LETTERS concepts featured in the interdisciplinary Critical Care Societies Collaborative “Choosing Wisely” list, a critical reappraisal of our sedation practices is now under the national spotlight (6). Let us heed this call to action and ensure that these conversations and changes are occurring in our ICUs.
References
2 Lipshutz AK, Fee C, Schell H, Campbell L, Taylor J, Sharpe BA, Nguyen J, Gropper MA. Strategies for success: a PDSA analysis of three QI initiatives in critical care. Jt Comm J Qual Patient Saf 2008;34: 435–444. 3 Girard TD, Kress JP, Fuchs BD, Thomason JW, Schweickert WD, Pun BT, Taichman DB, Dunn JG, Pohlman AS, Kinniry PA, et al. Efficacy and safety of a paired sedation and ventilator weaning protocol for mechanically ventilated patients in intensive care (Awakening and Breathing Controlled trial): a randomised controlled trial. Lancet 2008; 371:126–134. 4 Schweickert WD, Pohlman MC, Pohlman AS, Nigos C, Pawlik AJ, Esbrook CL, Spears L, Miller M, Franczyk M, Deprizio D, et al. Early physical and occupational therapy in mechanically ventilated, critically ill patients: a randomised controlled trial. Lancet 2009; 373:1874–1882. 5 Balas MC, Vasilevskis EE, Olsen KM, Schmid KK, Shostrom V, Cohen MZ, Peitz G, Gannon DE, Sisson J, Sullivan J, et al. Effectiveness and safety of the awakening and breathing coordination, delirium monitoring/management, and early exercise/mobility bundle. Crit Care Med 2014;42:1024–1036. 6 American Board of Internal Medicine. Critical Care Societies Collaborative: Critical Care—Five things physicians and patients should question. 2014 [cited 2014 April 7]. Available from: http:// www.choosingwisely.org/doctor-patient-lists/critical-care-societiescollaborative-critical-care/.
1 Hsieh SJ, Ely EW, Gong MN. Can intensive care unit delirium be prevented and reduced? Lessons learned and future directions. Ann Am Thorac Soc 2013;10:648–656.
Published 2014 by the American Thoracic Society
Author disclosures are available with the text of this letter at www.atsjournals.org. S. Jean Hsieh, M.D. Albert Einstein College of Medicine Bronx, New York E. Wesley Ely, M.D., M.P.H. Vanderbilt University Nashville, Tennessee and Tennessee Valley Veterans’ Affairs Healthcare Administration Nashville, Tennessee Michelle N. Gong, M.D., M.S. Albert Einstein College of Medicine Bronx, New York
Diffuse Alveolar Hemorrhage Induced by Sevoflurane To the Editor: We report a case of diffuse alveolar hemorrhage (DAH) (1, 2) attributed to the inhaled anesthetic sevoflurane, which was given during an elective surgery. Lung injury resolved with supportive care and intravenous administration of methylprednisolone. Our patient is a 31-year-old man with a history of recreational marijuana use who underwent elective surgical excision of a perirectal pilonidal cyst. His preoperative physical examination, chest radiograph (Figure 1A), and laboratory values were unremarkable. Surgery was performed without immediate complication after uneventful endotracheal intubation under general anesthesia achieved using intravenously administered midazolam (4 mg), fentanyl (200 mg), and inhaled sevoflurane. He developed hypoxemia and hemoptysis approximately 45 minutes after extubation. Arterial blood gas tensions measured while the patient breathed ambient air revealed a pH of 7.42, PaCO2 of 40 mm Hg, and PaO2 of 54 mm Hg, with an O2 saturation of 89%. His postoperative chest radiograph revealed interval development of bilateral alveolar infiltrates. Computed tomographic angiography of the chest demonstrated bilateral, centrally located ground glass opacities without evidence of pulmonary embolism (Figures 1B and 1C). Serum hemoglobin level dropped by approximately 2 g/dl postoperatively (from 14.4 to 12.1 g/dl) without evidence of overt bleeding. Platelet count was 246,000/ml, prothrombin time/ international normalized ratio was 12.9 seconds/1.0, and partial thromboplastin time was 23.3 seconds. Pulmonary function testing
This case was presented in poster format at CHEST 2013.
