Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 2 de 2
Filtrar
Mais filtros











Base de dados
Intervalo de ano de publicação
1.
Ther Hypothermia Temp Manag ; 13(4): 216-224, 2023 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-37140459

RESUMO

This study investigates the clinical profile and predictors of gastrointestinal/hepatic morbidities and feeding outcomes among neonates with hypoxic-ischemic encephalopathy (HIE). A single-center retrospective chart review of consecutive neonates >35 weeks of gestation admitted with a diagnosis of HIE between January 1, 2015, and December 31, 2020, and treated with therapeutic hypothermia, if met the institutional eligibility criteria. Outcomes assessed included necrotizing enterocolitis (NEC), conjugated hyperbilirubinemia, hepatic dysfunction, assisted feeding at discharge, and time to reach full enteral and oral feeds. Among 240 eligible neonates (gestational age 38.7 [1.7] weeks, birth weight 3279 [551] g), 148 (62%) received hypothermia therapy, and 7 (3%) and 5 (2%) were diagnosed with stage 1 NEC and stage 2-3 NEC, respectively. Twenty-nine (12%) were discharged home with a gastrostomy/gavage tube, conjugated hyperbilirubinemia (first week 22 [9%], at discharge 19 [8%]), and hepatic dysfunction (74 [31%]). Time to reach full oral feeds was significantly longer in hypothermic neonates compared with neonates who did not receive hypothermia (9 [7-12] days vs. 4.5 [3-9] days, p < 0.0001). Factors significantly associated with NEC were renal failure (odds ratio [OR] 9.24, 95% confidence interval [CI] 2.7-33), hepatic dysfunction (OR 5.69, 95% CI 1.6-26), and thrombocytopenia (OR 3.6, 95% CI 1.1-12), but no significant association with hypothermia, severity of brain injury, or stage of encephalopathy. Transient conjugated hyperbilirubinemia, hepatic dysfunction within first week of life, and need for assistive feeding are more common than NEC in HIE. Risk of NEC was associated with the severity of end-organ dysfunction in the first week of life, rather than severity of brain injury and hypothermia therapy per se.


Assuntos
Lesões Encefálicas , Hipotermia Induzida , Hipotermia , Hipóxia-Isquemia Encefálica , Recém-Nascido , Humanos , Adulto , Estudos Retrospectivos , Hipóxia-Isquemia Encefálica/diagnóstico , Hipotermia/terapia , Hipotermia Induzida/efeitos adversos , Morbidade , Lesões Encefálicas/terapia , Hiperbilirrubinemia/complicações , Hiperbilirrubinemia/terapia
2.
Clin Case Rep ; 11(1): e6770, 2023 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-36694646

RESUMO

Nitrous oxide is a gas frequently used in the medical/dental field for anesthesia and analgesic purposes and in the food industry as a spray propellant or foaming agent. Overexposure can lead to subacute combined degeneration (SACD) of the spinal cord through the mechanism of vitamin B12 deficiency. Because this drug is easily accessible, relatively inexpensive, and legal to possess, it has potential to be abused for recreational purposes. The number of published cases of nitrous oxide abuse has been increasing since 2010. Large-scale and long-term use of nitrous oxide have been found to cause nerve damage from vitamin B12 deficiency, thromboembolic phenomenon from elevated homocysteine levels, and even death from hypoxia. A 44-year-old male patient with past medical history of recently diagnosed type 2 diabetes, on Metformin, presented for 1 month of worsening bilateral upper and lower extremity weakness. On initial physical examination, he demonstrated pertinent abnormal findings of 2/5 hand strength bilaterally, 4/5 strength in his left upper extremity and right lower extremity, impaired coordination, ataxic gait, rigidity, and decreased but symmetrical reflexes. He reported using 50-100 canisters of nitrous oxide per day to obtain a feeling of relaxation and euphoria. Blood work revealed vitamin B12 deficiency, and abnormalities were seen on MRI. He was treated with 1000 µg of intramuscular vitamin B12 every other day for 3 doses, followed by 500 µg oral cyanocobalamin daily. He demonstrated a great amount of improvement in his neuropathy during his stay. However, he was still dependent in basic transfers, activities of daily living, and mobility and was discharged to acute rehabilitation. Vitamin B12 deficiency can lead to subacute combined degeneration, which presents with sensory deficits, weakness, ataxia, spasticity, and gait abnormalities. Treatment for SACD should be aggressive and rapid to prevent irreversible neurological deficits. Amid an opioid epidemic, practitioners can easily overlook the use of nitrous oxide and patients may consider this drug to be relatively harmless. This case demonstrates the importance of thorough history taking, patient education, and early recognition and treatment of vitamin B12 deficiency and the deleterious effects that may result without intervention.

SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA