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Spectacles were prescribed and she was commenced on a trial of amblyopia therapy which consisted of patching of the right eye for a period of 3-4 hours every day (after school). | [
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] | An eleven year old girl presented to the paediatric eye clinic of the University College Hospital, Ibadan, Nigeria with a history of squint and poor vision. Her mother had noticed a misalignment of the eyes three years previously and the patient had been complaining about poor distance vision for about a year. There was no history of antecedent trauma to the head or face. There was no history of double vision (diplopia) or pains on ocular movements. There was no associated headache, fever, vomiting, joint pains or skin rashes/lesions. The review of systems was essentially normal and she had enjoyed good health since early childhood. Her pregnancy and delivery were uneventful; and her development was normal. All other family members were well and there was no family history of squint. Unaided visual acuity was 6/24 in the right eye and counting fingers (CF) in the left eye. During refraction, her visual acuity improved to 6/9 and 6/60 in the right and left eyes respectively. The refractive error was a hypermetropia of +4.50 diopters in each eye. Examination revealed normal anterior and posterior segments bilaterally. There was about 10 prism diopters of left hypotropia with no horizontal deviation in the primary position and she did not have an abnormal head posture. Her palpebral fissures were normal and equal on both sides in the primary position of gaze. Examination of the ocular motility elicited marked limitation of elevation of the left eye when looking to the right, while elevation of the same eye was almost full on left gaze. The movements of the right eye were normal and there were no significant changes in the palpebral fissures of both eyes during eye movements. Forced duction test (performed under sedation) was positive and revealed marked restriction of passive elevation of the left eye in adduction. Her systemic examination was completely normal. A diagnosis of congenital left Brown syndrome with severe amblyopia was made. Spectacles were prescribed and she was commenced on a trial of amblyopia therapy which consisted of patching of the right eye for a period of 3-4 hours every day (after school). Her mother was counselled and educated about the condition as well as the treatment plan. Specifically, she was informed that surgery was necessary to correct the squint, irrespective of the outcome of the amblyopia therapy. A three month follow up visit was scheduled, however, the patient defaulted after the initial visit.
| EN100184 |
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] | An eleven year old girl presented to the paediatric eye clinic of the University College Hospital, Ibadan, Nigeria with a history of squint and poor vision. Her mother had noticed a misalignment of the eyes three years previously and the patient had been complaining about poor distance vision for about a year. There was no history of antecedent trauma to the head or face. There was no history of double vision (diplopia) or pains on ocular movements. There was no associated headache, fever, vomiting, joint pains or skin rashes/lesions. The review of systems was essentially normal and she had enjoyed good health since early childhood. Her pregnancy and delivery were uneventful; and her development was normal. All other family members were well and there was no family history of squint. Unaided visual acuity was 6/24 in the right eye and counting fingers (CF) in the left eye. During refraction, her visual acuity improved to 6/9 and 6/60 in the right and left eyes respectively. The refractive error was a hypermetropia of +4.50 diopters in each eye. Examination revealed normal anterior and posterior segments bilaterally. There was about 10 prism diopters of left hypotropia with no horizontal deviation in the primary position and she did not have an abnormal head posture. Her palpebral fissures were normal and equal on both sides in the primary position of gaze. Examination of the ocular motility elicited marked limitation of elevation of the left eye when looking to the right, while elevation of the same eye was almost full on left gaze. The movements of the right eye were normal and there were no significant changes in the palpebral fissures of both eyes during eye movements. Forced duction test (performed under sedation) was positive and revealed marked restriction of passive elevation of the left eye in adduction. Her systemic examination was completely normal. A diagnosis of congenital left Brown syndrome with severe amblyopia was made. Spectacles were prescribed and she was commenced on a trial of amblyopia therapy which consisted of patching of the right eye for a period of 3-4 hours every day (after school). Her mother was counselled and educated about the condition as well as the treatment plan. Specifically, she was informed that surgery was necessary to correct the squint, irrespective of the outcome of the amblyopia therapy. A three month follow up visit was scheduled, however, the patient defaulted after the initial visit.
| EN100184 |
Specifically, she was informed that surgery was necessary to correct the squint, irrespective of the outcome of the amblyopia therapy. | [
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| EN100184 |
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] | An eleven year old girl presented to the paediatric eye clinic of the University College Hospital, Ibadan, Nigeria with a history of squint and poor vision. Her mother had noticed a misalignment of the eyes three years previously and the patient had been complaining about poor distance vision for about a year. There was no history of antecedent trauma to the head or face. There was no history of double vision (diplopia) or pains on ocular movements. There was no associated headache, fever, vomiting, joint pains or skin rashes/lesions. The review of systems was essentially normal and she had enjoyed good health since early childhood. Her pregnancy and delivery were uneventful; and her development was normal. All other family members were well and there was no family history of squint. Unaided visual acuity was 6/24 in the right eye and counting fingers (CF) in the left eye. During refraction, her visual acuity improved to 6/9 and 6/60 in the right and left eyes respectively. The refractive error was a hypermetropia of +4.50 diopters in each eye. Examination revealed normal anterior and posterior segments bilaterally. There was about 10 prism diopters of left hypotropia with no horizontal deviation in the primary position and she did not have an abnormal head posture. Her palpebral fissures were normal and equal on both sides in the primary position of gaze. Examination of the ocular motility elicited marked limitation of elevation of the left eye when looking to the right, while elevation of the same eye was almost full on left gaze. The movements of the right eye were normal and there were no significant changes in the palpebral fissures of both eyes during eye movements. Forced duction test (performed under sedation) was positive and revealed marked restriction of passive elevation of the left eye in adduction. Her systemic examination was completely normal. A diagnosis of congenital left Brown syndrome with severe amblyopia was made. Spectacles were prescribed and she was commenced on a trial of amblyopia therapy which consisted of patching of the right eye for a period of 3-4 hours every day (after school). Her mother was counselled and educated about the condition as well as the treatment plan. Specifically, she was informed that surgery was necessary to correct the squint, irrespective of the outcome of the amblyopia therapy. A three month follow up visit was scheduled, however, the patient defaulted after the initial visit.
| EN100184 |
A 20-year-old right-handed female factory worker with no medical history is consulting in the emergency ward with an open trauma of the left hand resulting from an occupational accident. | [
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| EN100345 |
Her hand was crushed under a heavy object. | [
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| EN100345 |
Physical examination found an important swelling and obvious distortion at the dorsum of the hand associated with wounds of the ulnar and radial edges of the left hand. | [
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| EN100345 |
The neurovascular examination was normal; in particular no sensitive deficit in the median nerve area was noted. | [
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| EN100345 |
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] | A 20-year-old right-handed female factory worker with no medical history is consulting in the emergency ward with an open trauma of the left hand resulting from an occupational accident. Her hand was crushed under a heavy object. Physical examination found an important swelling and obvious distortion at the dorsum of the hand associated with wounds of the ulnar and radial edges of the left hand. The neurovascular examination was normal; in particular no sensitive deficit in the median nerve area was noted. Plain radiographs with front and lateral views showed a dislocation of the three lesser fingers associated with fractures of the hamatum and the second metacarpal. The three lesser metacarpals and the distal fragment of the hamatum were medially displaced. The patient was immediately brought to the operating theatre. The treatment consisted of a reduction and stabilisation using a multiple carpo-metacarpal and cross inter-metacarpal pinning. The wound was cleaned up trimmed and sutured. The had and the wrist were immobilized with a splint for six weeks. The patient had an intense and regular rehabilitation program. At one year follow-up, the outcome is good: the patient is painless with good bone consolidation in right position, strictly normal range of motion (metacarpophalangeal 90°, proximal interphalagienne 100° and distal interphalageal 90°) and a 80% grip strength compared to the right side.
| EN100345 |
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| EN100345 |
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| EN100345 |
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| EN100345 |
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| EN100345 |
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| EN100345 |
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| EN100345 |
At one year follow-up, the outcome is good: the patient is painless with good bone consolidation in right position, strictly normal range of motion (metacarpophalangeal 90°, proximal interphalagienne 100° and distal interphalageal 90°) and a 80% grip strength compared to the right side. | [
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| EN100345 |
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The patient was referred to her neurologist to provide a detailed history about her medical condition and to coordinate with him regarding the steroid dose take to avoid any complication during patient management. A consultation letter had been received from her neurologist explaining the patient medical condition which starts with difficulty in breathing, chewing and swallowing, there was no external ocular weakness, motor weakness, sphincter dysfunction, sensory deficits, muscle wasting and no signs of diplopia, dizziness, double vision, ptosis or any difficulty in maintaining balance. Patient underwent chest CT scan with contrast which show evidence of thymoma benign tumor of the thymus that has been the possible causes of MG. Diagnosis was confirmed with measuring serum level of acetylcholine receptor antibodies, later treatment plan had been formulated including drugs to control the condition and then thymectomy to avoid sever complication to the patient.
