Rehabilitation for critically ill patients aims to maintain, improve, and restore activities of daily living (ADL) to improve patients’ quality of life. Rehabilitation in this patient population should be considered a key element of the ABCDEF bundle, and comprehensive interventions should be included in this bundle to prevent post-intensive care syndrome (PICS). Although rehabilitation does not reduce the mortality in critically ill patients, such interventions are known to improve physical function and ADLs and are therefore recommended by national and international guidelines as a useful approach. Recently, in addition to interventions provided during ICU admission to prevent PICS, rehabilitation and follow-up after ICU discharge have received considerable clinical attention. Further studies are warranted to gain a deeper understanding of the optimal dose, frequency, intensity, and duration, as well as the type of rehabilitation in the ICU and following ICU discharge, for various disorders and diseases encountered in clinical settings.

Mechanical ventilation injures not only the lungs but also the diaphragm resulting in dysfunction associated with poor outcomes. The chief mechanisms of ventilator-induced diaphragm dysfunction are: disuse atrophy due to insufficient contraction and excessive ventilatory support; concentric load-induced injury due to excessive contraction and insufficient ventilatory support; eccentric load-induced injury due to contraction during the expiratory phase; and longitudinal atrophy caused by sudden decrease in high positive end-expiratory pressure. To protect the diaphragm during mechanical ventilation, maintaining proper levels of diaphragm contraction is paramount; thus, monitoring of respiratory effort, finely tuned ventilator settings, and maintaining of synchronization between the patient and the ventilator are necessary. As diaphragm dysfunction is more likely to occur in critically ill patients, diaphragm-protective mechanical ventilation strategies are essential to reduce the mortality rate of intensive care unit patients. This review outlines basic knowledge of diaphragm, clinical evidence of ventilator-induced diaphragm dysfunction and its underlying mechanisms, and strategies to facilitate diaphragm-protective mechanical ventilation.

Infant botulism is a disease characterized by generalized neurological paralysis due to botulinum toxin. Its symptoms are similar to those of intracranial diseases such as cerebral nerve palsy and respiratory impairment, and we rarely encounter and may overlook it in severe or atypical cases. We present the case of a 7-month-old girl who was referred to our hospital with chief complaints of fever and lethargy. On arrival, she had coma-like symptoms with almost no response to stimulation and frequent apnea. Since the electroencephalography (EEG) showed slow waves and the norovirus antigen test was positive, we initially diagnosed her condition as acute encephalopathy. Consequently, we provided nervous system-directed intensive care, including steroid pulse therapy. The head MRI and cerebrospinal fluid test showed no abnormalities, while the EEG showed diurnal variation and response to stimulation, suggesting neuromuscular junction disease. Based on the detection of botulinum toxin in a mouse assay of her blood and stool, we diagnosed the patient with infant botulism. Tracheostomy was performed, and she was weaned from the ventilator approximately one month later. These results suggest that we should consider infant botulism when infants present with coma-like symptoms or unexplained symptoms of cerebral nerve palsy.

ICU-acquired weakness (ICU-AW) is a general term used for acute diffuse muscle weakness that develops in critically ill patients and includes conditions such as critical illness polyneuropathy (CIP) and critical illness myopathy (CIM). In this case, lung transplantation was performed on a 6-year-old boy with severe respiratory failure. Due to a combination of many risk factors, the patient experienced ICU-AW with a Medical Research Council (MRC) score of 0. CT of the erector spinae muscles showed that the cross-sectional area of the patient’s muscles was maintained, suggesting that the main cause of muscle weakness was CIP. Rehabilitation did not proceed well because of the patient’s unstable respiratory condition, and the mass of the erector spinae muscles remained unchanged; nevertheless, muscle weakness showed a marked improvement. We speculated that this clinical course supports a diagnosis of CIP. While CIM recovery takes weeks to months, an improvement in CIP may take years; thus, a differentiation between the two is important when considering long-term prognosis. Critically ill children should undergo imaging tests, including CT, which help diagnose ICU-AW and accurately differentiate pathological conditions.

The patient is a 58-year-old woman who has symptom such as presented with fever, common cold, and dyspnea. She was diagnosed with pneumonia, therefore, and started antibiotic therapy. She was brought to our hospital because of the appearance of hemosputum. Her N-terminal pro-brain natriuretic peptide (NT-proBNP) level increased, but we diagnosed pneumonia based on a right predominant infiltrative shadow on chest X-ray, an increase in levels of procalcitonin (PCT), and no echocardiographic findings on valvular disease. Following this, she was intubated and treated with antibiotics. Both on days 3 and 4, her PCT and NT-proBNP levels decreased, but her oxygenation did not improve. We suspected heart failure or diffuse alveolar hemorrhage because her NT-proBNP levels increased again and the hemosputum worsened on day 7. We performed mitral valvuloplasty on day 26 after an echocardiogram revealed severe mitral regurgitation with chordae rupture on day 15. Acute mitral regurgitation may cause unilateral pulmonary edema and hemosputum, which can be misdiagnosed as pneumonia.

Pertussis is a severe infection that usually occurs in infancy. Patients who require extracorporeal membrane oxygenation (ECMO) support are at a high risk of death, and those that develop a thrombotic state during ECMO support need urgent attention and management. We report the case of a 46-day-old infant with severe Bordetella pertussis infection who required ECMO support and was suspected of having developed secondary thrombotic microangiopathy (TMA). He was transferred to our PICU due to apnea, respiratory failure, and hypoxemia caused by pertussis infection. He required ECMO support. Since early hospitalization, laboratory tests showed elevated LDH and free hemoglobin, along with the appearance of fragmented red blood cells; these findings were suggestive of thrombosis and hemolysis. Despite multiple interventions, the thrombosis and hemolysis did not improve. We diagnosed secondary thrombotic microangiopathy. Despite intensive care, the infant died. Pertussis infection can lead to secondary TMA, and urgent intervention is necessary; however, the pathophysiological pathways and optimal treatment for this condition are unclear.