right hemiplegic, and the left side is no longer localizing to pain. The overall mental status has been depressed further, and now painful stimulation does not lead to eye openings. Licox monitoring shows Pbto2 of 16 mm Hg in the left hemisphere frontal subcortical region where the probe is positioned. The decision to perform decompressive techniques is primarily based on the evacuation of a mass lesion, with temporal and frontal lesions more likely to result in decompression. The key is not to delay the procedure because the primary benefit is as a result of reducing sequelae from secondary injury. Once decompression is decided upon, resection of a larger bone fragment is performed to allow for greater dural expansion with a lower risk of herniation. The identification of any cervical spine injuries is part of the standard evaluation after the patient has been hemodynamically stabilized. In this population, the need for additional radiographic evaluations is based on the bedside examination. Those without pain (distracting, midline neck) and with no neurologic deficits localizing to the cervical spine and who are not intoxicated are very unlikely to have significant cervical spinal injury and can be cleared without radiographs. However, there is considerable concern that administering heparin and low-molecular-weight heparin will increase the risk for hematoma expansion. In addition, there is a very low risk for hematoma expansion with prophylactic doses of heparin or low-molecular-weight heparin, resulting in hematoma expansion in this patient population. For these reasons, a reasonable, safe approach toward this patient population is to begin prophylaxis 24 hours after radiographic demonstration of hematoma stability. Decisions regarding timing should balance the risk for intracranial as well as systemic bleeding with the urgency for therapy. However, each therapy does have a slightly different physiologic impact, which may lead to a preferential use of one therapy over another. There remains considerable uncertainty regarding how and when it should be used, but the recommended dose is 0. Some clinicians have advocated replacement of urinary losses to avoid intravascular volume depletion. Although improved outcomes may be obtained with higher doses, decisions regarding higher doses (> 1 g/kg) of mannitol administration should be made on a case-by-case basis. Hypertonic Saline Hypertonic saline is an osmotic agent that has traditionally been used as an adjunct to mannitol or in individuals who have become tolerant to mannitol. Hypertonic saline exerts its effect primarily by increasing serum sodium and osmolarity, thereby establishing an osmotic gradient. Although mannitol works similarly, sodium chloride has a better reflection coefficient (1. Hypertonic saline may also normalize resting membrane potential and cell volume by restoring normal intracellular electrolyte balance in injured cells. The dose and administration varies greatly, with boluses ranging between 30 mL of 23. Based on this evidence, some general clinical guidelines regarding the use of mannitol and hypertonic saline are as follows: 1. Mannitol may be of added benefit when there is intravascular volume overload, but careful attention should be paid to urine output so that patients do not become intravascular volume depleted. Although there is no ceiling as to when osmotic therapies should be discontinued, the likelihood of developing renal insufficiency does increase with supranormal serum sodium levels. Hypertonic saline should be administered with caution in patients with renal insufficiency or congestive heart failure. Regulation of blood carbon dioxide levels has a significant impact on cerebral blood flow and therefore intracranial volume and intracranial pressure. During mild hyperventilation, increased oxygen extraction can compensate for decreased blood flow and volume, allowing normal cellular metabolism to continue; however, prolonged hyperventilation may increase metabolic acidosis. However, this process depends on the availability of bicarbonate in the cerebrospinal fluid. Prolonged hyperventilation may deplete bicarbonate levels, which may in turn result in ischemia and poorer outcomes. The patient is reported to have dilated pupils, hypertension, tachycardia, tachypnea, high fever, and increased body tones with periodic self-extensor posturing during these episodes. Pleural effusion and pulmonary congestion are not uncommon, and these conditions can mimic the syndrome as well. Bromocriptine, -blockers such as propranolol, morphine sulfate, dantrolene, and clonidine may be helpful. It is not uncommon to observe prolonged phases of sporadically occurring storming events even weeks after the initial injury. According to the report, he fell and hit the icy surface of an object during a challenging jump. He immediately lost the motor function of his legs and became numb below his waist. Easily reproducible classification schemes are important methods by which to assess severity of injury, facilitate communication between practitioners, and, more importantly, aid in the determination of prognosis. Methylprednisolone was given to 162 patients, naloxone was given to 154 patients, and placebo was given to 171 patients. Most (95%) of the patients who were randomized to the steroid group received the drug within the first 14 hours of the injury. Only in a post-hoc subgroup analysis, which focused on the timing of the steroid administration, was there a positive 6-month outcome for some individuals who received the drug within the first 8 hours. Only positive reports are again based on the post-hoc analysis showing benefit in people who received the steroid between 3 and 8 hours of injury but no benefit in those who received the drug within the first 3 hours. As a result, the routine use of steroids remains controversial and is not recommended as a standard of care. It may be considered if the administration can be performed while minimizing the associated risks of high-dose steroids,32 making it an option and not a strong recommendation. Respiratory System Cervical cord injury is often associated with changes in respiratory patterns that are important to be aware of and can affect ventilatory strategy. High-level cervical lesions result in the recruitment of accessory muscles with inspiration, resulting in expansion of the upper rib cage with concomitant ascending diaphragm. This results in a paradoxical breathing pattern: reduction in all lung volumes (except residual volumes) but increased pulmonary and chest wall compliance and work of breathing. As a result, this population is at significant risk for developing aspiration pneumonia. The main goals of respiratory management are to provide aggressive pulmonary hygiene, routine bronchodilator therapy, and aggressive attempts at ventilator weaning. Attempting intermittent ventilation with high tidal volumes (10-15 mL/kg), sighs, or adequate positive end-expiratory pressure may reduce the incidence of atelectasis and related complications. Lesions involving the cervical and upper thoracic cord result in sympathetic denervation, resulting in arteriolar vasodilation, venous pooling, bradycardia, and reduced myocardial contractility. The end result of this is a shock state that is characterized by hypotension, low systemic vascular resistance, and sinus bradycardia. However, given the impairment in myocardial contractility, hypotension cannot be overcome just with volume resuscitation and often requires additional vasopressor and/or inotropic agents. In general, there is no advantage to either subcutaneous low-molecular-weight heparin or heparin. Urinary tract infection risk is elevated because of neurologic dysfunction resulting in incontinence, high bladder pressures, and reflux. There should be a low threshold for investigating for gastrointestinal tract infections in patients with persistent fever given the inability of patients to mount symptoms. Whether acute surgical intervention is needed to decompress the injured spinal cord has been a controversial topic. However, previous literature has shown conflicting outcomes with early decompression. Socalled "early" surgical decompressions in these previous studies were done in days to weeks after the injury and not in the first few minutes or hours. By the time a decompression is done, typically 3 to 5 days or a week later, the injury has been completed, and no further intervention is likely to provide any long-term benefit. It may be considered if the administration can be performed while minimizing the associated risks, making it an option and not a strong recommendation. Role of decompressive surgery in the management of severe head injuries: prognostic factors and patient selection. The management of patients with intradural posttraumatic mass lesions: a multicenter survey of current approaches to surgical management in 729 patients coordinated by the European Brain Injury Consortium. Cervical spine collar clearance in the obtunded adult blunt trauma patient: a systematic review and practice management guideline from the Eastern Association for the Surgery of Trauma.

Diseases

• Toni Fanconi syndrome
• Hypogonadism, isolated, hypogonadotropic
• Goodman camptodactyly
• Horn Kolb syndrome
• Spirurida infections
• Short stature microcephaly seizures deafness