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| EN100437 |
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Intraoral examination showed fair oral hygiene multiple fixed prosthodontic restorations and multiple carious teeth, multiple remaining roots and lipomatous tongue atrophy.
The patient was referred to her neurologist to provide a detailed history about her medical condition and to coordinate with him regarding the steroid dose take to avoid any complication during patient management. A consultation letter had been received from her neurologist explaining the patient medical condition which starts with difficulty in breathing, chewing and swallowing, there was no external ocular weakness, motor weakness, sphincter dysfunction, sensory deficits, muscle wasting and no signs of diplopia, dizziness, double vision, ptosis or any difficulty in maintaining balance. Patient underwent chest CT scan with contrast which show evidence of thymoma benign tumor of the thymus that has been the possible causes of MG. Diagnosis was confirmed with measuring serum level of acetylcholine receptor antibodies, later treatment plan had been formulated including drugs to control the condition and then thymectomy to avoid sever complication to the patient.
Before proceeding to the dental management of the case; CBC and blood chemistry had been requested form the patient. Creatinine level was below normal (42.23 umol/l), with normal levels of albumin, urea, uric acid, AST, ALT, cholesterol, triglycerides and bilirubin. Patient had elevated WBC “12.52 x 10 9 /L” and Platelet “453 x 10 9 /L” with reduction in RBC “4.4 x 10 9 /L” and Eosinophil count “0.07”. Consultation with patient neurologist regarding the steroid dose to reduce the susceptibility of developing adrenal crisis.
| EN100437 |
Upon taking medical history the patient revealed that was diagnosed with thymoma MG and on medication including pyridostigmine bromide 60 mg, azathioprine 50 mg and prednisone 20 mg. | [
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The patient was referred to her neurologist to provide a detailed history about her medical condition and to coordinate with him regarding the steroid dose take to avoid any complication during patient management. A consultation letter had been received from her neurologist explaining the patient medical condition which starts with difficulty in breathing, chewing and swallowing, there was no external ocular weakness, motor weakness, sphincter dysfunction, sensory deficits, muscle wasting and no signs of diplopia, dizziness, double vision, ptosis or any difficulty in maintaining balance. Patient underwent chest CT scan with contrast which show evidence of thymoma benign tumor of the thymus that has been the possible causes of MG. Diagnosis was confirmed with measuring serum level of acetylcholine receptor antibodies, later treatment plan had been formulated including drugs to control the condition and then thymectomy to avoid sever complication to the patient.
Before proceeding to the dental management of the case; CBC and blood chemistry had been requested form the patient. Creatinine level was below normal (42.23 umol/l), with normal levels of albumin, urea, uric acid, AST, ALT, cholesterol, triglycerides and bilirubin. Patient had elevated WBC “12.52 x 10 9 /L” and Platelet “453 x 10 9 /L” with reduction in RBC “4.4 x 10 9 /L” and Eosinophil count “0.07”. Consultation with patient neurologist regarding the steroid dose to reduce the susceptibility of developing adrenal crisis.
| EN100437 |
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Intraoral examination showed fair oral hygiene multiple fixed prosthodontic restorations and multiple carious teeth, multiple remaining roots and lipomatous tongue atrophy.
The patient was referred to her neurologist to provide a detailed history about her medical condition and to coordinate with him regarding the steroid dose take to avoid any complication during patient management. A consultation letter had been received from her neurologist explaining the patient medical condition which starts with difficulty in breathing, chewing and swallowing, there was no external ocular weakness, motor weakness, sphincter dysfunction, sensory deficits, muscle wasting and no signs of diplopia, dizziness, double vision, ptosis or any difficulty in maintaining balance. Patient underwent chest CT scan with contrast which show evidence of thymoma benign tumor of the thymus that has been the possible causes of MG. Diagnosis was confirmed with measuring serum level of acetylcholine receptor antibodies, later treatment plan had been formulated including drugs to control the condition and then thymectomy to avoid sever complication to the patient.
Before proceeding to the dental management of the case; CBC and blood chemistry had been requested form the patient. Creatinine level was below normal (42.23 umol/l), with normal levels of albumin, urea, uric acid, AST, ALT, cholesterol, triglycerides and bilirubin. Patient had elevated WBC “12.52 x 10 9 /L” and Platelet “453 x 10 9 /L” with reduction in RBC “4.4 x 10 9 /L” and Eosinophil count “0.07”. Consultation with patient neurologist regarding the steroid dose to reduce the susceptibility of developing adrenal crisis.
| EN100437 |
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Intraoral examination showed fair oral hygiene multiple fixed prosthodontic restorations and multiple carious teeth, multiple remaining roots and lipomatous tongue atrophy.
The patient was referred to her neurologist to provide a detailed history about her medical condition and to coordinate with him regarding the steroid dose take to avoid any complication during patient management. A consultation letter had been received from her neurologist explaining the patient medical condition which starts with difficulty in breathing, chewing and swallowing, there was no external ocular weakness, motor weakness, sphincter dysfunction, sensory deficits, muscle wasting and no signs of diplopia, dizziness, double vision, ptosis or any difficulty in maintaining balance. Patient underwent chest CT scan with contrast which show evidence of thymoma benign tumor of the thymus that has been the possible causes of MG. Diagnosis was confirmed with measuring serum level of acetylcholine receptor antibodies, later treatment plan had been formulated including drugs to control the condition and then thymectomy to avoid sever complication to the patient.
Before proceeding to the dental management of the case; CBC and blood chemistry had been requested form the patient. Creatinine level was below normal (42.23 umol/l), with normal levels of albumin, urea, uric acid, AST, ALT, cholesterol, triglycerides and bilirubin. Patient had elevated WBC “12.52 x 10 9 /L” and Platelet “453 x 10 9 /L” with reduction in RBC “4.4 x 10 9 /L” and Eosinophil count “0.07”. Consultation with patient neurologist regarding the steroid dose to reduce the susceptibility of developing adrenal crisis.
| EN100437 |
A consultation letter had been received from her neurologist explaining the patient medical condition which starts with difficulty in breathing, chewing and swallowing, there was no external ocular weakness, motor weakness, sphincter dysfunction, sensory deficits, muscle wasting and no signs of diplopia, dizziness, double vision, ptosis or any difficulty in maintaining balance. | [
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Intraoral examination showed fair oral hygiene multiple fixed prosthodontic restorations and multiple carious teeth, multiple remaining roots and lipomatous tongue atrophy.
The patient was referred to her neurologist to provide a detailed history about her medical condition and to coordinate with him regarding the steroid dose take to avoid any complication during patient management. A consultation letter had been received from her neurologist explaining the patient medical condition which starts with difficulty in breathing, chewing and swallowing, there was no external ocular weakness, motor weakness, sphincter dysfunction, sensory deficits, muscle wasting and no signs of diplopia, dizziness, double vision, ptosis or any difficulty in maintaining balance. Patient underwent chest CT scan with contrast which show evidence of thymoma benign tumor of the thymus that has been the possible causes of MG. Diagnosis was confirmed with measuring serum level of acetylcholine receptor antibodies, later treatment plan had been formulated including drugs to control the condition and then thymectomy to avoid sever complication to the patient.
Before proceeding to the dental management of the case; CBC and blood chemistry had been requested form the patient. Creatinine level was below normal (42.23 umol/l), with normal levels of albumin, urea, uric acid, AST, ALT, cholesterol, triglycerides and bilirubin. Patient had elevated WBC “12.52 x 10 9 /L” and Platelet “453 x 10 9 /L” with reduction in RBC “4.4 x 10 9 /L” and Eosinophil count “0.07”. Consultation with patient neurologist regarding the steroid dose to reduce the susceptibility of developing adrenal crisis.
| EN100437 |
Patient underwent chest CT scan with contrast which show evidence of thymoma benign tumor of the thymus that has been the possible causes of MG. | [
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Intraoral examination showed fair oral hygiene multiple fixed prosthodontic restorations and multiple carious teeth, multiple remaining roots and lipomatous tongue atrophy.
