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Typical daily electrolyte maintenance requirements for adults with normal kidney function are listed in table 100–3. 6,13 for additional details regarding management of fluid, electrolyte and acid–base disorders refer to chapters 27 and 28. »» calcium-phosphate solubility the fda published a safety alert in response to two deaths from microvascular pulmonary emboli associated with calcium–phosphate precipitation in pn. 14 because calcium and phosphate can bind and precipitate in solution, caution must be exercised when mixing these two electrolytes in pn admixtures. Several factors can affect calcium–phosphate solubility, including. •• amino acid concentration. Primary factor that affects ph of the pn admixture. The ph of amino acid stock solutions may vary between commercial products. In general, the higher the final amino acid concentration, the lower the ph of the final admixture. Phosphates can also bind with amino acids, leaving fewer phosphates available to bind with calcium. •• ph. Largely affected by the amino acid brand and concentration, to a lesser extent by the dextrose concentration. The lower the solution ph, the less chance for calcium–phosphate precipitation. Monobasic phosphates chapter 100  |  parenteral nutrition  1493 table 100–3  approximate daily maintenance electrolyte requirements for adults6,13 electrolyte approximate daily maintenance requirementsa electrolyte salts used in pn maximum concentration in pn sodium 1–2 meq/kg (1–2 mmol/kg) chloride, acetate, phosphate potassium phosphorus 1–2 meq/kg (1–2 mmol/kg) 20–40 mmol (~10–15 mmol per 1000 kcal [2. 4–3.

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T is is an example o transverse myelitis. What are the di erential diagnoses, diagnostic testing, and treatments?. Please see the chapter on demyelinating diseases. What is the most likely cause o transverse myelitis in this case?. T e subacute course, the mri imaging characteristics, and the presence o hilar lymphadenopathy all point to neurosarcoidosis. What other mani estations o neurosarcoidosis are commonly seen?. Sarcoidosis can present as a short or longitudinally extensive transverse myelitis, radiculopathy, and “basal meningitis” with cranial neuropathy. How is neurosarcoidosis diagnosed?. Mri. Cns neurosarcoidosis lesions are gadolinium enhancing on the mri. Lp. Raised ace levels (not very speci c or sensitive). Sometimes it mimics in ections with pleocytosis, low glucose, and raised protein. T e only reliable way to diagnose it is tissue diagnosis o en rom extra-cns sources such as the hilar lymph nodes in this case. How is neurosarcoidosis treated?. Steroids and in iximab are used or the acute disease. Note in iximab worsens multiple sclerosis, so a high diagnosis certainty should precede the choice o this agent. 630 ch a pt er 38 a b ▲ figure 38-10 postcontrast t1 images o the spine. Mid-sagittal images (a) and cross sectional images (b). Maintenance is achieved by chronic steroid therapy or steroid-sparing therapy such as azathioprine, methotrexate, or mycophenolate. What other autoimmune diseases can present with transverse myelitis?. Systemic lupus erythematosus (sle), sjögren’s disease, and mixed connective tissue disease can present with longitudinally extensive transverse myelitis. Reatment is directed toward the underlying condition. Toxic and metabolic myelopathies x ca s e 38-6 a 72-year-old woman presents with 5-month history o gait disequilibrium. On examination, she had brisk muscle stretch ref exes and bilateral babinski signs. She had lower limb parasthesias and loss o proprioception in the legs. Romberg testing was positive, and she had gait ataxia. Pain and temperature was intact. Mri shows t2 hyperintensities in the posterior s pina l cor d neur ology and lateral aspects o the spinal cord, which did not enhance. Emg/ncvs showed ndings consistent with sensory neuropathy. With what is this presentation consistent?. 12 t e presence o corticospinal and dorsal column dy unction and the preservation o spinothalamic unction point to subacute combined degeneration o the cord. What are some o the common reasons or this condition?. B12 de ciency:13 risk actors or b12 de ciency.

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Symptoms suggestive of end-organ dysfunction. Visual disturbances such as scotomata, diplopia or blindness, persistent severe headache, or epigastric pain. 4. Pulmonary edema. 5. Oliguria defined as <500 ml of urine per 24-hour collection. 6. Microangiopathic hemolysis. 7. Thrombocytopenia defined as a platelet count of <100,000. 8. Hepatocellular dysfunction. Elevated transaminases. 9. Intrauterine growth restriction (iugr) or oligohydramnios. C. Heilp syndrome {hemolysis, elevated liver enzymes, and low platelets) represents an alternative presentation of preeclampsia associated with disseminated intravascular coagulation (dic) and reflects systemic end-organ damage. Hellp syndrome often appears without hypertension or proteinuria and may, in fact, have a separate pathologic origin from that of preeclampsia. V. Complications of preeclampsia result in a maternal mortality rate of 3 per 100,000 live births in the united states. Maternal morbidity may include central nervous system complications (e.G., seizures, intracerebral hemorrhage, and blindness), dic, hepatic failure or rupture, pulmonary edema, and abruptio placentae leading to maternal hemorrhage and/or acute renal failure. Fetal mortality markedly increases with rising maternal diastolic blood pressure and proteinuria.

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2010 update by the society for healthcare epidemiology of america (shea) and the infectious diseases society of america (idsa). Infect control hosp epidemiol. 2010;31(5):431–455. Chapter 69  |  antimicrobial regimen selection  1045 15. Namdar r, lauzardo m, peloquin ca,. Tuberculosis. In. Dipiro jt, talbert rl, yee gc, et al.