Letters
was performed, which was notable for an elevated diffusing capacity (150% of predicted). Echocardiogram was unremarkable. Subsequent bronchoscopy with bronchoalveolar lavage recovered hemorrhagic fluid in serial samples (Figure 2). The cell count showed 92,000 red blood cells and 250 white blood cells (polymorphonuclear cells, 22%; lymphocytes, 15%; monocytes, 2%; macrophages, 56%). Bacterial, mycobacterial, and fungal cultures as well as cytology were negative. Serologic testing was negative for HIV, viral hepatitis, vasculitis, and connective tissue disease (anti-neutrophil cytoplasmic antibodies, proteinase 3, myeloperoxidase, rheumatoid factor, antinuclear antibodies, anti-dsDNA, anti-glomerular basement membrane antibody, cryoglobulins). Complement levels (C3, C4) were within normal limits. Urinalysis was negative for red blood cells and protein. Urine toxicology screen on admission was positive for cannabis. The patient was treated with intravenously administered methylprednisolone (1 g) daily for 3 days. His hypoxemia resolved, and his hemoglobin level stabilized. He had no additional episode of hemoptysis. One month after discharge, the patient was asymptomatic and had not experienced a recurrence. Our patient developed DAH without clinical or serological evidence of an underlying systemic disease. Given the immediate onset postoperatively and limited medication exposure, the most likely causative agent was inhaled sevoflurane. Sevoflurane is an inhalational anesthetic agent used for induction and maintenance of general anesthesia. Common side effects include nausea (25%), vomiting (18%), hypotension (4–11%), and bradyarrhythmia (3–5%) (3). Respiratory side effects include cough (5–11%), apnea (2–6%), laryngeal spasm (2–8%), and respiratory depression. Airway fires and acute respiratory distress syndrome/acute lung injury have been reported, but there are no published cases of sevoflurane causing DAH (4). 853
LETTERS
Figure 2. Bronchoscopy showing blood (A) and bronchoalveolar lavage sample confirming diffuse alveolar hemorrhage (B).
Figure 1. Interval development of bilateral patchy infiltrates and ground glass opacities between preoperative chest X-ray (A) and postoperative chest X-ray (B) and postoperative computed tomography (C).
854
Two previously published case reports have described postoperative DAH in patients who received inhaled halogenated agents (5, 6). A patient with end-stage renal disease and a history of cocaine use experienced DAH immediately after elective cataract surgery, during which he received sevoflurane, propofol, and midazolam (5). The authors ascribed the DAH to coagulopathy and platelet dysfunction secondary to the patient’s renal disease and cocaine use. In a second case report, a 25-year-old man with obstructive sleep apnea developed DAH immediately after tonsillectomy, during which he received desflurane gas (6). The authors speculated that the patient’s severe snoring may have damaged the alveolar wall, resulting in barotrauma during general anesthesia and causing DAH. Midazolam and fentanyl are less likely culprits because our patient’s clinical condition continued to improve despite repeated exposure to these medications during bronchoscopy. Midazolam is known to cause bronchospasm, hiccups, and anaphylaxis; fentanyl has been reported to cause acute pulmonary edema after receiving naloxone and other reversal agents. However, despite their widespread AnnalsATS Volume 11 Number 5 | June 2014
LETTERS use, there are no case reports of midazolam or fentanyl causing DAH. Marijuana use has been reported as a causative agent of DAH, but it is less likely to be the etiology in this case because our patient was asymptomatic and had a normal chest radiograph before surgery (7). In summary, the most likely cause of DAH in our patient was the inhaled anesthetic gas sevoflurane. Predisposing factors, if any, and the mechanism of lung injury in this instance are unknown. Author disclosures are available with the text of this letter at www.atsjournals.org. Caroline A. Kim, M.D. Harbor-UCLA Medical Center Los Angeles, California Rebecca Liu, M.D. UCLA Medical Center Los Angeles, California David W. Hsia, M.D. Harbor-UCLA Medical Center Los Angeles, California
2 Ioachimescu OC, Stoller JK. Diffuse alveolar hemorrhage: diagnosing it and finding the cause. Cleve Clin J Med 2008;75:258–280, 260, 264–265 passim. 3 Micromedex Healthcare Series [Internet database]. Greenwood Village, CO: Thomson Healthcare. Updated periodically [accessed 2014 Jan 20]. Available from: http://www. micromedex.com 4 Camus P. The drug-induced respiratory disease website, 2012 [Internet]. Dijon, France: Department of Pulmonary Medicine and Intensive Care University Hospital; 2012 [accessed 2014 Jan 20]. Available from: http://www. pneumotox.com 5 Khanna AK, Cummings KC III. Pulmonary hemorrhage in an outpatient ophthalmic anesthesia setting: it’s never “just a cataract.” J Anaesthesiol Clin Pharmacol 2012;28: 520–523. 6 Kim JP, Park JJ, Kim NJ, Woo SH. A case of diffuse alveolar hemorrhage after tonsillectomy: A case report. Korean J Anesthesiol 2012;63:165–168. 7 Grassin F, Andr e´ M, Rallec B, Combes E, Vinsonneau U, Paleiron N. Fatal alveolar haemorrhage following a “bang” of cannabis [in French]. Rev Mal Respir 2011;28: 919–923.
