Cold antibodies typically react best at temperatures less than 32°C cheap skelaxin 400mg with visa, with maximal reactivity at 4°C and lead to red cell agglutination [19] buy discount skelaxin 400mg. If the patient’s red cells have either IgG or C3 attached to them buy cheap skelaxin 400 mg on line, the red cells will agglutinate, indicating a positive test. The specificity of the antibody can be tested by testing the patient’s serum against panels of red cells that express different subsets of red cell antigens. Most commonly, these antibodies are directed against members of the Rh blood group, but the specificity of the pathogenic IgG antibodies is not always identified. As the shape with the smallest surface area-to-volume ratio is a sphere, the red cell becomes progressively more spherocytic with each pass through the splenic circulation [18]. Approximately 30% of patients with chronic lymphocytic leukemia have a positive Coombs test, although a much lower proportion develops hemolysis [21]. Older patients, and those with rapid hemolysis and ensuing severe anemia, may present with evidence of organ compromise such as dyspnea, angina, or syncope and can suffer myocardial ischemia, hypotension, and/or renal failure. If the patient has heart failure, angina, shock, or evidence of hypoperfusion to vital organs, or if compensatory erythrocytosis is absent or inadequate because of an underlying illness that suppresses the bone marrow, such as leukemia, prior chemotherapy, or renal failure, then red cell transfusion should be performed [18]. The anti-erythrocyte autoantibody itself can also be occasionally directed against red cell precursors in the marrow, leading to an inappropriately low reticulocyte count [18,22]. The offending antibody will frequently interfere with performing a crossmatch to identify compatible blood for transfusion. It is critical to obtain a thorough transfusion and pregnancy history to determine the likelihood of an underlying alloantibody which may be masked by the autoantibody; testing a red cell eluate may be helpful in this regard. Crossmatching can be done using low ionic strength solution which will minimize nonspecific interactions, allowing the stronger alloantibody interactions to appear. Each unit should be transfused slowly, while the patient’s clinical status is closely assessed for evidence of worsening hemolysis. The blood bank may require that samples of the patient’s blood be drawn soon after the transfusion begins to record any evidence of hemolysis. First-line therapy consists of glucocorticosteroids, either intravenously such as methylprednisolone or oral prednisone, typically at 1 to 2 mg per kg daily [19]. If steroids are ineffective, or if relapse occurs, then alternative immunosuppression should be considered. Splenectomy should also be considered as a reasonable second-line treatment option in eligible patients [18]. As with all hemolytic anemias, the administration of folic acid 1 to 5 mg per day, at least as long as hemolysis is ongoing, is recommended. IgM anti-erythrocyte antibodies fix complement to the red cell, leading to either intravascular or extravascular hemolysis. When episodic, cold- induced hemolytic episodes occur, intravascular hemolysis may be associated with shock, rigors, back pain, and renal failure. On Coombs testing, complement (C3) is typically positive whereas IgG is negative, reflecting the underlying IgM autoantibody which more efficiently fixes complement (Table 90. The thermal amplitude of the autoantibody, not the antibody titer, however, best determines the severity of clinical symptoms. If binding occurs only at 4°C to 30°C, it is less clinically important than if significant binding occurs at temperatures more than 34°C, approximating more physiologic conditions. In fact, many normal individuals will have cold agglutinins detected at 4°C but have no clinical symptoms. Other agents, such as