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By I. Ramirez. Asbury College.

Prophylaxis with subcutaneous heparin (5 buy levitra with dapoxetine 40/60 mg cheap,000 units twice a day) could be started as early as postoperative day 1 [44] levitra with dapoxetine 40/60 mg on line. Once identified cheap levitra with dapoxetine 40/60 mg with mastercard, treatment with anticoagulation may be problematic, especially in the immediate postoperative period because of fear of hemorrhage [46,47]. However, recent studies have shown that use of anticoagulation in the immediate post-op is safe and does not lead to increased risk of hemorrhage [42]. Cerebral Infarction About 15% of cancer patients have significant cerebrovascular pathology noted at autopsy [48]. Alternatively, because these patients may be older with premorbid atherosclerosis, they may suffer cerebral infarction. Coumadin, if indicated, should be reserved for a patient who has not had hemorrhage into the tumor and who is at least 2 weeks post-op. Systemic Infections Systemic infections are not uncommon, and most often include pneumonia, urinary tract infections, or sepsis secondary to line placement. Hopefully, the patient’s physicians have discussed these possibilities as the patient begins to show signs of decline. The most intensive interventions—surgery, ventriculostomy, and intubation for hyperventilation—may be most readily decided against. Prior to the onset of such cardiac difficulties, however, the patient may progress to the point of “brain death. The clinical exam shows the patient to be comatose, without any brain stem reflexes, motor responses, or spontaneous respirations, and on no sedative medications. If these criteria are present, the patient should be declared brain dead and supportive technologies be discontinued. It is important and mandated by statute that the organ bank be contacted so the organ donation can be discussed with the family prior to discontinuing supportive technologies. Bruce J, Criscuolo G, Merrill M, et al: Vascular permeability induced by protein product of malignant brain tumors: inhibition by dexamethasone. Muizelaar J, Wei E, Kontos H, et al: Mannitol causes compensatory cerebral vasoconstriction and vasodilation in response to blood viscosity changes. Dostal P, Dostalova V, Schreiberova J, et al: A comparison of equivolume, equiosmolar solutions of hypertonic saline and mannitol for brain relaxation in patients undergoing elective intracranial tumor surgery: a randomized clinical trial. Kumar B, Bhagat H: A comparison of 3% saline and mannitol for brain relaxation during elective supratentorial brain tumor surgery. Yamada K, Ushio Y, Hayakawa T, et al: Effects of methylprednisolone on peritumoral brain edema: a quantitative autoradiography study. Keddie S, Rohman L: Reviewing the reliability, effectiveness, and applications of Licox in traumatic brain injury. Weaver D, Winn R, Jane J: Differential intracranial pressure in patients with unilateral mass lesions. Raimondi A, Tomita T: Hydrocephalus and infratentorial tumors: incidence, clinical picture and treatment. Sekhar L, Moossy J, Guthkelch N: Malfunctioning ventriculoperitoneal shunts: clinical and pathological features. Aydin S, Yilmazlar S, Aker S, et al: Anatomy of the floor of the third ventricle in relation to endoscopic ventriculostomy. Chalk J, Ridgeway K, Brophy T, et al: Phenytoin impairs the bioavailability of dexamethasone in neurological and neurosurgical patients. Alroughani R, Javidan M, Qasem A et al: Non-convulsive status epilepticus; the rate of occurrence in a general hospital. Cohen N, Stauss G, Lew R, et al: Should prophylactic anticonvulsants be administered to patients with newly-diagnosed cerebral metastases? Fadul C, Wood J, Thaler H, et al: Morbidity and mortality of craniotomy for excision of supratentorial gliomas. Ross D, Rosegay H, Pons V: Differentiations of aseptic and bacterial meningitis in postoperative neurosurgical patients. Scheller C, Rachinger J, Strauss C et al: Therapeutic anticoagulation