Case
A 35-year-old female patient that developed CPM due to the rapid correction of hyponatremia in an external center was admitted to our hospital for neurorehabilitation and walking rehabilitation with robotics. The patient had a history of intensive care admission and a closed tracheostomy. At the time of admission to our hospital, she was spontaneously breathing without any problem except mild wheeze. The patient’s vital signs were as follows: oxygen saturation stable at 98 mmHg, pulse 62/min, respiratory rate 18 breaths per minute, body temperature 36.5 °C, and arterial blood pressure 100/70 mmHg. She had moderate dysarthric speech and was using warfarin sodium due to atrial fibrillation. There was no abnormal finding in her blood values during hospitalization and follow-up​​. She was conscious, cooperative, and oriented. In the neurological examination, muscle strength was grade 1 for the right upper extremity proximal and lower extremity distal groups and grade 3-4 for the remaining key motor muscle groups according to Lovett Scale. Spasticity was grade 1+ for upper extremities, grade 2 for the lower extremity proximal group, grade 3 for the gastrocnemius group on the right, and grade 2 for the gastrocnemius group on the left according to Modified Ashworth Scale. Her ambulation level was stage 1 according to Functional Ambulation Classification (FAC) Scale. The patient was observed to have ambulation potential but her spasticity was more prominent than loss of muscle strength. Therefore, first, the INR level was reduced below 2 with the adjustment of the warfarin sodium dose, and then a total of 300 units of BoNTA injection were applied as follows: 50 units each into the four points of the medial and lateral heads of the right gastrocnemius muscle group and 50 units each into the two different points of the medial and lateral heads of the left gastrocnemius muscle group.
After the injection, the patient’s general condition was good throughout the day and the next day, and she did not report any complaints. However, respiratory distress occurred on the third day of the injection. The patient’s respiratory rate was 36/min, pulse 52/min, blood pressure 100/60 mmHg, and body temperature 36.5 °C. Despite the provision of high oxygen support, the SaO2 value dropped from 97 mmHg to 92 and then 78 mmHg. The departments of chest diseases, anesthesia and reanimation, and cardiology were consulted immediately. The consultant cardiologist did not consider congestive heart failure in the patient since her ejection fraction was 55% on echocardiography. There were also no signs of congestive heart failure, such as right heart or hepatic vein dilatation, on the non-contrast thoracic computed tomography (CT) of the patient. Hypoxemia did not improve under 10 l/min O2 support and arterial blood gas pH was compatible with acidosis; therefore, the patient was admitted to the intensive care unit and intubated. The non-contrast thoracic CT revealed bilateral parenchymal ground glass opacities accompanied by consolidation areas in the lower lobes. The patient was ventilated following the ARDS protocol and dual broad-spectrum antibiotherapy, IV methylprednisolone at 40 mg 1x1, bronchodilator nebule, and IV acetylcysteine ​​were started. In the intensive care follow-up, the patient’s SaO2 values ​​improved but it was anticipated that she would have required mechanical ventilator support for a long time; thus, a tracheostomy was performed. During the follow-up, the patient’s vitals remained stable. At the request of the patient relatives, the patient was transferred to a closer hospital in their city of residence.