2018年·第98卷第43期

In 2018, the Neurocritical Care Collaboration Group of the Neurology Branch of the Chinese Medical Association and the Neurocritical Care Professional Committee of the Neurologist Branch of the Chinese Medical Doctors Association launched the "Chinese Expert Consensus on Monitoring and Treatment of Respiratory Pump Failure"^[1]。 The reason why respiratory pump failure has attracted much attention in the field of neurocritical disease is that whether it is hemisphere, midbrain, and pons lesions that adjust respiratory rhythm, or oblongus lesions that initiate respiratory movement, whether it is spinal cord, peripheral nerves, neuromuscular junction lesions that conduct and govern respiratory movement, or respiratory endplate (respiratory muscle) lesions that complete respiratory movement, it can lead to respiratory pump failure and be life-threatening. Unfortunately, not all neurologists, emergency physicians, and critical care physicians can keenly perceive and clearly distinguish respiratory pump failure, and give adequate monitoring and treatment.

respiratory pump failure is a critical disease that leads to poor prognosis or even death in patients with critical neurological diseases. Respiratory pump failure can occur regardless of central nervous system injury or peripheral nervous system disease, and rapid identification (diagnosis) and accurate treatment of respiratory pump failure can effectively reduce the mortality rate of patients and provide the opportunity for the recovery of nervous system function. To this end, the Neurocritical Care Collaboration Group of Neurology Branch of Chinese Medical Association and the Neurocritical Care Professional Committee of Neurologist Branch of Chinese Medical Doctors Association launched the Chinese Expert Consensus on Monitoring and Treatment of Respiratory Pump Failure, whose main contents include the definition of respiratory pump failure, monitoring of respiratory pump failure and treatment of respiratory pump failure.

Percutaneous coronary intervention (PCI) is an effective treatment for patients with acute coronary syndrome (ACS). Dual antiplatelet therapy (DAPT) with ticagrelor combined with aspirin after PCI is recommended by major guidelines^[1,2]。 Individualized assessment of DAPT effectively reduces thrombosis and bleeding events, and the CRUSADE bleeding score is a commonly used bleeding risk assessment tool for patients with ACS^[3,4]In-stent thrombosis risk score^[5](ST score) can effectively predict the occurrence of cardiovascular ischemic events. In the treatment of DAPT, there will be clinical intolerance of aspirin, and how to choose a reasonable treatment plan is a clinical doubt. Can ticagrelor be selected as a monotherapy for aspirin intolerant patients treated with DAPT in PCI in ACS patients with high bleeding and low in-stent thrombus during 1 to 12 months? In this study, the efficacy and safety of this protocol were evaluated by clinical observation and data collection.

Extracerebral hydrops in children is a benign self-limiting disease characterized by megacraniosis (enlarged head circumference). The imaging feature is low-density fluid accumulation outside the brain on CT. The vast majority of children with extracerebral hydrops are idiopathic^[1,2]Based on a population study in Norway, the incidence of benign extracerebral hydrops in children was 0.4‰^[2]。 Extracerebral hydrops in adults is relatively rare and rarely reported in the literature. The Department of Neurosurgery, Beijing Tiantan Hospital affiliated to Capital Medical University summarized the diagnosis and treatment experience of 4 adult patients with extracerebral hydrops from July 2016 to September 2018, and analyzed the clinical characteristics, etiology, pathophysiology, diagnosis and treatment principles of adult extracerebral hydrops.

The patient, a 32-year-old male, came to our hospital in October 2017 due to pain in his left foot for 1 1/2 months. The patient reported that he injured his left foot in a car collision with a car one and a half months ago. He was not treated, and the pain in his left foot recurred. Physical examination on admission: local bone bulging on the medial side of the left foot, obvious tenderness, red skin color, slightly higher skin temperature, unlimited flexion and extension of each toe, and no obvious abnormalities in skin sensation and blood supply at the tip of the toe. X-ray examination of left foot was performed after admission (Figure 1) and left foot CT examination (Figure 2), the results showed that the accessory scaphoid of the left foot, the soft tissue of the medial left foot was swollen, and no obvious bone interruption was seen. Laboratory tests: uric acid 591.6 μ mol/L (normal range: 208-428 μ mol/L, the same below), alanine aminotransferase 54.6 U/L (9-50 U/L), glutamate aminotransferase 48.8 U/L (15-40 U/L), glutamyl transpeptidase 276 U/L (10-60 U/L), C-reactive protein 4.3 mg/L (0-3 mg/L), and no obvious abnormalities were found in other test results. Combined with the patient's medical history, clinical manifestations, imaging examination and laboratory examination, the initial diagnosis was gout associated with accessory scaphoid of left foot.