after craniotomies: is the risk for secondary hemorrhage overestimated? Choucair A, Silver P, Levin V: Risk of intracranial hemorrhage in glioma patients receiving anticoagulant therapy for venous thromboembolism. These include: Suicidal hanging, electrical shock, acute carbon monoxide poisoning, and decompression sickness, which present so blatantly that the diagnosis is rarely in question, yet the range of clinical manifestations and their management may be unanticipated. Cerebral fat embolism, which is often not initially suspected if other surgical or medical issues take precedence. Singultus (hiccups), which is an all too common secondary problem that may further weaken the severely ill patient. Changes in techniques, with the victim dropped at least his height and the hangman’s knot placed in the submental location, have produced a consistently fatal bilateral axis pedicle fracture, resulting in complete herniation of the disc and severance of the ligaments between C2 and C3 [3]. This injury causes almost immediate death by destroying the cardiac and respiratory centers, lacerating the carotid artery, and injuring the pharynx [2,3]. Suicidal hangings are rarely so expert, and death usually results from strangulation due to interruption of cerebral blood flow [4]. A minimal amount of compression occludes the jugular veins, whereas an increased force occludes the carotid arteries [5]. Pressure on the jugular veins from the noose results in venous obstruction and stagnation of cerebral blood flow, causing hypoxia and loss of consciousness [3]. Cervical muscle tone then decreases, allowing airway obstruction and arterial compression, further exacerbating hypoxia [3]. In addition, external compression of the carotid bodies or vagal sheath can increase parasympathetic tone, whereas pressure on the pericarotid area stimulates sympathetic tone; either can result in cardiac arrest [4,5]. The altered autonomic tone may also cause a release of catecholamines, resulting in neurogenic pulmonary edema, as well as affect the respiratory smooth muscle tone, causing respiratory acidosis and a further insult to cerebral oxygenation [3]. If the blood flow is interrupted for more than a few minutes, however, hypoxia causes cell death and cytotoxic and vasogenic edema, with increased intracranial pressure. There is selective vulnerability of the cerebral cortex (particularly the pyramidal cell layer), the globus pallidus, thalamus, hippocampus, and the cerebellar Purkinje cells to anoxia and ischemia. Diagnosis Although the diagnosis is rarely in doubt, the patient may show a range of findings, varying from rope burns to coma. In the immediate posthanging period, the patient most commonly shows evidence of an altered level of consciousness, ranging from restlessness, delirium, or violent agitation to lethargy, stupor, or coma. Injury to the neck blood vessels occurs in 40% of patients, resulting in carotid dissection, thrombus formation, and distal ischemic infarcts [6]. In incomplete hanging, the patient may also show signs of laryngeal and pharyngeal edema, resulting in hoarseness, dysphagia, and stridor [3,7]. Although infrequent in suicidal hangings, fracture of the odontoid and injury to the spinal cord may occur. Careful neurologic examination should be performed, with particular attention to alterations in the level of consciousness and evidence of spinal cord injury, such as paraparesis, quadriparesis, or urinary retention. Owing to decreased blood flow and the resultant hypoxia, edema may be seen in the white matter tracts [9]. Subcortical and subarachnoid hemorrhages may result from venous occlusion, whereas ischemia may result from venous or arterial occlusion, particularly in the areas of greatest vulnerability: the basal ganglia, cortex, thalamus, and hippocampus [10]. The goals of treatment are to maintain an adequate level of cerebral oxygenation, to decrease the raised intracranial pressure, and to monitor and treat any cardiac arrhythmias or respiratory distress that may develop.