The patient was referred to her neurologist to provide a detailed history about her medical condition and to coordinate with him regarding the steroid dose take to avoid any complication during patient management. A consultation letter had been received from her neurologist explaining the patient medical condition which starts with difficulty in breathing, chewing and swallowing, there was no external ocular weakness, motor weakness, sphincter dysfunction, sensory deficits, muscle wasting and no signs of diplopia, dizziness, double vision, ptosis or any difficulty in maintaining balance. Patient underwent chest CT scan with contrast which show evidence of thymoma benign tumor of the thymus that has been the possible causes of MG. Diagnosis was confirmed with measuring serum level of acetylcholine receptor antibodies, later treatment plan had been formulated including drugs to control the condition and then thymectomy to avoid sever complication to the patient.
Before proceeding to the dental management of the case; CBC and blood chemistry had been requested form the patient. Creatinine level was below normal (42.23 umol/l), with normal levels of albumin, urea, uric acid, AST, ALT, cholesterol, triglycerides and bilirubin. Patient had elevated WBC “12.52 x 10 9 /L” and Platelet “453 x 10 9 /L” with reduction in RBC “4.4 x 10 9 /L” and Eosinophil count “0.07”. Consultation with patient neurologist regarding the steroid dose to reduce the susceptibility of developing adrenal crisis.
| EN100437 |
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Intraoral examination showed fair oral hygiene multiple fixed prosthodontic restorations and multiple carious teeth, multiple remaining roots and lipomatous tongue atrophy.
The patient was referred to her neurologist to provide a detailed history about her medical condition and to coordinate with him regarding the steroid dose take to avoid any complication during patient management. A consultation letter had been received from her neurologist explaining the patient medical condition which starts with difficulty in breathing, chewing and swallowing, there was no external ocular weakness, motor weakness, sphincter dysfunction, sensory deficits, muscle wasting and no signs of diplopia, dizziness, double vision, ptosis or any difficulty in maintaining balance. Patient underwent chest CT scan with contrast which show evidence of thymoma benign tumor of the thymus that has been the possible causes of MG. Diagnosis was confirmed with measuring serum level of acetylcholine receptor antibodies, later treatment plan had been formulated including drugs to control the condition and then thymectomy to avoid sever complication to the patient.
Before proceeding to the dental management of the case; CBC and blood chemistry had been requested form the patient. Creatinine level was below normal (42.23 umol/l), with normal levels of albumin, urea, uric acid, AST, ALT, cholesterol, triglycerides and bilirubin. Patient had elevated WBC “12.52 x 10 9 /L” and Platelet “453 x 10 9 /L” with reduction in RBC “4.4 x 10 9 /L” and Eosinophil count “0.07”. Consultation with patient neurologist regarding the steroid dose to reduce the susceptibility of developing adrenal crisis.
| EN100437 |
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Intraoral examination showed fair oral hygiene multiple fixed prosthodontic restorations and multiple carious teeth, multiple remaining roots and lipomatous tongue atrophy.
The patient was referred to her neurologist to provide a detailed history about her medical condition and to coordinate with him regarding the steroid dose take to avoid any complication during patient management. A consultation letter had been received from her neurologist explaining the patient medical condition which starts with difficulty in breathing, chewing and swallowing, there was no external ocular weakness, motor weakness, sphincter dysfunction, sensory deficits, muscle wasting and no signs of diplopia, dizziness, double vision, ptosis or any difficulty in maintaining balance. Patient underwent chest CT scan with contrast which show evidence of thymoma benign tumor of the thymus that has been the possible causes of MG. Diagnosis was confirmed with measuring serum level of acetylcholine receptor antibodies, later treatment plan had been formulated including drugs to control the condition and then thymectomy to avoid sever complication to the patient.
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Intraoral examination showed fair oral hygiene multiple fixed prosthodontic restorations and multiple carious teeth, multiple remaining roots and lipomatous tongue atrophy.
The patient was referred to her neurologist to provide a detailed history about her medical condition and to coordinate with him regarding the steroid dose take to avoid any complication during patient management. A consultation letter had been received from her neurologist explaining the patient medical condition which starts with difficulty in breathing, chewing and swallowing, there was no external ocular weakness, motor weakness, sphincter dysfunction, sensory deficits, muscle wasting and no signs of diplopia, dizziness, double vision, ptosis or any difficulty in maintaining balance. Patient underwent chest CT scan with contrast which show evidence of thymoma benign tumor of the thymus that has been the possible causes of MG. Diagnosis was confirmed with measuring serum level of acetylcholine receptor antibodies, later treatment plan had been formulated including drugs to control the condition and then thymectomy to avoid sever complication to the patient.
Before proceeding to the dental management of the case; CBC and blood chemistry had been requested form the patient. Creatinine level was below normal (42.23 umol/l), with normal levels of albumin, urea, uric acid, AST, ALT, cholesterol, triglycerides and bilirubin. Patient had elevated WBC “12.52 x 10 9 /L” and Platelet “453 x 10 9 /L” with reduction in RBC “4.4 x 10 9 /L” and Eosinophil count “0.07”. Consultation with patient neurologist regarding the steroid dose to reduce the susceptibility of developing adrenal crisis.
| EN100437 |
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] | A 28-year-old female patient presented to outpatient dental clinics for full mouth rehabilitation. On physical examination, the patient was awake, alert, oriented, and her blood pressure, temperature and heart rate were within normal limits. Upon taking medical history the patient revealed that was diagnosed with thymoma MG and on medication including pyridostigmine bromide 60 mg, azathioprine 50 mg and prednisone 20 mg.
Intraoral examination showed fair oral hygiene multiple fixed prosthodontic restorations and multiple carious teeth, multiple remaining roots and lipomatous tongue atrophy.
The patient was referred to her neurologist to provide a detailed history about her medical condition and to coordinate with him regarding the steroid dose take to avoid any complication during patient management. A consultation letter had been received from her neurologist explaining the patient medical condition which starts with difficulty in breathing, chewing and swallowing, there was no external ocular weakness, motor weakness, sphincter dysfunction, sensory deficits, muscle wasting and no signs of diplopia, dizziness, double vision, ptosis or any difficulty in maintaining balance. Patient underwent chest CT scan with contrast which show evidence of thymoma benign tumor of the thymus that has been the possible causes of MG. Diagnosis was confirmed with measuring serum level of acetylcholine receptor antibodies, later treatment plan had been formulated including drugs to control the condition and then thymectomy to avoid sever complication to the patient.
Before proceeding to the dental management of the case; CBC and blood chemistry had been requested form the patient. Creatinine level was below normal (42.23 umol/l), with normal levels of albumin, urea, uric acid, AST, ALT, cholesterol, triglycerides and bilirubin. Patient had elevated WBC “12.52 x 10 9 /L” and Platelet “453 x 10 9 /L” with reduction in RBC “4.4 x 10 9 /L” and Eosinophil count “0.07”. Consultation with patient neurologist regarding the steroid dose to reduce the susceptibility of developing adrenal crisis.
| EN100437 |
Consultation with patient neurologist regarding the steroid dose to reduce the susceptibility of developing adrenal crisis. | [
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] | A 28-year-old female patient presented to outpatient dental clinics for full mouth rehabilitation. On physical examination, the patient was awake, alert, oriented, and her blood pressure, temperature and heart rate were within normal limits. Upon taking medical history the patient revealed that was diagnosed with thymoma MG and on medication including pyridostigmine bromide 60 mg, azathioprine 50 mg and prednisone 20 mg.
Intraoral examination showed fair oral hygiene multiple fixed prosthodontic restorations and multiple carious teeth, multiple remaining roots and lipomatous tongue atrophy.
The patient was referred to her neurologist to provide a detailed history about her medical condition and to coordinate with him regarding the steroid dose take to avoid any complication during patient management. A consultation letter had been received from her neurologist explaining the patient medical condition which starts with difficulty in breathing, chewing and swallowing, there was no external ocular weakness, motor weakness, sphincter dysfunction, sensory deficits, muscle wasting and no signs of diplopia, dizziness, double vision, ptosis or any difficulty in maintaining balance. Patient underwent chest CT scan with contrast which show evidence of thymoma benign tumor of the thymus that has been the possible causes of MG. Diagnosis was confirmed with measuring serum level of acetylcholine receptor antibodies, later treatment plan had been formulated including drugs to control the condition and then thymectomy to avoid sever complication to the patient.