A 54-year-old male was admitted to the Second Affiliated Hospital of Zhejiang University School of Medicine on September 18, 2017 due to "facial numbness and tightness for 5 years and aggravation for 1 year". Five years ago, the patient experienced facial numbness and tightness without obvious inducement, involving both sides of the face and lips, rice grains stuck on both sides of the cheeks during meals, sometimes choking and coughing after drinking water, no dry mouth and eyes, no parotid gland swelling, no numbness, weakness and pain in the limbs, etc., and no systematic diagnosis and treatment was performed. In the past year, the patient felt that the symptoms had aggravated, and went to our outpatient clinic for electromyography to consider the possibility of trigeminal neuropathy, but there was no improvement after treatment such as nutritional nerve. Past physical fitness. Family history and genetic history were denied. Physical examination of the nervous system at admission: vague speech, pertinent answers, bilateral pupils of equal size and round, sensitive to light reflection, eyeball movement in all directions, bilateral corneal reflex weakening, bilateral facial and perioral acupuncture sensation decreasing, normal chewing movement, bilateral inability to bulge gills, bilateral facial muscle atrophy (Figure 1), bilateral frontal lines were symmetrical, bilateral nasolabial folds were not shallow, the mouth corners were not skewed, the taste was normal, the pharyngeal reflex disappeared, the head-up force was weak, the proximal and distal muscle strength of the limbs was grade 5, no muscle fibrillation was observed, no muscle atrophy of the limbs was observed, the muscle tone was normal, the depth and shallow sensation of the limbs was not abnormal, the tendon reflex of both upper limbs (+ +), the tendon reflex of both lower limbs (+ + +), the bilateral Hoffmann's sign was positive, the bilateral palmaromandibular reflex was positive, and the bilateral Babinski sign was negative. Auxiliary examinations: blood, urine, stool routine, blood biochemistry, complete set of antinuclear antibodies (including anti-SSA antibodies and anti-SSB antibodies), rheumatoid factor, thyroid function, immunoglobulin, IgG4, HIV, syphilis, hepatitis series, tumor series, etc. No abnormalities were found. Cerebrospinal fluid: Protein content 0.614 g/L (reference value 0.08~0.43 g/L), sugar, cell count and IgG synthesis index were normal. Whole exon gene test was negative. Cranial MRI plain scan + black water imaging showed no obvious abnormalities; MRI of trigeminal nerve showed that the right superior cerebellar artery was adjacent to the trigeminal nerve; Cervical MRI showed cervical 3/4, cervical 4/5 and cervical 5/6 disc herniation (Figure 2)。 Nerve conduction detection showed that the sensory nerve conduction velocity of the right and left superficial ulnar branches was slowed down, the amplitude of the evoked potential of the right and left superficial median branches and superficial peroneal nerves was reduced, and the amplitude of the motor conduction evoked potential of the left facial nerve (frontal muscle) was lower than that of the right side; Blink reflection measurement: incubation period of both R1 and R2 waves is prolonged (Figure 3)； Electromyography showed extensive neurogenic lesions in the three segments of medulla oblongata, cervix and thorax. Clinical diagnosis: FOSMN syndrome. Intravenous methylprednisolone 80 mg/d ×14 d + intravenous immunoglobulin 20 g/d ×5 d was administered, followed by oral prednisone 60 mg/d, and the dose was gradually reduced (10 mg per week) until discontinuation. On October 10, 2017, the patient's facial numbness and tightness improved, and facial muscle atrophy was reduced compared with before. At the last telephone follow-up on Oct. 3, 2018, the patient's symptoms were similar to those at discharge, and no disease progression was observed.