chlorambucil, cyclophosphamide, and rituximab, have been used successfully [19,29]. In patients who present with impending or actual end-organ damage such as myocardial ischemia or stroke, plasmapheresis may be effective because IgM remains primarily intravascular and can be efficiently removed. Plasmapheresis may need to be performed preoperatively in surgeries requiring cardiopulmonary bypass or cardioplegia [19,30]. In all patients, care must be taken to keep the extracorporeal tubing warm and to warm intravenous fluids and blood products, or hemolysis may worsen. This antibody is called the Donath–Landsteiner antibody and is directed against the “P” red cell antigen [19]. Red cell destruction occurs primarily via activation of the complement cascade and leads to subsequent intravascular hemolysis. The blood bank should be alerted to the possibility of this diagnosis, as special considerations are required for detection. Controls must be performed where red cells and serum are incubated at 37°C and in a separate test tube at 4°C. In both of these scenarios, there should be no lysis detected [31], as a positive test requires the extremes of temperature. Drug-Induced Hemolytic Anemias More than 130 drugs have been reported to cause immune-mediated hemolytic anemia [32]. Drugs can induce hemolytic anemia by three general mechanisms: the innocent bystander mechanism, hapten mechanism, and a true autoimmune mechanism [33,34]. It should be noted that many drugs may lead to a positive direct Coombs test in the absence of overt hemolysis. Thus, a positive direct Coombs test should not be inferred to represent hemolysis unless there is worsening anemia in conjunction with consistent laboratory evaluation. Other agents such as cyclosporine and tacrolimus may cause a microangiopathic hemolytic anemia due to endothelial damage (see “Microangiopathic Hemolytic Anemia” section). It is essential that the intensivist recognize the differential diagnosis of microangiopathic hemolytic anemia as many of the diagnoses require prompt recognition and treatment (Table 90. The diagnosis should be suspected in any patient who presents with unexplained microangiopathic hemolytic anemia and thrombocytopenia [36,38–40]. The “classic pentad” of microangiopathic hemolytic anemia, thrombocytopenia, mental status changes, renal failure, and fever is present in fewer than 25% of patients at presentation. Occlusion in blood vessels of the cardiac conduction system may lead to arrhythmias and sudden cardiac death. A dual-lumen, large-bore, dialysis-type catheter is often needed for the procedure, despite the coexisting thrombocytopenia. Plasma exchange is often tapered down to every other day upon remission, but this practice has not been critically studied and its efficacy in preventing relapse is uncertain [41]. Immunosuppressants such as glucocorticoids and cyclosporine as adjuncts to plasma exchange have been used, but efficacy remains uncertain [36,38–41]. Platelet transfusion is generally avoided, as it is thought to possibly exacerbate thrombosis, although evidence is conflicting [50,51]. Other Causes of Microangiopathic Hemolytic Anemia the differential diagnosis of microangiopathic hemolytic anemia includes other diagnoses listed in Table 90. An unstable form of hemoglobin (hemoglobin S) is produced which polymerizes in the setting of dehydration or hypoxia, leading to irreversible sickling of erythrocytes. Erythrocyte sickling is responsible for a variety of clinical conditions including extremely painful episodes in the back and extremities. Patients may be symptomatic if they are homozygous for hemoglobin S; if they are compound heterozygotes for hemoglobin S, hemoglobin C, hemoglobin D, and hemoglobin E; or if they also have concomitant β-thalassemia. In general, hematology consultation is indicated if transfusion is considered, as the need for transfusion usually suggests a more complicated clinical scenario.