Rarely purchase levitra with dapoxetine 40/60mg without a prescription, exogenous lipoid pneumonias are complicated by organisms of the Mycobacterium fortuitum complex [48] purchase 40/60mg levitra with dapoxetine with visa. Although corticosteroids may be helpful for cases of acute lipid aspiration buy levitra with dapoxetine 40/60 mg lowest price, acute exogenous lipoid pneumonias usually resolve on their own. Examples of conditions that predispose to an aspiration tracheobronchitis include a debilitated state, the postoperative period, endotracheal intubation, recent extubation, and neuromuscular diseases [3]. Aspiration tracheobronchitis should be suspected for patients with cough, wheezing, and bronchorrhea, defined as expectoration of more than 30 mL of phlegm in 24 hours. Matsuse T, Oka T, Kida K, et al: Importance of diffuse aspiration bronchiolitis caused by chronic occult aspiration in the elderly. Khorvash F, Abbasi S, Meidani M, et al: The comparison between proton pump inhibitors and sucralfate in the incidence of ventilator associated pneumonia in critically ill patients. Cook D, Guyatt G, Marshall J, et al: A comparison of sucralfate and ranitidine for the prevention of upper gastrointestinal bleeding in patients requiring mechanical ventilation. Brady S, Donzelli J: The modified barium swallow and the functional endoscopic evaluation of swallowing. Barquist E, Brown M, Cohn S, et al: Postextubation fiberoptic endoscopic evaluation of swallowing after prolonged endotracheal intubation: a randomized, prospective trial. Prigent H, Lejalle M, Terzi N, et al: Effect of a trachesotomy speaking valve on breathing—swallowing interaction. Mittal R, Stewart W, Schirmer B: Effect of a catheter in the pharynx on the frequency of transient lower esophageal sphincter relaxation. Ferrer M, Bauer T, Torres A, et al: Effect of nasogastric tube size on gastroesophageal reflux and microaspiration in intubated patients. Strong R, Condon S, Solinger M, et al: Equal aspiration rates from postpylorus and intragastric-placed small-bore nasoenteric feeding tubes: a randomized, prospective study. Baeten C, Hoefnagels J: Feeding via nasogastric tube or percutaneous endoscopic gastrostomy: a comparison. Montecalvo M, Steger K, Farber H, et al: Nutritional outcome and pneumonia in critical care patients randomized to gastric versus jejunal tube feedings. Reignier J, Mercier E, Le Gouge A, et al: Effect of not monitoring residual gastric volume on risk of ventilator-associated pneumonia in adults receiving mechanical ventilation and early enteral feeding: a randomized controlled trial. Tolep K, Getch C, Criner G: Swallowing dysfunction in patients receiving prolonged mechanical ventilation. Elpern E, Scott M, Petro L, et al: Pulmonary aspiration in mechanically ventilated patients with tracheostomies. Leder S, Sasaki C, Burrell M: Fiberoptic endoscopic evaluation of dysphagia to identify silent aspiration. Torres A, Serra-Batlles J, Ross E, et al: Pulmonary aspiration of gastric contents in patients receiving mechanical ventilation: the effect of body position. Orozco-Levi M, Torres A, Ferrer M, et al: Semirecumbent position protects from pulmonary aspiration but not completely from gastroesophageal reflux in mechanically ventilated patients. Schwartz D, Wynne J, Gibbs C, et al: The pulmonary consequences of aspiration of gastric contents at pH values greater than 2. Irwin R, Pratter M, Corwin R, et al: Pulmonary infection with Mycobacterium chelonei: successful treatment with one drug based on disk diffusion susceptibility data. Irwin R, Corrao W, Pratter M: Chronic persistent cough in the adult: the spectrum and frequency of causes and successful outcome of specific therapy. Implicit in this definition is that a liquid–air interface is present at the entrance of the victim’s airway, preventing the victim from breathing air. A victim can be rescued at any time during the drowning process and may not require an intervention or may receive appropriate resuscitative measures. Older terms, such as near- drowning, submersion or immersion injury, and dry or wet drowning are discouraged to facilitate clearer communication. It is the third most common cause of accidental injury death worldwide, claiming approximately 372,000 lives annually [3]. For most countries, drowning statistics do not include additional water-related deaths from boating accidents which are categorized separately. Drowning is most common among men, children younger than 14 years, North American Native populations, and African- Americans [2]. Statistics on nonfatal drowning are less exact because many nonfatal drowning victims do not seek medical attention. Estimates for the incidence of nonfatal drowning vary widely enough