Ebook Pediatric critical care medicine: Part 2
➤ Gửi thông báo lỗi ⚠️ Báo cáo tài liệu vi phạmNội dung chi tiết: Ebook Pediatric critical care medicine: Part 2
Ebook Pediatric critical care medicine: Part 2
IIClinical DisordersEndocrine DisordersMurray M. Pollack Paul KaploiuilzEndocrine Disorders of11Water RegulationSusan B. NunezCLINICAL SYNDROMES OF AB Ebook Pediatric critical care medicine: Part 2BNORMAL WATER REGULATIONManifestations of derangements in osmotic homeostasis are due to alterations in cell volume in the central nervous system (CNS), changes in ellcclive circulating volume and local disturbances produced, that is, by an intracranial neoplasm. In die steady slate, the net waler b Ebook Pediatric critical care medicine: Part 2alance should be zero. I lypertonicity occurs when the renal plus extrarenal water losses exceed water intake, causing the ratio of solutes to water iEbook Pediatric critical care medicine: Part 2
n the body fluids to increase. In hypotonic syndromes, waler intake exceeds die sum of renal plus exlrarenal waler losses; but in chronic hyponatremiaIIClinical DisordersEndocrine DisordersMurray M. Pollack Paul KaploiuilzEndocrine Disorders of11Water RegulationSusan B. NunezCLINICAL SYNDROMES OF AB Ebook Pediatric critical care medicine: Part 2alance in the setting of pediatric critical care. It can occur in children who are volume contracted and have lost sodium in excess of waler, as in severe diarrhea, or renal sodium losses due to adrenal insufficiency with inadequate aldosterone produnion. Ibis is particularly challenging in patients Ebook Pediatric critical care medicine: Part 2 with acute CNS disease, especially if the sodium is low (<125 ml-q per L), which can cause seizures and worsen neurologic status. I he dilferential dEbook Pediatric critical care medicine: Part 2
iagnosis is often between the syndrome of inappropriate secretion of antidiuretic hormone (SIADII) and the cerebral salt wasting (CSW) syndrome. DistiIIClinical DisordersEndocrine DisordersMurray M. Pollack Paul KaploiuilzEndocrine Disorders of11Water RegulationSusan B. NunezCLINICAL SYNDROMES OF AB Ebook Pediatric critical care medicine: Part 2ately concentrated urine. SIADII is associated with increased extracellular fluid volume (F.CF). In cswsyndrome, there is clinical evidence of a contracted F.CF volume.SYNDROME OF INAPPROPRIATE SECRETION OF ANTIDIURETIC HORMONEIbis syndrome, allhough common in die pediatric critical care setting, is Ebook Pediatric critical care medicine: Part 2 rarely the reason for admission to the pediatric intensive care unit (PIC.ll). The expansion of the ECI- volume in SIADI1 is due to a nonphysiologicEbook Pediatric critical care medicine: Part 2
or inappropriate secretion of die anlidiurelk hormone (ADI I), or due to the increased sensitivity of the kidneys to the effect of ADI I. ADIi acts onIIClinical DisordersEndocrine DisordersMurray M. Pollack Paul KaploiuilzEndocrine Disorders of11Water RegulationSusan B. NunezCLINICAL SYNDROMES OF AB Ebook Pediatric critical care medicine: Part 2. In response to the latter, the glomerular filtration rate and renal plasma flow increase, and proximal sodium reabsorption decreases, thereby increasing the urine sodium levels and decreasing die serum sodium level, rhe increased F.CF volume is accompanied hy weight gain hut is not associated with Ebook Pediatric critical care medicine: Part 2 distended neck veins or edema because only one third of retained waler is distributed in the ECF space.With progressively decreasing levels of sodiumEbook Pediatric critical care medicine: Part 2
, the patients gradually develop malaise, hypotonia, nausea, vom iting, anorexia, mental alterations, followed by convulsive crises, stupor, and coma.IIClinical DisordersEndocrine DisordersMurray M. Pollack Paul KaploiuilzEndocrine Disorders of11Water RegulationSusan B. NunezCLINICAL SYNDROMES OF AB Ebook Pediatric critical care medicine: Part 2have neurologic symptoms at higher levels of sodium (han those without such disorders.SIADII is uncommon in children.' A summary of the different conditions associated with SIADII is given in476Part II: Clinical DisordersTABLE 11.1CAUSES OF SYNDROME OF INAPPROPRIATE SECRETION OF ANTIDIURETIC HORMONE Ebook Pediatric critical care medicine: Part 2MalignanciesMedicationsBronchogenic carcinoma Thymoma ALL Lymphoma Neuroblastoma Duodenal or pancreatic adenocarcinoma Central Nervous System DisorderEbook Pediatric critical care medicine: Part 2
sVincristine Garba mazepire Cyclophosphamide (IV) SSRI antidepressants Opiates Clofibrate Chlorpropamide Lamotrigine Pulmonary DisordersInfection: menIIClinical DisordersEndocrine DisordersMurray M. Pollack Paul KaploiuilzEndocrine Disorders of11Water RegulationSusan B. NunezCLINICAL SYNDROMES OF AB Ebook Pediatric critical care medicine: Part 2a PsychosisInfection: pneumonia, tuberculosis Asthma Pneumothorax Positive pressure ventilationAl I, acute iymphobl.'ztic leukemia; SSRI, selective serotonin reuptake inhibitors; IV, inừavenous.Table 11.1. Hie release ul ADI I can be stimulated by pain, stress, increased intracranial pressure, and h Ebook Pediatric critical care medicine: Part 2ypovolemic stales/' S1AD11 can also develop 1 week alter transsphenoidal pituitary surgery in Ị5% of patients or as phase 2 in a triphasic phase folloEbook Pediatric critical care medicine: Part 2