IgE may play a role against parasites and is also and eradicating the carrier state discount 400 mg skelaxin with amex. It During acute infection skelaxin 400 mg visa, IgM antibodies appear within is predominantly IgM type with low titers order cheap skelaxin on-line. The response is a few days, peak at around 7–10 days and disappear in short lived, does not lead to boosting and such vaccines next few months to undetected levels. Hence presence of are actually revaccination rather than boosters when given IgM indicates recent infection. Similarly, IgM being a large repeatedly which produces the same type of response every molecule is not transferred transplacentally in a newborn. Lastly IgA is not produced Hence presence of IgM antibodies indicates congenital and hence there is no local mucosal protection with this 167 infection in the newborn. A T cell independent antigen like polysaccharide can be develops her/his own immunity after repeated exposure converted to T cell dependent antigen by the technique of to various antigens after birth. The protection offered by conjugation where a carrier protein is conjugated with the transplacental passive immunity depends on the half-life of polysaccharide. This technique is very useful in producing only does the passive immunity protect the child against vaccines like conjugated Hib, pneumococcal, typhoid and the specific diseases, it also interferes with the immune meningococcal vaccines. Cell Mediated Immunity Acquired Passive Immunity This type of immunity is transferable by the lymphocytes and not by antibodies and is mediated via T cells. T cell Immunoglobulins can be passively transferred by giving lymphocyte is a very important cell in the immune response. It can also be done inadvertently by infusing blood These cells are in circulation and in the lymphatic vessels. There are three types of preparations, which will help the B lymphocytes proliferate and produce antibodies. They are: T suppressor cells suppress various immune response and 1) pooled human immunoglobulin preparation; 2) homolo- cytotoxic T cells lead to lysis of the infected macrophages gous hyperimmune globulin and 3) heterologous hyperim- and cancer cells. T cell response is very important for T cell Human Immunoglobulins dependant humoral response as discussed before and for immunity against certain organisms which are essentially This is prepared by pooled plasma from more than 100 intercellular pathogens like M. As it contains a variety of antibodies it is ideally suffer from opportunistic infections, which are intracellular suitable for replacement therapy in congenital and acquired like tuberculosis and fungal infection as well as peculiar immune deficiency with antibody deficiency. It is also used for passive cells communicate with one another and with other types prophylaxis for measles or hepatitis A infection. Homologous Human Hyperimmune Globulins This is obtained by pooling plasma from specific donors Passive Immunity who have high titers of a specific antibody either due to Passive immunity is specific immunity which is transferred repeated past natural exposure or due to vaccination. It gives readymade immuno- preparation serves to protect against a specific disease. They are used for prophylaxis of diseases few weeks to few months depending upon the half-life like hepatitis B, tetanus, varicella or rabies. Besides the natural Heterologous Hyperimmune Globulins transplacental passive transfer of the immunoglobulins in the newborn, the other examples of the passive immunity These were used in past to prevent diseases like rabies or are infusing immunoglobulins in the person to protect him tetanus. Being an animal the most common form of passive immunity is that given product it can lead to severe allergic reactions including to the newborn from the mother. This means that at birth the child will have similar type of antibody pattern as the mother. This Active immunity is developed by stimulating the immune 168 protects the child for first few months till the time she/he system by antigens which can lead to specific humoral or cellular immune response or both. Immunization in Clinical Parts of this chapter including the figures are adapted from Practice. They occur at an incidence of 1 in 2000 live births are asymptomatic; others may have recurrent airway and are often under-diagnosed or diagnosed late. Early infections, severe sepsis, meningitis, recurrent diarrhea, oral diagnosis, correct classification and appropriate treatment candidiasis and severe varicella infection. Cellular immunodeficiencies common immunodeficiency disorders and usually occur in 3. Disorders of phagocyte function pneumococcal polysaccharide vaccine in children above 2 5. Disorders of the complement system years and should be suspected in the setting of repeated infections when all other immunodeficiencies are ruled out. The earliest recognized immunodeficiency disorder, Bruton’s agammaglobulinemia (X linked inheritance) is cellular immunodeficiencies characterized by severe depletion of circulating B cells and very low levels of IgG, IgM and IgA. Treatment consists of lifelong immunoglobulin the screening tests for B and T cell functions are normal. Class switch immunoglobulin deficiencies (earlier known Chronic mucocutaneous candidiasis is characterized by as hyper IgM syndromes and now reclassified as combined recurrent candidiasis of skin, nails and mucous membranes immunodeficiencies) are