Before proceeding to the dental management of the case; CBC and blood chemistry had been requested form the patient. Creatinine level was below normal (42.23 umol/l), with normal levels of albumin, urea, uric acid, AST, ALT, cholesterol, triglycerides and bilirubin. Patient had elevated WBC “12.52 x 10 9 /L” and Platelet “453 x 10 9 /L” with reduction in RBC “4.4 x 10 9 /L” and Eosinophil count “0.07”. Consultation with patient neurologist regarding the steroid dose to reduce the susceptibility of developing adrenal crisis.
| EN100437 |
A 12-year-old girl presented an abdominal pain, high persistent fever of (40°C) and severe fatigue. | [
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] | A 12-year-old girl presented an abdominal pain, high persistent fever of (40°C) and severe fatigue. The physical exam revealed pallor, hepatomegaly, and grade III splenomegaly. The investigation revealed an elevated white blood cell count (WBC): 545,000/mm³. PNN: 49,050/mm³, hemoglobin: 11.6g/dl, platelets: 328,000/mm³. The patient's peripheral blood smear revealed marked leukocytosis with a significant number of immature myeloid precursors and 21% blasts. The analysis of the BCR-ABL shows 94% in the peripheral blood. The patient was diagnosed with CML. She received a chemotherapy protocol made of hyperalkalinisation, allopurinol, hydroxyurea and a treatment based on imatinib at the dose of 400mg per day. Patient achieved complete hematological remission at three months and complete cytogenetic remission at 12 months. The patient was readmitted into our pediatric department with complains of severe headache, vomiting, pain and bilateral visual loss since three days. On examination, patient was afebrile and appeared pale. Blood pressure was 100/60mm/hg and the heart rate 98 beat/minute. There was no lymphadenopathy and the nervous system examination was normal. Intraocular muscle testing was normal; however, there was an exophthalmia in both eyes. The pupil was sluggish to react to light. Fundoscopy revealed bilateral stade III disc edema and hemorrhages of the retina. She underwent a brain computed tomography (CT) scan with the suspicion of leukemic involvement or any other intracranial event (cerebral edema); however, nothing was found. A subsequent bone marrow exam showed no morphologic or molecular evidence of CML or acute leukemia. Cytological evaluation of cerebrospinal fluid (CSF) was also negative. The patient had no other known pathology that could be held responsible for retina edema. We suggested that it was a side effect of imatinib so its administration was temporary interrupted. The patient was put on an anti-edema therapy (mannitol, dexamethasone). However, few months later, the patient presented in the emergency room with a headache and severe vomiting. She described a recurrence of the same character of headaches accompanied with weakness of extremities and seizures. Nervous system examination revealed neck rigidity, presence of meningeal signs and lower limb paraplegia. CT of the brain revealed subdural chronic hematoma and a serpenginous gyriform enhancement around the contusion in the right parietal and occipital lobes. Analysis of the CSF collected showed lymphoblasts in a WBC count of 11000cells/ml. Flow cytometry of the CSF showed that blast cells were positive for a cluster of differentiation markers (CD) (CD34, CD19, CD10, CD22 and partially positive for CD45) confirming CNS extramedullary lymphoid blast infiltration. A bone marrow aspiration was done to evaluate the status of her chronic myelogenous leukemia and result was consistent with a chronic phase. Fundus examination showed bilateral optic atrophy.
The diagnosis of extramedullary isolated CNS blast crises (lymphoid type) was based on the presence of blasts in CSF (confirmed by flow cytometry).
The patient received a high-dose systemic induction chemotherapy and intrathecal therapy (methotrexate, arabinoside and dexamethasone). The imatinib was replaced by dasatinib at the dose of 100 mg per day. She was treated with 24 Gy of whole-brain radiation therapy.
Allogenic stem cell transplantation was not feasible. We noticed a rapidly progressive amelioration in her neurological status after finishing systemic chemotherapy and physical therapy; however, the patient's visual loss showed no signs of improvement.
| EN100543 |
The physical exam revealed pallor, hepatomegaly, and grade III splenomegaly. | [
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] | A 12-year-old girl presented an abdominal pain, high persistent fever of (40°C) and severe fatigue. The physical exam revealed pallor, hepatomegaly, and grade III splenomegaly. The investigation revealed an elevated white blood cell count (WBC): 545,000/mm³. PNN: 49,050/mm³, hemoglobin: 11.6g/dl, platelets: 328,000/mm³. The patient's peripheral blood smear revealed marked leukocytosis with a significant number of immature myeloid precursors and 21% blasts. The analysis of the BCR-ABL shows 94% in the peripheral blood. The patient was diagnosed with CML. She received a chemotherapy protocol made of hyperalkalinisation, allopurinol, hydroxyurea and a treatment based on imatinib at the dose of 400mg per day. Patient achieved complete hematological remission at three months and complete cytogenetic remission at 12 months. The patient was readmitted into our pediatric department with complains of severe headache, vomiting, pain and bilateral visual loss since three days. On examination, patient was afebrile and appeared pale. Blood pressure was 100/60mm/hg and the heart rate 98 beat/minute. There was no lymphadenopathy and the nervous system examination was normal. Intraocular muscle testing was normal; however, there was an exophthalmia in both eyes. The pupil was sluggish to react to light. Fundoscopy revealed bilateral stade III disc edema and hemorrhages of the retina. She underwent a brain computed tomography (CT) scan with the suspicion of leukemic involvement or any other intracranial event (cerebral edema); however, nothing was found. A subsequent bone marrow exam showed no morphologic or molecular evidence of CML or acute leukemia. Cytological evaluation of cerebrospinal fluid (CSF) was also negative. The patient had no other known pathology that could be held responsible for retina edema. We suggested that it was a side effect of imatinib so its administration was temporary interrupted. The patient was put on an anti-edema therapy (mannitol, dexamethasone). However, few months later, the patient presented in the emergency room with a headache and severe vomiting. She described a recurrence of the same character of headaches accompanied with weakness of extremities and seizures. Nervous system examination revealed neck rigidity, presence of meningeal signs and lower limb paraplegia. CT of the brain revealed subdural chronic hematoma and a serpenginous gyriform enhancement around the contusion in the right parietal and occipital lobes. Analysis of the CSF collected showed lymphoblasts in a WBC count of 11000cells/ml. Flow cytometry of the CSF showed that blast cells were positive for a cluster of differentiation markers (CD) (CD34, CD19, CD10, CD22 and partially positive for CD45) confirming CNS extramedullary lymphoid blast infiltration. A bone marrow aspiration was done to evaluate the status of her chronic myelogenous leukemia and result was consistent with a chronic phase. Fundus examination showed bilateral optic atrophy.
The diagnosis of extramedullary isolated CNS blast crises (lymphoid type) was based on the presence of blasts in CSF (confirmed by flow cytometry).
The patient received a high-dose systemic induction chemotherapy and intrathecal therapy (methotrexate, arabinoside and dexamethasone). The imatinib was replaced by dasatinib at the dose of 100 mg per day. She was treated with 24 Gy of whole-brain radiation therapy.
Allogenic stem cell transplantation was not feasible. We noticed a rapidly progressive amelioration in her neurological status after finishing systemic chemotherapy and physical therapy; however, the patient's visual loss showed no signs of improvement.