wing intrasellar surgery? Hie retrograde neuronal degeneralion with cell death and vasopressin release has been lliougln lo be lire mechanism behind tIIClinical DisordersEndocrine DisordersMurray M. Pollack Paul KaploiuilzEndocrine Disorders of11Water RegulationSusan B. NunezCLINICAL SYNDROMES OF AB Ebook Pediatric critical care medicine: Part 2osmolality (>280 mOsin per L), decreased urine output to <1 ml/kg/hour with high urine osmolality (>600 niOsm per L), or an inappropriately high urine osmolality (with sodium ex cretion >20 to 25 mEq per I.) in the presence of a low-serum osmolality, and in the absence of clinically evident dehydrat Ebook Pediatric critical care medicine: Part 2ion. Measurement of plasma hormones including ADI I, natriuretic peptide, renin activity, and aldosterone are impractical because the results are notEbook Pediatric critical care medicine: Part 2
immediately available for use in making rapid clinical changes. In addi lion, the results may cause confusion because of the short half-life and mutuaIIClinical DisordersEndocrine DisordersMurray M. Pollack Paul KaploiuilzEndocrine Disorders of11Water RegulationSusan B. NunezCLINICAL SYNDROMES OF AB Ebook Pediatric critical care medicine: Part 2 to be given. Mortality may be as high as 50% in acute hyponatremiaif untreated? Treatment is based on the duration of the hyponatremia and the intensity of the neurologic disturbance such as seizure or altered mental status. There are two basic principles to be remembered when correcting hyponatrem Ebook Pediatric critical care medicine: Part 2ia: (i) the serum sodium level should be increased at a safe rate and (11) the underlying disease should be treated In general, lire serum sodium shouEbook Pediatric critical care medicine: Part 2
ld be corrected slowly at a rate not exceeding 1.3 mEq/I/hour with a total correction of no more than 10 inEq per I. in the first 24 hours and <20 mEqIIClinical DisordersEndocrine DisordersMurray M. Pollack Paul KaploiuilzEndocrine Disorders of11Water RegulationSusan B. NunezCLINICAL SYNDROMES OF AB Ebook Pediatric critical care medicine: Part 2order characterized by confusion, dysarthria, pseudobulbar palsy, and quadriplegia as a result of demyelination in the base of the pons.In severe "acute" hyponatremia with neurologic symptoms, occurring within <48 hours. 3% saline solution, 3.0 to 5.0 ml. per kg can be administered rapidly to increa Ebook Pediatric critical care medicine: Part 2se the senrm sodium faster at 1.5 to 2.0 mEq per I for 5 to 4 hours or until lire neurologic symptoms resolve. Ihe infusion rale may be calculated byEbook Pediatric critical care medicine: Part 2
multiplying the body weight in kilograms by the desired rate of increase in Na* level in ml-qfl/hour. A loop diuretic such as furosemide 1.0 to 2.0 mlIIClinical DisordersEndocrine DisordersMurray M. Pollack Paul KaploiuilzEndocrine Disorders of11Water RegulationSusan B. NunezCLINICAL SYNDROMES OF AB Ebook Pediatric critical care medicine: Part 2st treated with lluid restriction. This is usually sumdcnl to normalize the sodium level. In a young child, lluid intake may be restricted to the range of 30% to 75% of maintenance requirement or to 1,000 ml /m2/day? 9 If this fails to correct the hyponatremia, die addition OÍ demeclocycline, may be Ebook Pediatric critical care medicine: Part 2 indicated to allow for higher volume intake. Lithium may also be used for this purpose, but demeclocycline is superior in causing a nephrogenic diabeEbook Pediatric critical care medicine: Part 2
tes insipidus (DI) like stale, thereby decreasing the renal concentrating ability and decreasing waler reabsorption in the collecting ducts and tubuleIIClinical DisordersEndocrine DisordersMurray M. Pollack Paul KaploiuilzEndocrine Disorders of11Water RegulationSusan B. NunezCLINICAL SYNDROMES OF AB Ebook Pediatric critical care medicine: Part 2 pediatric patient, csw syndrome and SIADII have many similar clinical findings, that is, hyponatremia, high urine osmo lalily, and elevated urinary sodium concentration higher than 150 inEq per 1.. llicy can both be caused by the same intracerebral diseases. Vasopressin level is also elevated in cs Ebook Pediatric critical care medicine: Part 2w syndrome, however, it is an appropriate response to volume depletion. Unlike SIAD1I, in csw syndrome, the urinary output is not low and the ECF voluEbook Pediatric critical care medicine: Part 2
me is decreased due to primary natriuresis.11 Clinical signs of dehydration are evident. Therefore, volume restriction is not effective in restoring nIIClinical DisordersEndocrine DisordersMurray M. Pollack Paul KaploiuilzEndocrine Disorders of11Water RegulationSusan B. NunezCLINICAL SYNDROMES OF ABGọi ngay
Chat zalo
Facebook