characterized by low levels of IgG (systemic or invasive candidiasis is rare) and in some with and IgA and normal or high levels of IgM. Treatment is with prolonged T cell deficiency and neutropenia and propensity for severe administration of antifungal agents. Management is by antimicrobial ulomatous inflammation of the lungs and gastrointestinal prophylaxis. The nadir in cyclic neutropenia is combined immunodeficiencies usually 21 days but may range from 14-36 days. These children present in the first few months by chronic eczematous dermatitis, recurrent skin and of life with recurrent, persistent, severe and disseminated respiratory infections, and in an autosomal dominant variant bacterial, viral, or fungal infections and failure to thrive, skeletal or bony abnormalities with delayed shedding of diarrhea, and rashes. The eosinophil count and IgE levels is severe lymphopenia and depletion of all lymphocyte are high. Treatment consists Ataxia telangiectasia related disorders are characterized of antibiotic prophylaxis and immunization (especially by ocular telangiectasia, ataxia and recurrent severe bacterial meningococcal vaccine). The Primary immunodeficiencies should be suspected in the immune deficiency is variable and very severe lymphopenia setting of infections that are: is rare. It is characterized Children less than 5 years of age who get recurrent upper by recurrent skin, soft tissue and lymph node infections and respiratory tract infections is the most common setting granulomatous abscesses in internal organs. Commonly implicated organisms are Staphylococcus aureus, Aspergillus, when immunodeficiency is suspected but rarely established. Cellular immunodeficiencies present with infections of skin, respiratory tract with oculocutaneous infection with intracellular organisms such as mycobacteria, albinism, neurologic defects and propensity to develop an Salmonella, fungi, pneumocystis and viruses. There complement component deficiencies are suggested by is significant neutrophilia even in the absence of infection neisserial infections. Diagnosis at the genetic or molecular level is and less than 1500 in older children is lymphopenia. The platelet count is low and platelet size of specific disorders now and in the future. In practice, this term applies present the immunogenic epitopes to T and B lymphocytes; to the inoculation of vaccine, regardless of the success or T and B cells that are thus stimulated to respond; and a set failure of inducing the desired immune response. Th-2 pathway the injection of pre-formed antibodies to a specific antigen, regulates antibody production by B cells. Th-17 cells modulate in the form of “antiserum” or “immune globulin” is termed autoimmunity (antibody-related). The term “gammaglobulin” is mediated through immunoglobulins (antibodies) which used to denote that the product is not “hyperimmune” to belong to class IgM, IgG, IgA, IgD and IgE. When stimulated, B any specific antigen, but contains antibodies to all common cells transform into plasma cells and secrete antibodies.

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Methamphetamine produces a euphoric and anorexic effect 400 mg skelaxin otc, with smoked and injected administration producing a greater “rush purchase skelaxin 400 mg without a prescription. Hyperthermia may be more common and worse in patients with uncontrolled psychomotor agitation purchase 400 mg skelaxin visa, especially when patients are physically but not chemically restrained. The cathinones or “bath salts” are notorious for causing extreme agitation, hyperthermia, and rapid demise. Focal neurologic deficit may be secondary to cerebral ischemia or infarction, vasospasm, or direct injection trauma. On arteriography, multiple occlusions or “beading” of the arteries has been observed; this is thought to represent some combination of local vasospasm or vasculitis [23,24]. Seizures may occur in association with and independent of intracranial hemorrhage or cerebral infarction. Some abusers develop stereotyped, compulsive behavior such as cleaning or buttoning shirts; in some cases, it has been observed that addicts compulsively disassemble appliances, usually without reassembly. Psychosis from amphetamines can present as paranoid delusions and perceptual disturbances; these may persist long after the drug has been stopped and can result in homicidal or self-destructive behavior [16,25,26]. Severe and prolonged psychosis following cathinones or “bath salts” abuse may be more common than from amphetamines. After binge use of amphetamines, patients may develop a withdrawal pattern of symptoms consisting of generalized fatigue, dysphoria, decreased level of consciousness, and profound lethargy. One occasionally sees choreiform, ballistic, bruxism, torticollis, or athetoid involuntary movements with amphetamine, methamphetamine, and cathinone abuse [27]. These movements usually begin after prolonged abuse of amphetamine or methamphetamine and may worsen or reoccur with additional drug abuse. The mechanism for these movements is not well understood, and may involve a disruption of the normal dopamine neurotransmitter system [28]. Abdominal findings may include increased bowel sounds, bowel obstruction from body packing, and abdominal pain due to intestinal ischemia or bowel perforation [29]. Dehydration, increased anion gap metabolic acidosis associated with increased lactate, and hypokalemia are common in patients with