| EN100543 |
The investigation revealed an elevated white blood cell count (WBC): 545,000/mm³. | [
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] | A 12-year-old girl presented an abdominal pain, high persistent fever of (40°C) and severe fatigue. The physical exam revealed pallor, hepatomegaly, and grade III splenomegaly. The investigation revealed an elevated white blood cell count (WBC): 545,000/mm³. PNN: 49,050/mm³, hemoglobin: 11.6g/dl, platelets: 328,000/mm³. The patient's peripheral blood smear revealed marked leukocytosis with a significant number of immature myeloid precursors and 21% blasts. The analysis of the BCR-ABL shows 94% in the peripheral blood. The patient was diagnosed with CML. She received a chemotherapy protocol made of hyperalkalinisation, allopurinol, hydroxyurea and a treatment based on imatinib at the dose of 400mg per day. Patient achieved complete hematological remission at three months and complete cytogenetic remission at 12 months. The patient was readmitted into our pediatric department with complains of severe headache, vomiting, pain and bilateral visual loss since three days. On examination, patient was afebrile and appeared pale. Blood pressure was 100/60mm/hg and the heart rate 98 beat/minute. There was no lymphadenopathy and the nervous system examination was normal. Intraocular muscle testing was normal; however, there was an exophthalmia in both eyes. The pupil was sluggish to react to light. Fundoscopy revealed bilateral stade III disc edema and hemorrhages of the retina. She underwent a brain computed tomography (CT) scan with the suspicion of leukemic involvement or any other intracranial event (cerebral edema); however, nothing was found. A subsequent bone marrow exam showed no morphologic or molecular evidence of CML or acute leukemia. Cytological evaluation of cerebrospinal fluid (CSF) was also negative. The patient had no other known pathology that could be held responsible for retina edema. We suggested that it was a side effect of imatinib so its administration was temporary interrupted. The patient was put on an anti-edema therapy (mannitol, dexamethasone). However, few months later, the patient presented in the emergency room with a headache and severe vomiting. She described a recurrence of the same character of headaches accompanied with weakness of extremities and seizures. Nervous system examination revealed neck rigidity, presence of meningeal signs and lower limb paraplegia. CT of the brain revealed subdural chronic hematoma and a serpenginous gyriform enhancement around the contusion in the right parietal and occipital lobes. Analysis of the CSF collected showed lymphoblasts in a WBC count of 11000cells/ml. Flow cytometry of the CSF showed that blast cells were positive for a cluster of differentiation markers (CD) (CD34, CD19, CD10, CD22 and partially positive for CD45) confirming CNS extramedullary lymphoid blast infiltration. A bone marrow aspiration was done to evaluate the status of her chronic myelogenous leukemia and result was consistent with a chronic phase. Fundus examination showed bilateral optic atrophy.
The diagnosis of extramedullary isolated CNS blast crises (lymphoid type) was based on the presence of blasts in CSF (confirmed by flow cytometry).
The patient received a high-dose systemic induction chemotherapy and intrathecal therapy (methotrexate, arabinoside and dexamethasone). The imatinib was replaced by dasatinib at the dose of 100 mg per day. She was treated with 24 Gy of whole-brain radiation therapy.
Allogenic stem cell transplantation was not feasible. We noticed a rapidly progressive amelioration in her neurological status after finishing systemic chemotherapy and physical therapy; however, the patient's visual loss showed no signs of improvement.
| EN100543 |
PNN: 49,050/mm³, hemoglobin: 11.6g/dl, platelets: 328,000/mm³. | [
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] | A 12-year-old girl presented an abdominal pain, high persistent fever of (40°C) and severe fatigue. The physical exam revealed pallor, hepatomegaly, and grade III splenomegaly. The investigation revealed an elevated white blood cell count (WBC): 545,000/mm³. PNN: 49,050/mm³, hemoglobin: 11.6g/dl, platelets: 328,000/mm³. The patient's peripheral blood smear revealed marked leukocytosis with a significant number of immature myeloid precursors and 21% blasts. The analysis of the BCR-ABL shows 94% in the peripheral blood. The patient was diagnosed with CML. She received a chemotherapy protocol made of hyperalkalinisation, allopurinol, hydroxyurea and a treatment based on imatinib at the dose of 400mg per day. Patient achieved complete hematological remission at three months and complete cytogenetic remission at 12 months. The patient was readmitted into our pediatric department with complains of severe headache, vomiting, pain and bilateral visual loss since three days. On examination, patient was afebrile and appeared pale. Blood pressure was 100/60mm/hg and the heart rate 98 beat/minute. There was no lymphadenopathy and the nervous system examination was normal. Intraocular muscle testing was normal; however, there was an exophthalmia in both eyes. The pupil was sluggish to react to light. Fundoscopy revealed bilateral stade III disc edema and hemorrhages of the retina. She underwent a brain computed tomography (CT) scan with the suspicion of leukemic involvement or any other intracranial event (cerebral edema); however, nothing was found. A subsequent bone marrow exam showed no morphologic or molecular evidence of CML or acute leukemia. Cytological evaluation of cerebrospinal fluid (CSF) was also negative. The patient had no other known pathology that could be held responsible for retina edema. We suggested that it was a side effect of imatinib so its administration was temporary interrupted. The patient was put on an anti-edema therapy (mannitol, dexamethasone). However, few months later, the patient presented in the emergency room with a headache and severe vomiting. She described a recurrence of the same character of headaches accompanied with weakness of extremities and seizures. Nervous system examination revealed neck rigidity, presence of meningeal signs and lower limb paraplegia. CT of the brain revealed subdural chronic hematoma and a serpenginous gyriform enhancement around the contusion in the right parietal and occipital lobes. Analysis of the CSF collected showed lymphoblasts in a WBC count of 11000cells/ml. Flow cytometry of the CSF showed that blast cells were positive for a cluster of differentiation markers (CD) (CD34, CD19, CD10, CD22 and partially positive for CD45) confirming CNS extramedullary lymphoid blast infiltration. A bone marrow aspiration was done to evaluate the status of her chronic myelogenous leukemia and result was consistent with a chronic phase. Fundus examination showed bilateral optic atrophy.
The diagnosis of extramedullary isolated CNS blast crises (lymphoid type) was based on the presence of blasts in CSF (confirmed by flow cytometry).
The patient received a high-dose systemic induction chemotherapy and intrathecal therapy (methotrexate, arabinoside and dexamethasone). The imatinib was replaced by dasatinib at the dose of 100 mg per day. She was treated with 24 Gy of whole-brain radiation therapy.
Allogenic stem cell transplantation was not feasible. We noticed a rapidly progressive amelioration in her neurological status after finishing systemic chemotherapy and physical therapy; however, the patient's visual loss showed no signs of improvement.
| EN100543 |
The patient's peripheral blood smear revealed marked leukocytosis with a significant number of immature myeloid precursors and 21% blasts. | [
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] | A 12-year-old girl presented an abdominal pain, high persistent fever of (40°C) and severe fatigue. The physical exam revealed pallor, hepatomegaly, and grade III splenomegaly. The investigation revealed an elevated white blood cell count (WBC): 545,000/mm³. PNN: 49,050/mm³, hemoglobin: 11.6g/dl, platelets: 328,000/mm³. The patient's peripheral blood smear revealed marked leukocytosis with a significant number of immature myeloid precursors and 21% blasts. The analysis of the BCR-ABL shows 94% in the peripheral blood. The patient was diagnosed with CML. She received a chemotherapy protocol made of hyperalkalinisation, allopurinol, hydroxyurea and a treatment based on imatinib at the dose of 400mg per day. Patient achieved complete hematological remission at three months and complete cytogenetic remission at 12 months. The patient was readmitted into our pediatric department with complains of severe headache, vomiting, pain and bilateral visual loss since three days. On examination, patient was afebrile and appeared pale. Blood pressure was 100/60mm/hg and the heart rate 98 beat/minute. There was no lymphadenopathy and the nervous system examination was normal. Intraocular muscle testing was normal; however, there was an exophthalmia in both eyes. The pupil was sluggish to react to light. Fundoscopy revealed bilateral stade III disc edema and hemorrhages of the retina. She underwent a brain computed tomography (CT) scan with the suspicion of leukemic involvement or any other intracranial event (cerebral edema); however, nothing was found. A subsequent bone marrow exam showed no morphologic or molecular evidence of CML or acute leukemia. Cytological evaluation of cerebrospinal fluid (CSF) was also negative. The patient had no other known pathology that could be held responsible for retina edema. We suggested that it was a side effect of imatinib so its administration was temporary interrupted. The patient was put on an anti-edema therapy (mannitol, dexamethasone). However, few months later, the patient presented in the emergency room with a headache and severe vomiting. She described a recurrence of the same character of headaches accompanied with weakness of extremities and seizures. Nervous system examination revealed neck rigidity, presence of meningeal signs and lower limb paraplegia. CT of the brain revealed subdural chronic hematoma and a serpenginous gyriform enhancement around the contusion in the right parietal and occipital lobes. Analysis of the CSF collected showed lymphoblasts in a WBC count of 11000cells/ml. Flow cytometry of the CSF showed that blast cells were positive for a cluster of differentiation markers (CD) (CD34, CD19, CD10, CD22 and partially positive for CD45) confirming CNS extramedullary lymphoid blast infiltration. A bone marrow aspiration was done to evaluate the status of her chronic myelogenous leukemia and result was consistent with a chronic phase. Fundus examination showed bilateral optic atrophy.