that a definitive statement cannot be made at this time. Alcoholic beverages reduce the ability to deal with emergency situations by depressing coordination, increasing response time, and decreasing awareness of stimuli. Furthermore, alcohol consumption by a potential rescuer or by the adult responsible for supervising a child in the water can destroy that person’s ability to function effectively, often resulting in a double tragedy. Studies have shown lower rates of drowning for areas where swimming pools are required by law to be surrounded by a fence [2,5]. Diving and sliding headfirst may produce serious head and neck injuries as a result of striking the bottom or side of a shallow body of water. Appropriate sign posting in hazardous areas, effective educational programs on the dangers of water recreation, and the presence of lifeguards minimize risk and improve survival [5,9]. The use of infant bath seats, while providing some sense of security to parents, may actually predispose to submersion accidents because the child may slip and become trapped by the seat, making it impossible to escape the water [10]. The practice of leaving infants to bathe in the custody of a toddler is inappropriate and should be discouraged. One study indicated that 29% of all nonfatal pediatric drownings in bathtubs were purposely caused to inflict harm on the child. In general, these children are younger than average for submersion injuries, and many have signs of previous abuse on close examination. Inadequate Swimming Skills Both objective data and common sense support the idea that improved swimming skill can reduce the risk of drowning. Although the exact magnitude of this reduction is imprecise, some reports have estimated it as high as 88% for young children [12,13]. Seizures Drowning is 15 to 19 times more common in people with epilepsy than in the general population [14]. Tonic seizures include a forced exhalation component that increases body density and causes the victim to sink. When the tonic component relaxes, the negative intrathoracic pressure leads to an inhalation that will then be composed of water [16]. Boating Accidents Of the 710 boating fatalities in the United States in 2006, 70% were caused by drowning [17]. In addition, injuries associated with the use of personal watercraft share many features with boating accidents and are associated with drowning [19]. Drugs Centrally acting drugs cause disorientation, induce sleep, impair coordination, and reduce the ability to swim. In almost every case, there are eventually involuntary breaths with aspiration of varying amounts of water. Survival after extremely long submersion is generally considered possible only when the victim has been submerged in icy water.

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Yield of bone marrow examination in diagnosing the source of fever of unknown origin order 40/60mg levitra with dapoxetine amex. From prolonged febrile illness to fever of unknown origin: the challenge continues order levitra with dapoxetine 40/60 mg fast delivery. What are the symptoms levitra with dapoxetine 40/60mg cheap, signs, and diagnostic tests that help to differentiate viral from bacterial pneumonia? How useful is sputum Gram stain, and what are the parameters that are used to assess the adequacy of a sputum sample? How should the clinician interpret the sputum culture, and should sputum cultures be obtained in the absence of sputum Gram stain? What are some of the difficulties encountered in trying to determine the cause of acute pneumonia? How often should chest X-ray be repeated, and how long do the radiologic changes associated with acute pneumonia persist? Which antibiotic regimens are recommended for empiric therapy of community-acquired pneumonia and why? Estimates suggest that pneumonia is responsible for more than 10 million physician visits, 500,000 hospitalizations, and 45,000 deaths annually. Overall, 258 people per 100,000 population require hospitalization for pneumonia, and that number rises to 962 per 100,000 among or nearly 1/100 for those over the age of 65 years. It is estimated that, annually, 1 in 50 people over 65 years of age and 1 in 20 over 85 years will develop a pneumonia. Causes Improved diagnostic techniques have shown that the number of pathogens that cause acute pneumonia is ever expanding (Table 4. Mycoplasma and Chlamydophila pneumoniae also account for a significant percentage of acute pneumonias. Legionella species vary in importance, depending on the season and geographic area. Anaerobes such as anaerobic streptococci and bacteroides can cause acute pneumonia following aspiration of mouth contents. Common viral pathogens include influenza, parainfluenza, and respiratory