References 1 Lara AR, Schwarz MI. Diffuse alveolar hemorrhage. Chest 2010;137: 1164–1171.
Guillain-Barre´ Syndrome Related to Pulmonary Tuberculosis To the Editor: Guillain-Barr´e syndrome is a rare disorder presenting as an acute areflexic paralysis. There is considerable evidence suggesting an autoimmune mechanism of injury. Guillain-Barr´e Syndrome typically follows acute gastrointestinal or respiratory infections such as Campylobacter jejuni, Mycoplasma pneumoniae, vaccines, or a member of the herpes virus family (1, 2). We present a case of rapidly progressing and destructive pulmonary tuberculosis (TB) with severe constitutional symptoms complicated by constrictive pericarditis and permanent neurological impairments. We believe that this may be the first case of Guillain-Barr´e Syndrome associated with TB reported in North America. Rare sporadic cases of Guillain-Barr´e Syndrome in relation to tuberculosis have been noted globally (3–8). Some prior case reports linking Guillain-Barr´e Syndrome to TB have lacked the following: bacteriologic confirmation, nerve conduction studies, spinal fluid analysis, spinal imaging, and other illnesses potentially playing a role in Guillain-Barr´e Syndrome. A 25-year-old man reported that he was in good health until April 2008, at which time he developed a relentlessly productive cough that was followed by hemoptysis, fatigue, fevers, chills, and anorexia, with an eventual weight loss of 40 pounds (18 kg). He did not immediately seek medical attention regarding these symptoms. Approximately 6 weeks into this illness, he began to complain of swelling in his feet accompanied by sharp, lancinating foot pain initially noted while playing basketball Author Contributions: Both authors contributed to the drafting and preparation of this manuscript and to consultation on behalf of this patient.
Letters
Copyright © 2014 by the American Thoracic Society
that made walking difficult; weakness, foot numbness, and feet dragging followed. After 8 weeks of symptoms, he was too weak to get out of bed, and was taken emergently to a community hospital critically ill. Radiographic imaging revealed bilateral cavitary pneumonia (Figure 1); sputa were 41 positive for acid-fast bacilli, and cultures yielded heavy growth of Mycobacterium tuberculosis susceptible to all first-line agents. Therapy was promptly begun with isoniazid, rifampin, ethambutal, and pyrazinamide. A large pericardial effusion with signs of tamponade was discovered, and 600 ml of pericardial fluid was drained. A neurological examination was performed. Upper extremity strength was 5/5 bilaterally in the biceps and deltoids. Strength in the lower extremity was 2/5 bilaterally for plantar flexion, 0/5 bilaterally for dorsiflexion, and 5/5 on the right, 4/5 on the left for hip flexion. Deep tendon reflexes were absent at the ankles, and present at both knees, wrists, and elbows. Severe proprioceptive deficits were found in both lower extremities. Pinprick was decreased in both feet and legs up to the knees, but was normal in both upper extremities. Testing of light touch revealed no sensation throughout. The patient was unable to ambulate. A lumber puncture yielded clear cerebral spinal fluid without leukocytes and normal protein and glucose; all spinal fluid cultures were negative. A stool sample tested negative for Campylobacter jejuni. Urine testing was negative for heavy metals, coxsackie, and echovirus antibodies. Magnetic resonance imaging of lumbar spine revealed mild degenerative changes of the lower lumbar spine without other abnormalities. An electromyogram and nerve conduction studies were performed. All nerve conduction studies and motor responses in the right lower extremity were absent. Right median distal motor latency was prolonged; compound muscle action potential was 855