The diagnosis of extramedullary isolated CNS blast crises (lymphoid type) was based on the presence of blasts in CSF (confirmed by flow cytometry).
The patient received a high-dose systemic induction chemotherapy and intrathecal therapy (methotrexate, arabinoside and dexamethasone). The imatinib was replaced by dasatinib at the dose of 100 mg per day. She was treated with 24 Gy of whole-brain radiation therapy.
Allogenic stem cell transplantation was not feasible. We noticed a rapidly progressive amelioration in her neurological status after finishing systemic chemotherapy and physical therapy; however, the patient's visual loss showed no signs of improvement.
| EN100543 |
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The diagnosis of extramedullary isolated CNS blast crises (lymphoid type) was based on the presence of blasts in CSF (confirmed by flow cytometry).
The patient received a high-dose systemic induction chemotherapy and intrathecal therapy (methotrexate, arabinoside and dexamethasone). The imatinib was replaced by dasatinib at the dose of 100 mg per day. She was treated with 24 Gy of whole-brain radiation therapy.
Allogenic stem cell transplantation was not feasible. We noticed a rapidly progressive amelioration in her neurological status after finishing systemic chemotherapy and physical therapy; however, the patient's visual loss showed no signs of improvement.
| EN100543 |
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The diagnosis of extramedullary isolated CNS blast crises (lymphoid type) was based on the presence of blasts in CSF (confirmed by flow cytometry).
The patient received a high-dose systemic induction chemotherapy and intrathecal therapy (methotrexate, arabinoside and dexamethasone). The imatinib was replaced by dasatinib at the dose of 100 mg per day. She was treated with 24 Gy of whole-brain radiation therapy.
Allogenic stem cell transplantation was not feasible. We noticed a rapidly progressive amelioration in her neurological status after finishing systemic chemotherapy and physical therapy; however, the patient's visual loss showed no signs of improvement.
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The diagnosis of extramedullary isolated CNS blast crises (lymphoid type) was based on the presence of blasts in CSF (confirmed by flow cytometry).
The patient received a high-dose systemic induction chemotherapy and intrathecal therapy (methotrexate, arabinoside and dexamethasone). The imatinib was replaced by dasatinib at the dose of 100 mg per day. She was treated with 24 Gy of whole-brain radiation therapy.
Allogenic stem cell transplantation was not feasible. We noticed a rapidly progressive amelioration in her neurological status after finishing systemic chemotherapy and physical therapy; however, the patient's visual loss showed no signs of improvement.
| EN100543 |
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The diagnosis of extramedullary isolated CNS blast crises (lymphoid type) was based on the presence of blasts in CSF (confirmed by flow cytometry).
The patient received a high-dose systemic induction chemotherapy and intrathecal therapy (methotrexate, arabinoside and dexamethasone). The imatinib was replaced by dasatinib at the dose of 100 mg per day. She was treated with 24 Gy of whole-brain radiation therapy.
Allogenic stem cell transplantation was not feasible. We noticed a rapidly progressive amelioration in her neurological status after finishing systemic chemotherapy and physical therapy; however, the patient's visual loss showed no signs of improvement.
| EN100543 |
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The diagnosis of extramedullary isolated CNS blast crises (lymphoid type) was based on the presence of blasts in CSF (confirmed by flow cytometry).
The patient received a high-dose systemic induction chemotherapy and intrathecal therapy (methotrexate, arabinoside and dexamethasone). The imatinib was replaced by dasatinib at the dose of 100 mg per day. She was treated with 24 Gy of whole-brain radiation therapy.
Allogenic stem cell transplantation was not feasible. We noticed a rapidly progressive amelioration in her neurological status after finishing systemic chemotherapy and physical therapy; however, the patient's visual loss showed no signs of improvement.
| EN100543 |
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The diagnosis of extramedullary isolated CNS blast crises (lymphoid type) was based on the presence of blasts in CSF (confirmed by flow cytometry).
The patient received a high-dose systemic induction chemotherapy and intrathecal therapy (methotrexate, arabinoside and dexamethasone). The imatinib was replaced by dasatinib at the dose of 100 mg per day. She was treated with 24 Gy of whole-brain radiation therapy.
Allogenic stem cell transplantation was not feasible. We noticed a rapidly progressive amelioration in her neurological status after finishing systemic chemotherapy and physical therapy; however, the patient's visual loss showed no signs of improvement.
| EN100543 |
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The diagnosis of extramedullary isolated CNS blast crises (lymphoid type) was based on the presence of blasts in CSF (confirmed by flow cytometry).
The patient received a high-dose systemic induction chemotherapy and intrathecal therapy (methotrexate, arabinoside and dexamethasone). The imatinib was replaced by dasatinib at the dose of 100 mg per day. She was treated with 24 Gy of whole-brain radiation therapy.
Allogenic stem cell transplantation was not feasible. We noticed a rapidly progressive amelioration in her neurological status after finishing systemic chemotherapy and physical therapy; however, the patient's visual loss showed no signs of improvement.
| EN100543 |
There was no lymphadenopathy and the nervous system examination was normal. | [
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The diagnosis of extramedullary isolated CNS blast crises (lymphoid type) was based on the presence of blasts in CSF (confirmed by flow cytometry).
The patient received a high-dose systemic induction chemotherapy and intrathecal therapy (methotrexate, arabinoside and dexamethasone). The imatinib was replaced by dasatinib at the dose of 100 mg per day. She was treated with 24 Gy of whole-brain radiation therapy.
Allogenic stem cell transplantation was not feasible. We noticed a rapidly progressive amelioration in her neurological status after finishing systemic chemotherapy and physical therapy; however, the patient's visual loss showed no signs of improvement.
| EN100543 |
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] | A 12-year-old girl presented an abdominal pain, high persistent fever of (40°C) and severe fatigue. The physical exam revealed pallor, hepatomegaly, and grade III splenomegaly. The investigation revealed an elevated white blood cell count (WBC): 545,000/mm³. PNN: 49,050/mm³, hemoglobin: 11.6g/dl, platelets: 328,000/mm³. The patient's peripheral blood smear revealed marked leukocytosis with a significant number of immature myeloid precursors and 21% blasts. The analysis of the BCR-ABL shows 94% in the peripheral blood. The patient was diagnosed with CML. She received a chemotherapy protocol made of hyperalkalinisation, allopurinol, hydroxyurea and a treatment based on imatinib at the dose of 400mg per day. Patient achieved complete hematological remission at three months and complete cytogenetic remission at 12 months. The patient was readmitted into our pediatric department with complains of severe headache, vomiting, pain and bilateral visual loss since three days. On examination, patient was afebrile and appeared pale. Blood pressure was 100/60mm/hg and the heart rate 98 beat/minute. There was no lymphadenopathy and the nervous system examination was normal. Intraocular muscle testing was normal; however, there was an exophthalmia in both eyes. The pupil was sluggish to react to light. Fundoscopy revealed bilateral stade III disc edema and hemorrhages of the retina. She underwent a brain computed tomography (CT) scan with the suspicion of leukemic involvement or any other intracranial event (cerebral edema); however, nothing was found. A subsequent bone marrow exam showed no morphologic or molecular evidence of CML or acute leukemia. Cytological evaluation of cerebrospinal fluid (CSF) was also negative. The patient had no other known pathology that could be held responsible for retina edema. We suggested that it was a side effect of imatinib so its administration was temporary interrupted. The patient was put on an anti-edema therapy (mannitol, dexamethasone). However, few months later, the patient presented in the emergency room with a headache and severe vomiting. She described a recurrence of the same character of headaches accompanied with weakness of extremities and seizures. Nervous system examination revealed neck rigidity, presence of meningeal signs and lower limb paraplegia. CT of the brain revealed subdural chronic hematoma and a serpenginous gyriform enhancement around the contusion in the right parietal and occipital lobes. Analysis of the CSF collected showed lymphoblasts in a WBC count of 11000cells/ml. Flow cytometry of the CSF showed that blast cells were positive for a cluster of differentiation markers (CD) (CD34, CD19, CD10, CD22 and partially positive for CD45) confirming CNS extramedullary lymphoid blast infiltration. A bone marrow aspiration was done to evaluate the status of her chronic myelogenous leukemia and result was consistent with a chronic phase. Fundus examination showed bilateral optic atrophy.
The diagnosis of extramedullary isolated CNS blast crises (lymphoid type) was based on the presence of blasts in CSF (confirmed by flow cytometry).
