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.