References
2 Lipshutz AK, Fee C, Schell H, Campbell L, Taylor J, Sharpe BA, Nguyen J, Gropper MA. Strategies for success: a PDSA analysis of three QI initiatives in critical care. Jt Comm J Qual Patient Saf 2008;34: 435–444. 3 Girard TD, Kress JP, Fuchs BD, Thomason JW, Schweickert WD, Pun BT, Taichman DB, Dunn JG, Pohlman AS, Kinniry PA, et al. Efficacy and safety of a paired sedation and ventilator weaning protocol for mechanically ventilated patients in intensive care (Awakening and Breathing Controlled trial): a randomised controlled trial. Lancet 2008; 371:126–134. 4 Schweickert WD, Pohlman MC, Pohlman AS, Nigos C, Pawlik AJ, Esbrook CL, Spears L, Miller M, Franczyk M, Deprizio D, et al. Early physical and occupational therapy in mechanically ventilated, critically ill patients: a randomised controlled trial. Lancet 2009; 373:1874–1882. 5 Balas MC, Vasilevskis EE, Olsen KM, Schmid KK, Shostrom V, Cohen MZ, Peitz G, Gannon DE, Sisson J, Sullivan J, et al. Effectiveness and safety of the awakening and breathing coordination, delirium monitoring/management, and early exercise/mobility bundle. Crit Care Med 2014;42:1024–1036. 6 American Board of Internal Medicine. Critical Care Societies Collaborative: Critical Care—Five things physicians and patients should question. 2014 [cited 2014 April 7]. Available from: http:// www.choosingwisely.org/doctor-patient-lists/critical-care-societiescollaborative-critical-care/.
1 Hsieh SJ, Ely EW, Gong MN. Can intensive care unit delirium be prevented and reduced? Lessons learned and future directions. Ann Am Thorac Soc 2013;10:648–656.
Published 2014 by the American Thoracic Society
Author disclosures are available with the text of this letter at www.atsjournals.org. S. Jean Hsieh, M.D. Albert Einstein College of Medicine Bronx, New York E. Wesley Ely, M.D., M.P.H. Vanderbilt University Nashville, Tennessee and Tennessee Valley Veterans’ Affairs Healthcare Administration Nashville, Tennessee Michelle N. Gong, M.D., M.S. Albert Einstein College of Medicine Bronx, New York
Diffuse Alveolar Hemorrhage Induced by Sevoflurane To the Editor: We report a case of diffuse alveolar hemorrhage (DAH) (1, 2) attributed to the inhaled anesthetic sevoflurane, which was given during an elective surgery. Lung injury resolved with supportive care and intravenous administration of methylprednisolone. Our patient is a 31-year-old man with a history of recreational marijuana use who underwent elective surgical excision of a perirectal pilonidal cyst. His preoperative physical examination, chest radiograph (Figure 1A), and laboratory values were unremarkable. Surgery was performed without immediate complication after uneventful endotracheal intubation under general anesthesia achieved using intravenously administered midazolam (4 mg), fentanyl (200 mg), and inhaled sevoflurane. He developed hypoxemia and hemoptysis approximately 45 minutes after extubation. Arterial blood gas tensions measured while the patient breathed ambient air revealed a pH of 7.42, PaCO2 of 40 mm Hg, and PaO2 of 54 mm Hg, with an O2 saturation of 89%. His postoperative chest radiograph revealed interval development of bilateral alveolar infiltrates. Computed tomographic angiography of the chest demonstrated bilateral, centrally located ground glass opacities without evidence of pulmonary embolism (Figures 1B and 1C). Serum hemoglobin level dropped by approximately 2 g/dl postoperatively (from 14.4 to 12.1 g/dl) without evidence of overt bleeding. Platelet count was 246,000/ml, prothrombin time/ international normalized ratio was 12.9 seconds/1.0, and partial thromboplastin time was 23.3 seconds. Pulmonary function testing
This case was presented in poster format at CHEST 2013.
