A-70-year-old male patient with a history of chronic obstructive pulmonary disease (COPD) over the previous 10 years was referred from Physical Therapy Department for etiological investigations on his inability to walk. His medical history revealed that he had been discharged from pulmonology 3 weeks ago after the administration of medications for COPD exacerbation. He was hospitalized for 2 weeks and received antibiotherapy of ceftriaxone (2 g intravenous daily for 1 week) for pneumonia, medication for COPD, as well as bilevel positive airway pressure (BIPAP) therapy

Onder, Halil

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Columbia University Academic Commons

1New Observations LetterA Case of Severe Myoclonus due to Carbon Dioxide Retention  in the Setting of Chronic Obstructive Pulmonary Disease ExacerbationHalil OnderNeurology Clinic, Yozgat City Hospital, Yozgat, TurkeyDear EditorA-70-year-old male patient with a history of  chronic obstructive pul-monary disease (COPD) over the previous 10 years was referred from Physical Therapy Department for etiological investigations on his inability to walk. His medical history revealed that he had been discharged from pulmonology 3 weeks ago after the administration of  medications for COPD exacerbation. He was hospitalized for 2 weeks and received anti-biotherapy of  ceftriaxone (2 g intravenous daily for 1 week) for pneumo-nia, medication for COPD, as well as bilevel positive airway pressure (BIPAP) therapy. However, after discharge, BIPAP therapy could not be administered due to social problems (his relatives did not show any interest in the patient, and he had no support for the administration of  BIPAP therapy at home). After being discharged from hospital, it was noticed that he could not walk or even mobilize due to severe involuntary jerks in his whole body. Therefore, he has applied to physical therapy polyclinic (2 weeks after being discharged), from which he was referred to neurology clinic. At admission to neurology polyclinic, the patient was not taking any medication except for bronchodilator therapy including salbutamol and ipratropium inhaler. He was evaluated as fully orientated and cooperated. However, he had poor mobilization, and he was dependent on a wheel-chair. There were severe, sudden, brief  jerks in his whole body, which were aggravated during mobilization (Video 1). These jerks were so powerful that he could not move from lying to a sitting position without any support due to severe jerks compatible with myoclonus. Other neurological  examinations including motor and sensory examination were within normal ranges. The patient was hospitalized in order to conduct etiologi-cal investigations for myoclonus. Vital signs were regular (temperature: 36.2°C, pulse: 90, SPO2: 90%). Cranial magnetic resonance imaging (MRI) was in normal range (Figure 1). Laboratory investigations revealed mild leukocytosis (hemoglobin [Hb]: 12.7/dL, white blood cell counts [WBC]: 16,000/mm3, plt: 233,000/mm3), and hypocalcemia (7.9 mg/dL). However, arterial blood gas test showed carbon dioxide retention (pH: 7.33, pCO2: 76, pO2: 26.8, HCO3: 41.2). Taken together, carbon dioxide retention was considered as the cause of  myoclonus in the forefront, and the patient was referred to pulmonology department to receive therapy for COPD exacerbation on the same day of  hospitalization. Increases in bronchial secretions were apparent, and wheezing was detected on aus-cultation. Chest X-ray showed chronic signs of  COPD. BIPAP treatment was suggested, with initiation of  piperacillin/tazobactam (4.5 g thrice daily) at first due to the diagnosis of  atypical pneumonia. However, BIPAP therapy did not provide any amelioration in blood gas test results. Hence, the patient was intubated and taken to intensive care unit (on the second day of  hospitalization). After the following 3 days, decrease in bronchial secretions was achieved and the need for aspiration was significantly reduced. Remarkably, the myoclonic movements were almost recovered following intubation, soon after normalization of  hypercarbia. After final evaluation by pulmonology department, it was decided that the patient was able to protect the airway and maintain sufficient ventilation. Hence, following gradual preparation for pre-extubation, extubation was per-formed (the patient could easily tolerate intubation into such a level that Columbia University LibrariesFreely available onlineTremor and Other Hyperkinetic Movementshttp://www.tremorjournal.orgKeywords: Myoclonus, chronic obstructive lung disease, carbon dioxide retention, BIPAP, pathophysiology.Citation: Onder H. A Case of  Severe Myoclonus due to Carbon Dioxide Retention in the