significant sympathomimetic toxicity. Acute tubular necrosis may occur secondary to hyperthermia, hypovolemia, hypotension, and rhabdomyolysis. Scarring and hyperpigmentation (“track marks”) in areas above veins suggest chronic intravenous drug use. Subcutaneous injection of the drug (“skin popping”) can result in scabs, circular scars, and lesions in a variety of areas. In general, the toxicity observed in patients using methamphetamine is attributable to the drug and not to any adulterants. Adulterants are not usually present in large enough quantities, and methamphetamine is relatively pure and sufficiently toxic in its own right. Talc pulmonary emboli have been reported as well, which probably contribute to pulmonary hypertension. In addition to having some sympathomimetic qualities, nearly all of the ring-substituted amphetamines (e. Given the increased serotonin levels produced, at least part of this toxicity should be characterized as serotonin syndrome. Hyperthermia is more common with the ring- substituted amphetamines, likely from contribution from serotonin toxicity and possibly from mitochondrial uncoupling [34]. Patients with abnormal vital signs or mental status should have an electrocardiogram, complete blood cell count, electrolyte, blood urea nitrogen, creatinine, glucose, and arterial blood gas determinations. Patients with chest pain, dysrhythmias, or persistent pulse or blood pressure abnormalities should be evaluated for acute coronary or vascular syndromes. Several imaging studies may be warranted for an amphetamine toxic patient, depending on his or her clinical presentation. The results of toxicology screening for most drugs of abuse rarely contribute to or alter patient management. However, in the case of sympathomimetic toxicity, the urine drug screen is reasonably sensitive to the recent use of methamphetamine/amphetamine as well as cocaine and can assist in differentiating these syndromes, which can be important in management. If toxicology drug screening is essential, health care providers should contact their clinical laboratory to determine included substances as well as causes of false-positive and false-negative results. A positive drug screen can confirm the presence of amphetamine or a similar structured drug, whereas a negative drug screen is nondiagnostic. For amphetamines, the screen is typically reasonably sensitive for use within the last few days, but has limited specificity. A sampling of some common substances that may cause a positive amphetamine screen are bupropion, chloroquine, clobenzorex, ephedrine, methylphenidate, phenelzine, phentermine, phenylpropanolamine, pseudoephedrine, selegiline, tranylcypromine, trazodone, and Vicks(R) inhaler [37]. One should remember that if the result of a toxicology screen is to be used for forensic purposes, the chain of custody should be maintained, and results will need to be confirmed using a more rigorous analytical method such as gas chromatography/mass spectrometry. Toxicologic and nontoxicologic conditions that may have a similar presentation or that present concomitantly (Table 100. A serum lactate level may be helpful for patients with increased anion gap metabolic acidosis of unclear origin. The possibility of concomitant poisoning with by- products or impurities related to the illicit synthesis of methamphetamine (e. The overall approach to these patients is aggressive supportive care with supplemental oxygen, sedation, fluid administration, prevention and treatment of hyperthermia, and close monitoring while addressing the specific myriad complications that can occur. Mild sinus tachycardia and hypertension not associated with psychomotor agitation or evidence of end-organ damage usually do not require pharmacologic treatment. If sufficient benzodiazepines do not provide adequate improvement, rate-related cardiac ischemia may be treated with a β- blocker, preferably a short-acting and easily titratable agent such as esmolol, or a calcium channel blocker, being cautious to exclude cocaine toxicity if a β-blocker is being used. Patients with life-threatening dysrhythmias who are hemodynamically unstable should be cardioverted or defibrillated. However in the author’s experience interventions specifically directed at reducing the heart rate have occasionally precipitated cardiovascular collapse. Persistent hypertension, especially if there is evidence of end-organ damage or hyperthermia, should be treated with benzodiazepines as well as phentolamine, nitroprusside, or nitroglycerin with careful dose titration. Patients presenting with chest pain should be evaluated for acute coronary syndromes and managed accordingly [20]. In these circumstances, cardiology consultation is recommended, especially since coronary vasospasm is a possibility. Other important potential causes of chest pain such as pneumothorax, pneumomediastinum, infection, septic emboli, and aortic dissection should be ruled out. Persistent symptomatic hypotension that is refractory to fluids necessitates treatment with a direct acting vasopressor such as norepinephrine, epinephrine, or phenylephrine. At times, the choice and dose of vasopressor should be guided by their different pharmacological properties as well as potentially pulmonary artery catheter hemodynamic monitoring or bedside ultrasound. Management of bronchospasm should include nebulized β2 agonists (such as albuterol) and anticholinergic agents (such as ipratropium bromide).