Letters
was performed, which was notable for an elevated diffusing capacity (150% of predicted). Echocardiogram was unremarkable. Subsequent bronchoscopy with bronchoalveolar lavage recovered hemorrhagic fluid in serial samples (Figure 2). The cell count showed 92,000 red blood cells and 250 white blood cells (polymorphonuclear cells, 22%; lymphocytes, 15%; monocytes, 2%; macrophages, 56%). Bacterial, mycobacterial, and fungal cultures as well as cytology were negative. Serologic testing was negative for HIV, viral hepatitis, vasculitis, and connective tissue disease (anti-neutrophil cytoplasmic antibodies, proteinase 3, myeloperoxidase, rheumatoid factor, antinuclear antibodies, anti-dsDNA, anti-glomerular basement membrane antibody, cryoglobulins). Complement levels (C3, C4) were within normal limits. Urinalysis was negative for red blood cells and protein. Urine toxicology screen on admission was positive for cannabis. The patient was treated with intravenously administered methylprednisolone (1 g) daily for 3 days. His hypoxemia resolved, and his hemoglobin level stabilized. He had no additional episode of hemoptysis. One month after discharge, the patient was asymptomatic and had not experienced a recurrence. Our patient developed DAH without clinical or serological evidence of an underlying systemic disease. Given the immediate onset postoperatively and limited medication exposure, the most likely causative agent was inhaled sevoflurane. Sevoflurane is an inhalational anesthetic agent used for induction and maintenance of general anesthesia. Common side effects include nausea (25%), vomiting (18%), hypotension (4–11%), and bradyarrhythmia (3–5%) (3). Respiratory side effects include cough (5–11%), apnea (2–6%), laryngeal spasm (2–8%), and respiratory depression. Airway fires and acute respiratory distress syndrome/acute lung injury have been reported, but there are no published cases of sevoflurane causing DAH (4). 853
LETTERS
Figure 2. Bronchoscopy showing blood (A) and bronchoalveolar lavage sample confirming diffuse alveolar hemorrhage (B).
Figure 1. Interval development of bilateral patchy infiltrates and ground glass opacities between preoperative chest X-ray (A) and postoperative chest X-ray (B) and postoperative computed tomography (C).
854
Two previously published case reports have described postoperative DAH in patients who received inhaled halogenated agents (5, 6). A patient with end-stage renal disease and a history of cocaine use experienced DAH immediately after elective cataract surgery, during which he received sevoflurane, propofol, and midazolam (5). The authors ascribed the DAH to coagulopathy and platelet dysfunction secondary to the patient’s renal disease and cocaine use. In a second case report, a 25-year-old man with obstructive sleep apnea developed DAH immediately after tonsillectomy, during which he received desflurane gas (6). The authors speculated that the patient’s severe snoring may have damaged the alveolar wall, resulting in barotrauma during general anesthesia and causing DAH. Midazolam and fentanyl are less likely culprits because our patient’s clinical condition continued to improve despite repeated exposure to these medications during bronchoscopy. Midazolam is known to cause bronchospasm, hiccups, and anaphylaxis; fentanyl has been reported to cause acute pulmonary edema after receiving naloxone and other reversal agents. However, despite their widespread AnnalsATS Volume 11 Number 5 | June 2014
LETTERS use, there are no case reports of midazolam or fentanyl causing DAH. Marijuana use has been reported as a causative agent of DAH, but it is less likely to be the etiology in this case because our patient was asymptomatic and had a normal chest radiograph before surgery (7). In summary, the most likely cause of DAH in our patient was the inhaled anesthetic gas sevoflurane. Predisposing factors, if any, and the mechanism of lung injury in this instance are unknown. Author disclosures are available with the text of this letter at www.atsjournals.org. Caroline A. Kim, M.D. Harbor-UCLA Medical Center Los Angeles, California Rebecca Liu, M.D. UCLA Medical Center Los Angeles, California David W. Hsia, M.D. Harbor-UCLA Medical Center Los Angeles, California
2 Ioachimescu OC, Stoller JK. Diffuse alveolar hemorrhage: diagnosing it and finding the cause. Cleve Clin J Med 2008;75:258–280, 260, 264–265 passim. 3 Micromedex Healthcare Series [Internet database]. Greenwood Village, CO: Thomson Healthcare. Updated periodically [accessed 2014 Jan 20]. Available from: http://www. micromedex.com 4 Camus P. The drug-induced respiratory disease website, 2012 [Internet]. Dijon, France: Department of Pulmonary Medicine and Intensive Care University Hospital; 2012 [accessed 2014 Jan 20]. Available from: http://www. pneumotox.com 5 Khanna AK, Cummings KC III. Pulmonary hemorrhage in an outpatient ophthalmic anesthesia setting: it’s never “just a cataract.” J Anaesthesiol Clin Pharmacol 2012;28: 520–523. 6 Kim JP, Park JJ, Kim NJ, Woo SH. A case of diffuse alveolar hemorrhage after tonsillectomy: A case report. Korean J Anesthesiol 2012;63:165–168. 7 Grassin F, Andr e´ M, Rallec B, Combes E, Vinsonneau U, Paleiron N. Fatal alveolar haemorrhage following a “bang” of cannabis [in French]. Rev Mal Respir 2011;28: 919–923.