syncytial virus. Pathogenesis and Pathology Under normal conditions, the tracheobronchial tree is sterile. The respiratory tract has a series of protective mechanisms that prevent pathogens from gaining entry [ure 4. The epiglottis covers the trachea and prevents secretions or food from entering the trachea. Mucin contains a number of antibacterial compounds including immunoglobulin A antibodies, defensins, lysozymes, and lactoferrin. Mucin also is sticky, and it traps bacteria or other foreign particles that manage to pass the epiglottis. Cilia lining the inner walls of the trachea and bronchi beat rapidly, acting as a conveyer belt to move mucin out of the tracheobronchial tree to the larynx. When significant volumes of fluid or large particles gain access to the trachea, the cough reflex is activated, and the unwanted contents are quickly forced out of the tracheobronchial tree. If pathogens are able to bypass all of the above protective mechanisms and gain entry into the alveoli, they encounter a space that, under normal circumstances, is dry and relatively inhospitable. The presence of an invading pathogen induces the entry of neutrophils and alveolar macrophages that ingest and kill infecting organisms. The lymphatic channels adjacent to the alveoli serve to drain this space and transport fluid, macrophages, and lymphocytes to the mediastinal lymph nodes. Bacterial pathogens usually gain entry into the lung by aspiration of mouth flora or by inhalation of small aerosolized droplets (<3 μm in diameter) that can be transported by airflow to the alveoli. The nasal turbinates trap foreign particles, and the epiglottis covers the trachea. First, an outpouring of edema fluid into the alveoli occurs, serving as an excellent culture media for further bacterial growth. As fluid accumulates, it spills over to adjacent alveoli through the pores of Kohn and the terminal bronchioles, resulting in a centrifugal spread of infection. Bacterial invasion of the alveoli induces a) edema fluid that spreads to other alveoli through the pores of Kohn, and b) infiltration by polymorphonuclear leukocytes and red blood cells, followed by macrophages. Infection spreads centrifugally: a) Newer regions in the periphery appear red (“red hepatization”). On lower power microscopy, this region has an appearance similar to the architecture of the liver—an effect termed “red hepatization. Gram-negative rods and anaerobic bacteria also cause permanent tissue destruction. Predisposing Factors Most bacterial pneumonias are preceded by a viral upper respiratory infection [ure 4. Viral infections of the upper respiratory tract can damage the bronchial epithelium and cilia. Virus-mediated cell damage also results in the production of serous fluid that can pool in the pulmonary alveoli, serving as an excellent culture media for bacteria. The low viscosity of this fluid, combined with depressed ciliary motility, enables the viral exudate to carry nasopharyngeal bacteria past the epiglottis into the lungs. Smoking also damages the bronchial epithelial cells and impairs mucociliary function. Congenital defects in ciliary function (such as Kartagener syndrome) and diseases resulting in highly viscous mucous (such as cystic fibrosis) predispose patients to recurrent pneumonia. An active cough and normal epiglottal function usually prevent nasopharyngeal contents from gaining access to the tracheobronchial tree. However, drugs such as alcohol, sedatives, and anesthetics can depress the level of consciousness and impair these functions, predisposing the patient to pneumonia. Elderly individuals, particularly after a cerebrovascular accident, often develop impairments in swallowing that predispose them to aspiration. In addition, elderly people demonstrate reduced humoral and cell-mediated immunity, rendering them more susceptible to viral and bacterial pneumonia. Patients with impairments in immunoglobulin production, T- and B-cell function, and neutrophil and macrophage function are also at greater risk of developing pneumonia. Chronic diseases, including multiple myeloma, diabetes, chronic renal failure, and sickle cell disease, have been associated with an increased risk of pneumonia. Viral infections damage cilia and produce serous exudate that can transport nasopharyngeal bacteria into the alveoli. Elderly patients have reduced humoral and cell-mediated immunity, and may have impaired swallowing because of stroke. Cold weather dries the mucous membranes and increases person-to- person spread of infection. Cold, dry weather can alter the viscosity of mucous and impair bacterial clearance. Cold weather also encourages people to remain indoors, a situation that enhances person-to-person spread of respiratory infections.

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The physical examination should focus on the vital signs order levitra with dapoxetine 40/60mg fast delivery, neurologic function buy cheap levitra with dapoxetine 40/60mg on-line, and cardiovascular status discount levitra with dapoxetine 40/60 mg line. Lithium levels should be obtained at least 12 hours after the last lithium dose and repeated at intervals of 4 to 6 hours after acute overdose until peak levels are observed. If the levels are elevated, they should be repeated until they are in the therapeutic range and the patient becomes asymptomatic [12]. Blood for thyroid function testing and calcium and magnesium levels may be warranted in some cases [2]. Patients with chronic lithium overdose are typically brought to medical attention by a family member or therapist because of gradual onset of neurologic symptoms. There is usually a recent history of excessive fluid loss caused by gastroenteritis, other infective illness, renal insufficiency, or the addition of new drugs such as diuretics and nonsteroidal anti- inflammatory agents [12]. After acute lithium overdose, the predominant initial symptoms are nausea, vomiting, abdominal pain, or diarrhea [2]. Patients do not usually have significant neurologic manifestations despite high serum lithium levels during the first 12 hours or more after ingestion because lithium is taken up slowly by the brain and other tissues [11]. However, toxicity may develop during the subsequent 24 to 48 hours, even as serum levels fall [15,17]. There does not appear to be any clinical variable that accurately predicts which patients will deteriorate. However, cerebrospinal fluid levels do not reflect intracellular brain tissue levels or predict the level of coma [6,9]. Patients with acute-on-chronic lithium overdose have a clinical course similar to those following an acute overdose. However, a smaller total dose may produce severe intoxication, depending on the preoverdose serum lithium level. Elevated blood urea nitrogen and creatinine reflect renal insufficiency and suggest that intoxication results from gradual accumulation of lithium rather than acute ingestion. Elevated creatinine may also be caused by cross-reactivity of the assay with creatinine from muscle destruction and should prompt the measurement of serum creatinine phosphokinase and urinalysis for myoglobinuria. A reduced or absent anion gap may occur with severe lithium carbonate intoxication, probably because the carbonate anion (but not the lithium cation) is measured and used in calculating the anion gap [25]. In a patient with hyperthermia and rigidity who is also taking antipsychotic medications, neuroleptic malignant syndrome and serotonin syndrome should be considered. If hyperthermia is present, cooling measures should be instituted, including evaporative cooling, tepid sponging, and fanning. Neuromuscular paralysis and endotracheal intubation, a reliable approach to rapidly lower body temperature, can be considered as needed. Cardiac dysrhythmias do not usually require treatment, but should respond to the current recommended pharmacologic treatment of dysrhythmias. Gastrointestinal tract decontamination should be considered after acute ingestion to prevent continued absorption of lithium. Activated charcoal does not effectively bind lithium and should be given only if coingestion of another drug is suspected [28]. Whole-bowel irrigation (see Chapter 97) has been recommended for large ingestions, especially if they involve modified-release tablets [29]. If a tablet mass or concretion is suspected because of sustained high levels after 2 to 3 days, contrast imaging studies, ultrasound, or gastroduodenal endoscopy and endoscopic removal should be considered [30]. Preliminary evidence in animals and human volunteers suggests that the cation exchange resin sodium polystyrene sulfonate (Kayexalate) binds lithium and may enhance its elimination [31–33]. The clinical effectiveness of sodium polystyrene sulfonate treatment in lithium overdose remains to be determined. Observation in asymptomatic patients following an acute or acute-on- chronic overdose of lithium in conventional formulation should be for a minimum of 6 hours, and observation for a minimum of 24 hours following an overdose of lithium