The patient received a high-dose systemic induction chemotherapy and intrathecal therapy (methotrexate, arabinoside and dexamethasone). The imatinib was replaced by dasatinib at the dose of 100 mg per day. She was treated with 24 Gy of whole-brain radiation therapy.
Allogenic stem cell transplantation was not feasible. We noticed a rapidly progressive amelioration in her neurological status after finishing systemic chemotherapy and physical therapy; however, the patient's visual loss showed no signs of improvement.
| EN100543 |
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] | A 12-year-old girl presented an abdominal pain, high persistent fever of (40°C) and severe fatigue. The physical exam revealed pallor, hepatomegaly, and grade III splenomegaly. The investigation revealed an elevated white blood cell count (WBC): 545,000/mm³. PNN: 49,050/mm³, hemoglobin: 11.6g/dl, platelets: 328,000/mm³. The patient's peripheral blood smear revealed marked leukocytosis with a significant number of immature myeloid precursors and 21% blasts. The analysis of the BCR-ABL shows 94% in the peripheral blood. The patient was diagnosed with CML. She received a chemotherapy protocol made of hyperalkalinisation, allopurinol, hydroxyurea and a treatment based on imatinib at the dose of 400mg per day. Patient achieved complete hematological remission at three months and complete cytogenetic remission at 12 months. The patient was readmitted into our pediatric department with complains of severe headache, vomiting, pain and bilateral visual loss since three days. On examination, patient was afebrile and appeared pale. Blood pressure was 100/60mm/hg and the heart rate 98 beat/minute. There was no lymphadenopathy and the nervous system examination was normal. Intraocular muscle testing was normal; however, there was an exophthalmia in both eyes. The pupil was sluggish to react to light. Fundoscopy revealed bilateral stade III disc edema and hemorrhages of the retina. She underwent a brain computed tomography (CT) scan with the suspicion of leukemic involvement or any other intracranial event (cerebral edema); however, nothing was found. A subsequent bone marrow exam showed no morphologic or molecular evidence of CML or acute leukemia. Cytological evaluation of cerebrospinal fluid (CSF) was also negative. The patient had no other known pathology that could be held responsible for retina edema. We suggested that it was a side effect of imatinib so its administration was temporary interrupted. The patient was put on an anti-edema therapy (mannitol, dexamethasone). However, few months later, the patient presented in the emergency room with a headache and severe vomiting. She described a recurrence of the same character of headaches accompanied with weakness of extremities and seizures. Nervous system examination revealed neck rigidity, presence of meningeal signs and lower limb paraplegia. CT of the brain revealed subdural chronic hematoma and a serpenginous gyriform enhancement around the contusion in the right parietal and occipital lobes. Analysis of the CSF collected showed lymphoblasts in a WBC count of 11000cells/ml. Flow cytometry of the CSF showed that blast cells were positive for a cluster of differentiation markers (CD) (CD34, CD19, CD10, CD22 and partially positive for CD45) confirming CNS extramedullary lymphoid blast infiltration. A bone marrow aspiration was done to evaluate the status of her chronic myelogenous leukemia and result was consistent with a chronic phase. Fundus examination showed bilateral optic atrophy.
The diagnosis of extramedullary isolated CNS blast crises (lymphoid type) was based on the presence of blasts in CSF (confirmed by flow cytometry).
The patient received a high-dose systemic induction chemotherapy and intrathecal therapy (methotrexate, arabinoside and dexamethasone). The imatinib was replaced by dasatinib at the dose of 100 mg per day. She was treated with 24 Gy of whole-brain radiation therapy.
Allogenic stem cell transplantation was not feasible. We noticed a rapidly progressive amelioration in her neurological status after finishing systemic chemotherapy and physical therapy; however, the patient's visual loss showed no signs of improvement.
| EN100543 |
Fundoscopy revealed bilateral stade III disc edema and hemorrhages of the retina. | [
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The diagnosis of extramedullary isolated CNS blast crises (lymphoid type) was based on the presence of blasts in CSF (confirmed by flow cytometry).
The patient received a high-dose systemic induction chemotherapy and intrathecal therapy (methotrexate, arabinoside and dexamethasone). The imatinib was replaced by dasatinib at the dose of 100 mg per day. She was treated with 24 Gy of whole-brain radiation therapy.
Allogenic stem cell transplantation was not feasible. We noticed a rapidly progressive amelioration in her neurological status after finishing systemic chemotherapy and physical therapy; however, the patient's visual loss showed no signs of improvement.
| EN100543 |
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] | A 12-year-old girl presented an abdominal pain, high persistent fever of (40°C) and severe fatigue. The physical exam revealed pallor, hepatomegaly, and grade III splenomegaly. The investigation revealed an elevated white blood cell count (WBC): 545,000/mm³. PNN: 49,050/mm³, hemoglobin: 11.6g/dl, platelets: 328,000/mm³. The patient's peripheral blood smear revealed marked leukocytosis with a significant number of immature myeloid precursors and 21% blasts. The analysis of the BCR-ABL shows 94% in the peripheral blood. The patient was diagnosed with CML. She received a chemotherapy protocol made of hyperalkalinisation, allopurinol, hydroxyurea and a treatment based on imatinib at the dose of 400mg per day. Patient achieved complete hematological remission at three months and complete cytogenetic remission at 12 months. The patient was readmitted into our pediatric department with complains of severe headache, vomiting, pain and bilateral visual loss since three days. On examination, patient was afebrile and appeared pale. Blood pressure was 100/60mm/hg and the heart rate 98 beat/minute. There was no lymphadenopathy and the nervous system examination was normal. Intraocular muscle testing was normal; however, there was an exophthalmia in both eyes. The pupil was sluggish to react to light. Fundoscopy revealed bilateral stade III disc edema and hemorrhages of the retina. She underwent a brain computed tomography (CT) scan with the suspicion of leukemic involvement or any other intracranial event (cerebral edema); however, nothing was found. A subsequent bone marrow exam showed no morphologic or molecular evidence of CML or acute leukemia. Cytological evaluation of cerebrospinal fluid (CSF) was also negative. The patient had no other known pathology that could be held responsible for retina edema. We suggested that it was a side effect of imatinib so its administration was temporary interrupted. The patient was put on an anti-edema therapy (mannitol, dexamethasone). However, few months later, the patient presented in the emergency room with a headache and severe vomiting. She described a recurrence of the same character of headaches accompanied with weakness of extremities and seizures. Nervous system examination revealed neck rigidity, presence of meningeal signs and lower limb paraplegia. CT of the brain revealed subdural chronic hematoma and a serpenginous gyriform enhancement around the contusion in the right parietal and occipital lobes. Analysis of the CSF collected showed lymphoblasts in a WBC count of 11000cells/ml. Flow cytometry of the CSF showed that blast cells were positive for a cluster of differentiation markers (CD) (CD34, CD19, CD10, CD22 and partially positive for CD45) confirming CNS extramedullary lymphoid blast infiltration. A bone marrow aspiration was done to evaluate the status of her chronic myelogenous leukemia and result was consistent with a chronic phase. Fundus examination showed bilateral optic atrophy.
The diagnosis of extramedullary isolated CNS blast crises (lymphoid type) was based on the presence of blasts in CSF (confirmed by flow cytometry).
The patient received a high-dose systemic induction chemotherapy and intrathecal therapy (methotrexate, arabinoside and dexamethasone). The imatinib was replaced by dasatinib at the dose of 100 mg per day. She was treated with 24 Gy of whole-brain radiation therapy.