References 1 Lara AR, Schwarz MI. Diffuse alveolar hemorrhage. Chest 2010;137: 1164–1171.
Guillain-Barre´ Syndrome Related to Pulmonary Tuberculosis To the Editor: Guillain-Barr´e syndrome is a rare disorder presenting as an acute areflexic paralysis. There is considerable evidence suggesting an autoimmune mechanism of injury. Guillain-Barr´e Syndrome typically follows acute gastrointestinal or respiratory infections such as Campylobacter jejuni, Mycoplasma pneumoniae, vaccines, or a member of the herpes virus family (1, 2). We present a case of rapidly progressing and destructive pulmonary tuberculosis (TB) with severe constitutional symptoms complicated by constrictive pericarditis and permanent neurological impairments. We believe that this may be the first case of Guillain-Barr´e Syndrome associated with TB reported in North America. Rare sporadic cases of Guillain-Barr´e Syndrome in relation to tuberculosis have been noted globally (3–8). Some prior case reports linking Guillain-Barr´e Syndrome to TB have lacked the following: bacteriologic confirmation, nerve conduction studies, spinal fluid analysis, spinal imaging, and other illnesses potentially playing a role in Guillain-Barr´e Syndrome. A 25-year-old man reported that he was in good health until April 2008, at which time he developed a relentlessly productive cough that was followed by hemoptysis, fatigue, fevers, chills, and anorexia, with an eventual weight loss of 40 pounds (18 kg). He did not immediately seek medical attention regarding these symptoms. Approximately 6 weeks into this illness, he began to complain of swelling in his feet accompanied by sharp, lancinating foot pain initially noted while playing basketball Author Contributions: Both authors contributed to the drafting and preparation of this manuscript and to consultation on behalf of this patient.
Letters
Copyright © 2014 by the American Thoracic Society
that made walking difficult; weakness, foot numbness, and feet dragging followed. After 8 weeks of symptoms, he was too weak to get out of bed, and was taken emergently to a community hospital critically ill. Radiographic imaging revealed bilateral cavitary pneumonia (Figure 1); sputa were 41 positive for acid-fast bacilli, and cultures yielded heavy growth of Mycobacterium tuberculosis susceptible to all first-line agents. Therapy was promptly begun with isoniazid, rifampin, ethambutal, and pyrazinamide. A large pericardial effusion with signs of tamponade was discovered, and 600 ml of pericardial fluid was drained. A neurological examination was performed. Upper extremity strength was 5/5 bilaterally in the biceps and deltoids. Strength in the lower extremity was 2/5 bilaterally for plantar flexion, 0/5 bilaterally for dorsiflexion, and 5/5 on the right, 4/5 on the left for hip flexion. Deep tendon reflexes were absent at the ankles, and present at both knees, wrists, and elbows. Severe proprioceptive deficits were found in both lower extremities. Pinprick was decreased in both feet and legs up to the knees, but was normal in both upper extremities. Testing of light touch revealed no sensation throughout. The patient was unable to ambulate. A lumber puncture yielded clear cerebral spinal fluid without leukocytes and normal protein and glucose; all spinal fluid cultures were negative. A stool sample tested negative for Campylobacter jejuni. Urine testing was negative for heavy metals, coxsackie, and echovirus antibodies. Magnetic resonance imaging of lumbar spine revealed mild degenerative changes of the lower lumbar spine without other abnormalities. An electromyogram and nerve conduction studies were performed. All nerve conduction studies and motor responses in the right lower extremity were absent. Right median distal motor latency was prolonged; compound muscle action potential was 855
