Objective: to verify whether the use of invasive mechanical ventilation (IMV) with positive pressure predisposes to the appearance of acute kidney injury (AKI) in critically ill patients. Method: prospective cohort of quantitative approach developed in intensive care unit (ICU) of a public hospital. Eligible patients were selected by convenience sampling. For data collection, a questionnaire consisting of items on clinical and laboratory variables was applied. The information was extracted from the medical records during a period of 15 days. Data analysis was descriptive and inferential. Significant results with p≤0.05 were considered significant. Results: hypertension was among the most incident comorbidities (29. 1%) of the 79 patients evaluated. Among the patients analyzed, 59.5% required IMV with PEEP ≥10 cmH 2 O. Of the total number of patients, 91. 1% evolved with renal dysfunction, according to the KDIGO classification. As an outcome, 34.2% of patients died. Patients who used PEEP >5 cmH 2 0 showed significant predisposition to renal dysfunction (p≤0.05). Conclusion: invasive mechanical ventilation with positive pressure (PEEP) was a factor that contributed to aggravate renal function in different gradations. It was found that patients receiving IMV with PEEP >5 cmH 2 O are more predisposed to the onset of AKI in the ICU, due to the tendency to advanced age, overweight, long time of mechanical ventilation and also hypertension.
A.V.S., 57-year-old, had delayed motor development milestones, walking at the age of three with slow progression of symptoms which later stabilized. At the age 31 he noticed a new worsening, with proximal lower limbs weakness and the need for unilateral support while walking. He reports a history of Poliomyelitis. Neurological examination showed thoracic kyphosis and lumbar hyperlordosis, flaccid areflex and asymmetric tetraparesis predominantly in lower limbs (worse on the left side) and proximally in upper limbs. He also had muscle atrophy on those sites with fasciculations and a pawing gait. The hypothesis of Spinal Muscular Atrophy (SMA) was raised. The electroneuromyography identified chronic severe denervation in L3-S2 and moderate in C5-C7 myotomes. Thighs and legs magnetic resonance imaging identified liposuction in the anterior, posterior and lateral compartments bilaterally with myoedema. A gene panel testing showed no variants that would justify the case. Considering the asymmetry as well as its evolution and the possible infection by Poliomyelitis, we considered the hypothesis of Post-Poliomyelitis Syndrome (PPS) to be more likely, admitting SMA with lower limbs predominance as a differential diagnosis. Poliomyelitis was a prevalent disease during pre-vaccination era and is currently restricted to surviving patients who may present a phenomenon of progression after years of stability, triggered by overtraining with dysfunction of motor neurons, recognized as PPS, with impairment of functionality. There are few reports of muscle imaging in PPS that could be crucial for investigation of atypical cases and a potential marker of progression and natural history of the syndrome.
Female, 54-year-old, began with weakness in her right hand and loss of dexterity. Four months after initial symptoms, patient developed sudden onset vertigo. She progressed with difficulties in coordination, dystonic posture and involuntary movements in her right arm. Family also reported insomnia and cognitive impairment. Ten days later, she had no recognition of family members, and developed myoclonia. After two weeks, progression of ataxia rendered her unable to walk and she also had urinary incontinence. Neurological examination revealed perseveration of speech, oculomotor apraxia, severe gait and limb ataxia, intention tremors and generalized hiperrreflexia. She had marked tenar, first dorsal and palmar interosseus amyotrophy. Video-EEG showed markedly disorganized activity and generalized periodic complexes. Neuroimaging had no signs of spinal cord suffering. Electroneuromyography showed preganglionic chronic neurogenic involvement in cervical and lumbosacral myotomes, and acute denervation bilateral of C5–C7. Cerebrospinal fluid examination showed discrete hyperproteinorraquia and positivity for protein research 14-3-3. Genetic testing showed M129M variant in the PRNP gene. Brain tissue neuropathology revealed histologic spongiform encephalopathy associated with reactional gliosis and neuronal loss. Creutzfeldt-Jakob disease is a rare neurodegenerative disease caused by prion propagation. It has been mainly associated with central nervous system involvement, but lower neuron signs have been described. We report a case of motor neurone symptoms as initial clinical manifestation of Creutzfeldt-Jakob disease.
A male patient, 44-year-old, presents with severe abrupt myalgia in the upper and lower limbs, with evolution to muscle weakness after two weeks. After 40 days, he developed intermittent fever and night sweats. Personal history of anorectal abscess drainage. The neurological exam evidenced discreet muscular hypotrophy of the lateral and medial portion of the thighs, global hyperreflexia, proximal muscle weakness, and bilateral antalgic gait. A right vastus lateralis muscle biopsy showed muscle atrophy and congested vessels. Magnetic resonance imaging of the thighs visualizes diffuse inflammation of the fascia and muscles of the thigh. After beginning the use of corticosteroids, there was a significant improvement. A genetic test showing the c.1129G>A variant (p.Gly377Ser) in the NFKB1 gene was also requested, followed by corticoid weaning and human immunoglobulin initiation.Myofasciitis is a painful inflammatory condition affecting the muscles and the tissues around them. One of them is the fascia, a fibrous connective tissue that surrounds and connects the body’s muscles, tendons, and bones. The pathogenesis may be founded on the mutation of the NFkB gene, which regulates our body’s inflammatory and immune processes, which may result in autoinflammatory diseases, immunodeficiencies, and, consequently, tissue damage. Symptoms are varied and can include muscle weakness, arthralgia, and skin rashes. Diagnosis is based on blood tests, imaging, muscle biopsy, and genetic testing. Treatment involves rehabilitation and immunosuppressive medications to control the immune system’s response. Although NFkB-associated myofasciitis is rare, awareness and understanding of its symptoms are essential to ensure early diagnosis and appropriate treatment.
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