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Treatment of Hyponatremia Saline or Water Restriction In general order skelaxin cheap, the plasma sodium concentration can be raised by giving patients salt (either as saline or salt tablets) or by restricting their water intake to below the level of excretion skelaxin 400 mg free shipping. Salt administration purchase skelaxin 400 mg without a prescription, usually as isotonic saline, is appropriate in those with true volume depletion or adrenal insufficiency, in which cortisol replacement is also indicated. Each liter of saline infused raises the plasma sodium by 1 to 2 mEq per L because saline has a higher sodium concentration (154 mEq per L) than plasma. In primary polydipsia, the initiation of water restriction may result in a dramatic rise in the plasma sodium concentration. These patients may be less predisposed to osmotic demyelination because their hyponatremia often is of rapid onset, with less brain cell adaptation apt to occur. In asymptomatic patients, who are more likely to have chronic hyponatremia, the plasma sodium concentration should be raised at a maximum rate of approximately 0. More rapid initial correction is indicated for patients with symptomatic hyponatremia, particularly those presenting with seizures or other severe neurologic manifestations, which primarily result from cerebral edema induced by acute (developing during 2 to 3 days) hyponatremia. This appears to be particularly important in premenopausal women, who may progress from minimal symptoms (headache and nausea) to coma and respiratory arrest; furthermore, irreversible neurologic damage or death is relatively common in younger women with symptomatic hyponatremia, even if the hyponatremia is corrected at an appropriate rate. In comparison, men are at much less risk of symptomatic hyponatremia and of permanent neurologic injury. After the initial 3 to 4 hours of rapid correction, the rate should be slowed down so that the total rise in plasma sodium does not exceed approximately 8 mEq during the initial 24 hours. If the initial aim in an asymptomatic hyponatremic 60-kg woman is to raise the plasma sodium concentration from 110 to 120 mEq per L, then Sodium deficit for initial therapy = 0. In this setting, the administered salt in the hypertonic 3% saline is excreted because plasma volume expansion is present. Because there are approximately 1,000 mEq of solute (Na and Cl) in a liter of 3% saline, the fluid in the renal collecting tubule is relatively hyperosmotic. The result would be no change in total body sodium and that the plasma sodium concentration would increase because of the loss of 1 L of water. Effects of Potassium Potassium is as osmotically active as sodium, and giving potassium can raise the plasma sodium concentration and osmolality in a hyponatremic subject. Because most of the excess potassium goes into the cells, electroneutrality is maintained in one of three ways, each of which raises the plasma sodium concentration: (a) intracellular sodium moves into the extracellular fluid; (b) extracellular chloride moves into the cells with potassium; the increase in cell osmolality promotes free water entry into the cells; and (c) intracellular hydrogen moves into the extracellular fluid. These hydrogen ions are buffered by extracellular bicarbonate and, to a much lesser degree, by plasma proteins. This buffering renders the hydrogen ions osmotically inactive; the ensuing fall in extracellular osmolality leads to water movement into the cells. This relationship becomes clinically important in the patient with severe diuretic or vomiting-induced hyponatremia who is also hypokalemic. Risk of Osmotic Demyelination Severe hyponatremia, especially if acute in onset, can lead to cerebral edema, potentially irreversible neurologic damage, and death. Within 24 hours, however, the brain begins to lose extracellular water into the cerebrospinal fluid and loses intracellular water by extruding sodium and potassium salts and osmolytes, thereby lowering the brain volume toward normal. In this setting, in which brain volume has fallen toward normal, rapid correction of severe hyponatremia may lead within 1 to several days to the development of a neurologic disorder called osmotic demyelination or central pontine myelinolysis. Rapid elevation in the plasma sodium concentration leads to water movement out of the brain, which can lower the brain volume below normal. Such osmotically induced shrinkage in axons could sever