Cuidados Intensivos Pediatricos Ruza Pdf

Cuidados Intensivos Pediatricos Ruza Pdf Rating: 8,2/10 3517 reviews

MANUAL DE CUIDADOS INTENSIVOS PEDIATRICOS del autor FRANCISCO RUZA TARRIO (ISBN 048). Comprar libro completo al MEJOR PRECIO nuevo o. Dec 27, 2018  PEDIATRICOS, Francisco Ruza (3 edicin) y al MANUAL DE CUIDADOS. Descargar Libro: Cuidados intensivos peditricos de Francisco Ruza en PDF Capitel Editores, 2003. Publicado por Elida. TRATADO DE CUIDADOS INTENSIVOS PEDIATRICOS (2 VOLS.) del autor FRANCISCO RUZA (ISBN 031). Comprar libro completo al MEJOR PRECIO nuevo o.

Hypercalcemia is a rare metabolic disorder in children and is potentiallyfatal. It has a wide differential diagnosis, including cancer. Here, wereport the case of a previously healthy 3-year-old who was admitted to theemergency room with fatigue, hyporeactivity, fever and limping gait thathad evolved over 5 days and that was progressively worsening. Onexamination the patient was unconscious (Glasgow coma score: 8). Laboratorytests indicated severe hypercalcemia (total calcium 21.39mg/dL, ionizedcalcium 2.93mmol/L) and microcytic anemia. Hyperhydration was initiated,and the child was transferred to the pediatric intensive care unit.Continuous venovenous hemodiafiltration with calcium-free solution wasinstituted, which brought progressive normalization of serum calcium and animproved state of consciousness.

Zoledronate was administered, andmetabolic and infectious causes and poisoning were excluded. The bonemarrow smear revealed a diagnosis of acute lymphoblastic leukemia.Hypercalcemia associated with malignancy in children is rare and occurs asa form of cancer presentation or recurrence. Continuous venovenoushemodiafiltration should be considered in situations where there isimminent risk to life. INTRODUCTIONHypercalcemia is an uncommon metabolic disorder in children. The differentialdiagnosis is complex and varies with age at presentation.

Metabolic,nutritional, drug-induced, genetic, inflammatory and neoplastic factors may alsobe involved. Although common in adults, malignancy-associated hypercalcemia (MAH) is a rarecomplication at pediatric age and occurs in 0.4 to 1.3% of cancers, of whichacute lymphoblastic leukemia is the most common in this age group. (,)Treatment of MAH consists in the treatment of the underlying malignancy. In severeand persistent hypercalcemia, the initial approach is hyperhydration. As a part of standardtreatment, prednisolone is effective in cases of moderate severity.

Calcitonin is often reportedas a treatment for pediatric MAH but has a modest hypocalcemic effect and is notmarketed in Portugal. Bisphosphonates have been extensively studied and areeffective in adult MAH. However, due to the rarity of the disease in childrenand the potential adverse effects with respect to osteogenesis, studies ofefficacy and safety in this age group are limited. Nonetheless, small case series have confirmedits effectiveness. Severesymptomatic hypercalcemia requires emergency correction with continuousvenovenous hemodiafiltration.

CASE REPORTA 3-year-old male child weighting 16kg with unremarkable past medical historypresented with tiredness that had evolved over 1 week. Five days beforeadmission, he started fever, left coxalgia and limping gait in the context ofrecent trauma. Due to symptom maintenance, the child was re-evaluated 3 daysbefore admission. Imaging and laboratory studies did not suggest osteoarticularinfection, and the child was given symptomatic treatment. Since the clinicalpicture persisted and was, accompanied by prostration, hyporeactivity andrefusal to eat, he returned to the emergency room.On admission, the patient was unconscious (Glasgow coma score: 8) with themaintenance of osteotendinous reflexes.

He was hemodynamically stable and didnot present any other alterations, such as rash, blood dyscrasia,lymphadenopathy, hepatomegaly or splenomegaly.Laboratory evaluation revealed compensated metabolic alkalosis (pH of 7.41,partial pressure of carbon dioxide PaCO 2 of 48.7mmHg, bicarbonateHCO 3 of 32.5mmol/L and base excess of 9.6) and severehypercalcemia (total calcium 21.8mg/dL, ionized calcium 2.93mmol/L). Otherevaluations are shown in.Craniocephalic computed tomography and renal, abdominal and hip joint ultrasoundshowed no significant changes. AnalysisResultReference valueHemoglobin (g/dL)9.311.5 - 11.5Hematocrit (%)26.634 - 43Mean corpuscular volume (fL)73.175 - 90Leukocytes (/uL)5,5004,000 - 12,000Neutrophils (/uL)2,300Lymphocytes (/uL)2,500Platelets (/uL)186,000150,000 - 350,000C-reactive protein (mg/dL)7.96.