in modified-release formulation [6–8]. Symptomatic patients, patients with a massive acute ingestion, and those whose levels continue to rise beyond 6 hours after ingestion should be admitted to an intensive care setting. Delayed clinical manifestations and peak serum lithium concentrations may occur in patients who overdose on modified-release formulations of lithium. However, the gradual onset and the duration required of hydrochlorothiazide, carbamazepine, and amiloride therapy would limit their clinical usefulness. Intravenous fluid therapy is effective in restoring glomerular filtration rate and maintaining renal elimination of lithium in most patients with mild or moderate intoxication. A crystalloid solution (half-normal or normal saline) aiming for urine output of 1 to 3 mL/kg/h should be administered after an initial saline bolus (10 to 20 mL per kg), depending on the degree of dehydration. A crude estimate of renal lithium clearance can be calculated from simultaneous urine and serum lithium levels and urine flow rate: Renal lithium clearance = urine flow rate (mL per minute) × urine lithium (mmol per L)/serum lithium (mmol per L). If the clearance is below normal in a patient without underlying cardiac or renal dysfunction, the rate of fluid administration should be increased because this suggests low renal perfusion secondary to dehydration. In human studies, water loading, furosemide, thiazide, ethacrynic acid, ammonium chloride, and spironolactone did not increase lithium clearance. Hemodialysis is the most efficient method for removing lithium, achieving clearance rates of up to 170 to 180 mL per minute [7,35,36]. However, lithium is only slowly removed from intracellular tissue compartments, especially the brain, and rebound increases of serum lithium levels often occur within several hours after dialysis. Hemodialysis should be repeated frequently until the serum level drawn 6 to 8 hours after the last dialysis is 1 mmol per L or less [7,12,36]. However, despite repeated dialyses, patients with significant neurologic toxicity do not promptly improve. The indications for hemodialysis are not well established, and hence recommendations for management of lithium poisoning vary widely, as demonstrated in a survey of 163 health care professionals from 33 countries [37]. It is generally agreed that patients with severe clinical toxicity and those with renal dysfunction should undergo dialysis. Asymptomatic patients or those with mild-to-moderate intoxication who are otherwise healthy may be managed with intravenous fluids as long as they remain clinically stable or are improving with satisfactory lithium clearance (>15 to 20 mL per minute). In one case, 14 hours of continuous arteriovenous hemodiafiltration was estimated to achieve lithium elimination equivalent to 5. In another case report, clearances of up to 38 mL per minute were achieved with continuous venovenous hemodiafiltration [40]. However, in the acute setting, hemodialysis is most effective for quickly reducing the serum lithium concentration, and it can be followed by continuous renal replacement therapy to maintain a slow but continuous removal of lithium, thus mitigating a rebound in the central compartment lithium concentration. The systematic review indicated there is a very low quality of evidence for all recommendations, because most publications were case reports. Serinken M, Karcioglu O, Korkmaz A: Rarely seen cardiotoxicity of lithium overdose: complete heart block. Erden A, Karagoz H, Basak M, et al: Lithium intoxication and nephrogenic diabetes insipidus: a case report and review of literature. Leon M, Graeber C: Absence of high anion gap metabolic acidosis in severe ethylene glycol poisoning: a potential effect of simultaneous lithium carbonate ingestion. Teece S, Crawford I: Best evidence topic report: no clinical evidence for gastric lavage in lithium overdose. Bellomo R, Kearly Y, Parkin G, et al: Treatment of life-threatening lithium toxicity with continuous arterio-venous hemodiafiltration. Until recently, theophylline was used exclusively as a bronchodilator for the management of reversible obstructive pulmonary diseases and as a respiratory stimulant for the treatment of apnea of prematurity in neonates.

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