their connections with surrounding myelin sheaths. Alternatively, the initial brain cell response to brain shrinkage may be the uptake of potassium and sodium from the extracellular fluid; this elevation in cell cation concentration could be toxic to the cells. The manifestations of osmotic demyelination, which may be irreversible, include mental status changes, dysarthria, dysphagia, paraparesis or quadriparesis, and coma; seizures may occur but are less common. Patients in whom the plasma sodium concentration is raised to more than 20 mEq per L in the first 24 hours or is overcorrected to greater than 140 mEq per L are at greatest risk. Other putative risk factors for osmotic demyelination include chronic alcoholism, malnutrition, prolonged diuretic use, liver failure and transplantation, and burns [15]. On the contrary, late neurologic deterioration is rare if the hyponatremia is corrected at an average rate equal to or less than 0. Studies in experimental animals indicate that the total rate of correction during the first 24 hours is more important than the maximum rate in any given hour [16]. Demyelinating lesions are most common when the plasma sodium concentration in severe hyponatremia is raised by more than 20 mEq/L/d and are rare at a rate less than 10 to 12 mEq/L/d. Recommendations the preferred rate at which the plasma sodium concentration should be increased varies with the clinical presentation. Owing to the cerebral adaptation previously described, patients with chronic asymptomatic hyponatremia are generally at little risk for neurologic symptoms. Although the optimal rate of correction is not clearly proven, the current recommendation in asymptomatic patients is that the plasma sodium concentration be raised at a maximum rate of 4 to 8 mEq/L/d (which represents an average correction of 0. Although it may be safe to increase the plasma sodium concentration at a rate of more than 8 mEq per day, there is no reason to correct it more rapidly in the absence of symptoms. It is not known whether there is a potential benefit to administering water to previously hypoosmolar patients whose hyponatremia has been corrected much too rapidly. In rodents, a marked reduction in the incidence and severity of brain lesions was demonstrated if overly rapid correction (30 mEq per L or more during several hours) was partially reversed so that the net daily elevation in the plasma sodium concentration was less than 20 mEq per L [17]. This improvement was seen if therapy was begun before the onset of neurologic symptoms; benefit was much less likely in animals with symptomatic demyelination. The primary problem in these patients is cerebral edema, and the risk of delayed therapy is greater than the potential risk of too rapid correction. Even in this setting, however, the plasma sodium concentration should probably not be raised by more than 8 mEq per L in the first 24 hours because partial cerebral adaptation has already occurred. It is usually not necessary to continue hypertonic saline once the plasma sodium concentration is greater than 120 mEq per L. Appropriate therapy for this disorder depends on the severity of the hyponatremia and, on the fact that, although water excretion is impaired, sodium handling is intact because there is no abnormality in volume-regulating mechanisms such as the renin–angiotensin– aldosterone system. If the plasma sodium concentration is to be elevated, the osmolality of the fluid given must exceed that of the urine. If 1,000 mL of isotonic saline is given (containing 154 mEq each of Na and Cl or 308 mOsm), all of the salt is excreted (because sodium handling is intact), but in only 500 mL of water (308 mOsm in 500 mL of water equals 616 mOsm per kg). The retention of half of the administered water leads to a further reduction in the plasma sodium concentration. Recent data suggest that a single 20 mg bolus intravenously over 30 minutes results in a sustained water diuresis and may avoid vascular injury. It must also be initiated in the hospital but can be2 administered in the outpatient setting after that. The choice of initial therapy in symptomatic patients is usually 3% saline, and this is the preferred treatment with severe neuropathology (such as seizures). When they are administered, it is important to relax fluid restriction during the initial titration with these agents to avoid an excessive rise in the serum sodium concentration.

Z. Sigmor. Nazareth College. 2019.

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