RuzaPara

Given the clinical and laboratory severity of hypercalcemia, on suspicion ofosteoarticular infection, intravenous hyperhydration was initiated(2,500mL/m 2/day), and antibiotics were given (flucloxacillin andgentamicin). The child was transferred to the pediatric intensive care unit.Continuous venovenous hemodiafiltration was initiated after a 6.5F hemodialysiscentral venous catheter was placed in the right femoral vein. An HF20 filter wasused and priming was performed with 5,000 UI of heparin in 1L of 0.9% sodiumchloride. Continuous venovenous hemodiafiltration was programmed in accordancewith the pediatric protocol (25 - 40mL/kg/h = 1/3 dialysis fluid + 2/3 fluidreplacement (2/3 prefilter + 1/3 post-filter)). Ultrafiltrate was calculatedaccording to the desired fluid balance. A replacement and calcium-free dialysis solution wasused (Prism0Cal ®, Gambro - Lund, Sweden).

Regionalanticoagulation was performed with machine-perfused unfractionated heparin, thedose of which was adjusted according to the patient's activated partialthromboplastin time. The technique was maintained for 72 hours and took placewithout complications. As a therapeutic supplement, intravenous zoledronate(0.025mg/kg) was administered on the third day of hospitalization. There was aprogressive decrease in total and ionized calcium levels and an improved stateof consciousness. AnalysisResultReference valuePTH intact. DISCUSSIONHypercalcemia is a potentially fatal disorder, regarding its neurological andcardiac complications.

Cuidados Intensivos En Ingles

The treatment includes hyperhydration, bisphosphonatesand treatment of the underlying disease. Occasionally, rapid correction of the disturbancebecomes crucial, particularly in the setting of loss of consciousness or whenthe hypercalcemia is refractory to conventional measures. In such situations,the use of continuous venovenous hemodiafiltration has been identified as aneffective treatment. (,) Its successful use in severehypercalcemia has been reported in adults, (-) but the useof the technique in pediatrics has rarely been described in theliterature. (,) In this case report, due tosevere hypercalcemia on admission, the use of dialysis solution withcalcium-free replacement was chosen. Regular analytical calcemia controls wereperformed in order to avoid a sudden decrease and below-normal values.

The renalreplacement therapy settings were set in order to provide a gradual decrease inserum calcium, thereby avoiding complications such as circuit clotting. As thepatient did not present spontaneous diuresis, it was decided to program lossesto ensure a neutral fluid balance. Following clinical and laboratorystabilization, zoledronate was introduced to maintain normocalcemia, as theeffect of continuous venovenous hemodiafiltration is temporary. Continuous monitoring ofserum calcium levels was assured due to the risk of hypocalcemia observed inthis case. The etiological investigation suggested an independent PTH mechanism. Metabolicand infectious causes and vitamin or drug poisoning were excluded. Progressivepancytopenia led to the suspicion of MAH, which ultimately led to the finaldiagnosis.The pathogenesis of MAH includes the stimulation of bone resorption, mediated byproteins and cytokines produced by the tumor cells or by the tumoralmicroenvironment. Flashpoint digital image copier driver.

Two distinct mechanisms are described, which includehypercalcemia by local osteolytic lesions (bone metastasis) and humoralhypercalcemia by the activation of RANK-RANKL (receptor activator of nuclearfactor κB and its ligand). Parathyroid hormone-related protein (PTHrP) isthe most frequently involved mediator, but other mediators, such as interleukin(IL)-1, IL-6, tumor necrosis factor alpha (TNF-α), transforming growthfactor beta (TGF-β), prostaglandins and even calcitriol and ectopic PTHproduction may be involved. In acute lymphoblastic leukemia, an association with hypercalcemia in patientswith t (17;19) has been reported, suggesting the possible induction ofPTHrP. (,) In this case, thiscytogenetic abnormality was not observed, and high levels of PTHrP were notdetected, thus excluding this mechanism as the primum movens ofhypercalcemia. CONCLUSIONThe described case shows an infrequent complication, not only at pediatric age,but also in children with oncological diseases, suggesting that this metabolicemergency unveils of the underlying disease. Continuous venovenoushemodiafiltration with calcium-free solution as a first-line treatment in casesof severe and symptomatic hypercalcemia was found to be effective in the rapidinduction of normocalcemia and neurological improvement, buying valuable timeuntil maintenance treatment focused on the etiology can exert a sustainedeffect.

. 43 Downloads.AbstractWe report 31 episodes of hypertensive crises in children, managed with sublingual nifedipine at the following dosages: 10 mg in children with body weight (BW) higher than 20 kg, 5 mg in children with BW between 10 and 20 kg, and 2.5 mg in children with BW below 10 kg. The mean initial blood pressures were 161.41 mm Hg for the systolic pressure (mSBP) and 111.25 mm Hg for the diastolic pressure (mDBP).

After nifedipine, both the mSBP and the mDBP decreased, with onset of effect five minutes after dosage and maximum decrease at 60 min (mSBP 134.93 mm Hg, mDBP 79.23 mm Hg, for decreases of 16.4 and 28.7%, respectively), and this effect persisted for 180 min. Blood pressure increased again from min 240 to min 360, yet without reaching the initial levels. One case did not respond to the first dose of nifedipine and required a second one. The effect of nifedipine was more pronounced on the DBP than on the SBP, and greater reductions of both pressures were achieved in the cases with higher initial readings. No side of medication were observed in our patients.