Setting of  Chronic Obstructive Pulmonary Disease Exacerbation. Tremor Other Hyperkinet Mov. 2019; 9. doi: 10.7916/d8-85y8-rr41*To whom correspondence should be addressed. E-mail: halilnder@yahoo.comEditor: Elan D. Louis, Yale University, USAReceived: January 26, 2019; Accepted: March 7, 2019; Published: June 21, 2019Copyright: ©2019 Halil Onder. This is an open-access article distributed under the terms of  the Creative Commons Attribution–Noncommercial–No Derivatives License, which permits the user to copy, distribute, and transmit the work provided that the original authors and source are credited; that no commercial use is made of  the work; and that the work is not altered or transformed.Funding: None.Financial Disclosures: None.Conflicts of Interest: The authors report no conflicts of  interest.Ethics Statement: This study was reviewed by the author’s institutional ethics committee and was considered exempted from further review.Onder H Myoclonus due to Carbon Dioxide RetentionColumbia University LibrariesTremor and Other Hyperkinetic Movementshttp://www.tremorjournal.org 2no sedation and analgesia were required during the pre- and post-intu-bation periods). On neurological examination, it was observed that myoclonic jerks were significantly reduced (Video 2). Concurrently per-formed arterial blood gas test revealed significant improvement of  hypercarbia (pCO2: 42.5, ph: 7.49, pO2: 79.7, HCO3: 33). After 1 week of  hospitalization, piperacillin/tazobactam was stopped, and the patient was discharged with the recommendation of  BIPAP therapy.DiscussionMyoclonus is characterized by sudden, brief, shock-like involuntary movements, associated with bursts of  muscular activity or  silencing of  muscular activity. There are many classifications of  myoclonus, includ-ing clinical, neuroanatomical, and etiological aspects. Neurodegenerative diseases, stroke, and ictal events can be postulated as the forefront  etiological causes of  myoclonus.1 On the other hand, Figure 1. Cranial MRI. Cranial MRI (T2 and T1 Sequences) of  the Patient, Showing Normal Findings. Video 1. Myoclonic Movement Which Was Recorded Soon after Hospitalization at the Same Day of  Admission (Concurrently pCO2:76). (a) Images recorded while the patient was trying to mobilize from lying position to sitting position. (b) Images recorded while the patient was trying to put his body into standing position.Onder H Myoclonus due to Carbon Dioxide RetentionColumbia University LibrariesTremor and Other Hyperkinetic Movementshttp://www.tremorjournal.org 3metabolic encephalopathies are also considered as a common cause of  myoclonus, which are typically seen in the intensive care unit.1 Hyponatremia, hepatic encephalopathy, uremia, hypophosphatemia, hypo or hyperglycemia, hyperthyroidism, and pulmonary encephalop-athy (carbon dioxide retention) have been reported as the major causes of  myoclonus associated with metabolic encephalopathies.1 Among those, carbon dioxide retention has been acknowledged as an inducer of  myoclonus for quite a long time.1,2 However, to our knowl-edge, there is no proper demonstration of  a case with myoclonus induced by carbon dioxide retention in the literature. Therefore, we think that the presentation of  this patient, in whom a significant ame-lioration of  myoclonus was achieved after COPD therapy, may provide a substantial perspective for clinicians. Through the presentation of  this patient, first, we attract attention to the fact that carbon dioxide retention is a crucial cause of  myoclonus among metabolic agents. In addition, remarkably, the patient did not suffer from dyspnea. Besides, on neurological examination, he was evaluated as orientated and coop-erated (findings not compatible with encephalopathy). We think that the recognition of  this point may be crucial for timely etiological diag-nosis such that it can even be the only manifestation of  COPD exacer-bation, as in our case.References1. Eberhardt O, Topka H. Myoclonic disorders. Brain Sci 2017;7,103. doi:10.3390/brainsci7080103.2. Kilburn KH. Neurologic manifestations of  respiratory failure. Arch Intern Med 1965;116:409–415. doi:10.1001/archinte.1965.03870030089015Video 2. Post-treatment. Video, Recorded on the 6th Day of  Hospitalization, Showing Recovery of  Myoclonic Jerks after Treatment of  Carbon Dioxide Retention (pCO2:42.5).

A Case of Severe Myoclonus due to Carbon Dioxide Retention in the Setting of Chronic Obstructive Pulmonary Disease Exacerbation

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A Case of Severe Myoclonus due to Carbon Dioxide Retention in the Setting of Chronic Obstructive Pulmonary Disease Exacerbation

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