Allogenic stem cell transplantation was not feasible. We noticed a rapidly progressive amelioration in her neurological status after finishing systemic chemotherapy and physical therapy; however, the patient's visual loss showed no signs of improvement.
| EN100543 |
A subsequent bone marrow exam showed no morphologic or molecular evidence of CML or acute leukemia. | [
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] | A 12-year-old girl presented an abdominal pain, high persistent fever of (40°C) and severe fatigue. The physical exam revealed pallor, hepatomegaly, and grade III splenomegaly. The investigation revealed an elevated white blood cell count (WBC): 545,000/mm³. PNN: 49,050/mm³, hemoglobin: 11.6g/dl, platelets: 328,000/mm³. The patient's peripheral blood smear revealed marked leukocytosis with a significant number of immature myeloid precursors and 21% blasts. The analysis of the BCR-ABL shows 94% in the peripheral blood. The patient was diagnosed with CML. She received a chemotherapy protocol made of hyperalkalinisation, allopurinol, hydroxyurea and a treatment based on imatinib at the dose of 400mg per day. Patient achieved complete hematological remission at three months and complete cytogenetic remission at 12 months. The patient was readmitted into our pediatric department with complains of severe headache, vomiting, pain and bilateral visual loss since three days. On examination, patient was afebrile and appeared pale. Blood pressure was 100/60mm/hg and the heart rate 98 beat/minute. There was no lymphadenopathy and the nervous system examination was normal. Intraocular muscle testing was normal; however, there was an exophthalmia in both eyes. The pupil was sluggish to react to light. Fundoscopy revealed bilateral stade III disc edema and hemorrhages of the retina. She underwent a brain computed tomography (CT) scan with the suspicion of leukemic involvement or any other intracranial event (cerebral edema); however, nothing was found. A subsequent bone marrow exam showed no morphologic or molecular evidence of CML or acute leukemia. Cytological evaluation of cerebrospinal fluid (CSF) was also negative. The patient had no other known pathology that could be held responsible for retina edema. We suggested that it was a side effect of imatinib so its administration was temporary interrupted. The patient was put on an anti-edema therapy (mannitol, dexamethasone). However, few months later, the patient presented in the emergency room with a headache and severe vomiting. She described a recurrence of the same character of headaches accompanied with weakness of extremities and seizures. Nervous system examination revealed neck rigidity, presence of meningeal signs and lower limb paraplegia. CT of the brain revealed subdural chronic hematoma and a serpenginous gyriform enhancement around the contusion in the right parietal and occipital lobes. Analysis of the CSF collected showed lymphoblasts in a WBC count of 11000cells/ml. Flow cytometry of the CSF showed that blast cells were positive for a cluster of differentiation markers (CD) (CD34, CD19, CD10, CD22 and partially positive for CD45) confirming CNS extramedullary lymphoid blast infiltration. A bone marrow aspiration was done to evaluate the status of her chronic myelogenous leukemia and result was consistent with a chronic phase. Fundus examination showed bilateral optic atrophy.
The diagnosis of extramedullary isolated CNS blast crises (lymphoid type) was based on the presence of blasts in CSF (confirmed by flow cytometry).
The patient received a high-dose systemic induction chemotherapy and intrathecal therapy (methotrexate, arabinoside and dexamethasone). The imatinib was replaced by dasatinib at the dose of 100 mg per day. She was treated with 24 Gy of whole-brain radiation therapy.
Allogenic stem cell transplantation was not feasible. We noticed a rapidly progressive amelioration in her neurological status after finishing systemic chemotherapy and physical therapy; however, the patient's visual loss showed no signs of improvement.
| EN100543 |
Cytological evaluation of cerebrospinal fluid (CSF) was also negative. | [
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The diagnosis of extramedullary isolated CNS blast crises (lymphoid type) was based on the presence of blasts in CSF (confirmed by flow cytometry).
The patient received a high-dose systemic induction chemotherapy and intrathecal therapy (methotrexate, arabinoside and dexamethasone). The imatinib was replaced by dasatinib at the dose of 100 mg per day. She was treated with 24 Gy of whole-brain radiation therapy.
Allogenic stem cell transplantation was not feasible. We noticed a rapidly progressive amelioration in her neurological status after finishing systemic chemotherapy and physical therapy; however, the patient's visual loss showed no signs of improvement.
| EN100543 |
The patient had no other known pathology that could be held responsible for retina edema. | [
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The diagnosis of extramedullary isolated CNS blast crises (lymphoid type) was based on the presence of blasts in CSF (confirmed by flow cytometry).
The patient received a high-dose systemic induction chemotherapy and intrathecal therapy (methotrexate, arabinoside and dexamethasone). The imatinib was replaced by dasatinib at the dose of 100 mg per day. She was treated with 24 Gy of whole-brain radiation therapy.
Allogenic stem cell transplantation was not feasible. We noticed a rapidly progressive amelioration in her neurological status after finishing systemic chemotherapy and physical therapy; however, the patient's visual loss showed no signs of improvement.
| EN100543 |
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The diagnosis of extramedullary isolated CNS blast crises (lymphoid type) was based on the presence of blasts in CSF (confirmed by flow cytometry).
The patient received a high-dose systemic induction chemotherapy and intrathecal therapy (methotrexate, arabinoside and dexamethasone). The imatinib was replaced by dasatinib at the dose of 100 mg per day. She was treated with 24 Gy of whole-brain radiation therapy.
Allogenic stem cell transplantation was not feasible. We noticed a rapidly progressive amelioration in her neurological status after finishing systemic chemotherapy and physical therapy; however, the patient's visual loss showed no signs of improvement.
| EN100543 |
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The diagnosis of extramedullary isolated CNS blast crises (lymphoid type) was based on the presence of blasts in CSF (confirmed by flow cytometry).
The patient received a high-dose systemic induction chemotherapy and intrathecal therapy (methotrexate, arabinoside and dexamethasone). The imatinib was replaced by dasatinib at the dose of 100 mg per day. She was treated with 24 Gy of whole-brain radiation therapy.
Allogenic stem cell transplantation was not feasible. We noticed a rapidly progressive amelioration in her neurological status after finishing systemic chemotherapy and physical therapy; however, the patient's visual loss showed no signs of improvement.
| EN100543 |
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The diagnosis of extramedullary isolated CNS blast crises (lymphoid type) was based on the presence of blasts in CSF (confirmed by flow cytometry).
The patient received a high-dose systemic induction chemotherapy and intrathecal therapy (methotrexate, arabinoside and dexamethasone). The imatinib was replaced by dasatinib at the dose of 100 mg per day. She was treated with 24 Gy of whole-brain radiation therapy.
Allogenic stem cell transplantation was not feasible. We noticed a rapidly progressive amelioration in her neurological status after finishing systemic chemotherapy and physical therapy; however, the patient's visual loss showed no signs of improvement.
| EN100543 |
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The diagnosis of extramedullary isolated CNS blast crises (lymphoid type) was based on the presence of blasts in CSF (confirmed by flow cytometry).
The patient received a high-dose systemic induction chemotherapy and intrathecal therapy (methotrexate, arabinoside and dexamethasone). The imatinib was replaced by dasatinib at the dose of 100 mg per day. She was treated with 24 Gy of whole-brain radiation therapy.
Allogenic stem cell transplantation was not feasible. We noticed a rapidly progressive amelioration in her neurological status after finishing systemic chemotherapy and physical therapy; however, the patient's visual loss showed no signs of improvement.
| EN100543 |
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The diagnosis of extramedullary isolated CNS blast crises (lymphoid type) was based on the presence of blasts in CSF (confirmed by flow cytometry).
The patient received a high-dose systemic induction chemotherapy and intrathecal therapy (methotrexate, arabinoside and dexamethasone). The imatinib was replaced by dasatinib at the dose of 100 mg per day. She was treated with 24 Gy of whole-brain radiation therapy.
Allogenic stem cell transplantation was not feasible. We noticed a rapidly progressive amelioration in her neurological status after finishing systemic chemotherapy and physical therapy; however, the patient's visual loss showed no signs of improvement.
| EN100543 |
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The diagnosis of extramedullary isolated CNS blast crises (lymphoid type) was based on the presence of blasts in CSF (confirmed by flow cytometry).
The patient received a high-dose systemic induction chemotherapy and intrathecal therapy (methotrexate, arabinoside and dexamethasone). The imatinib was replaced by dasatinib at the dose of 100 mg per day. She was treated with 24 Gy of whole-brain radiation therapy.
Allogenic stem cell transplantation was not feasible. We noticed a rapidly progressive amelioration in her neurological status after finishing systemic chemotherapy and physical therapy; however, the patient's visual loss showed no signs of improvement.
| EN100543 |
Analysis of the CSF collected showed lymphoblasts in a WBC count of 11000cells/ml. | [
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] | A 12-year-old girl presented an abdominal pain, high persistent fever of (40°C) and severe fatigue. The physical exam revealed pallor, hepatomegaly, and grade III splenomegaly. The investigation revealed an elevated white blood cell count (WBC): 545,000/mm³. PNN: 49,050/mm³, hemoglobin: 11.6g/dl, platelets: 328,000/mm³. The patient's peripheral blood smear revealed marked leukocytosis with a significant number of immature myeloid precursors and 21% blasts. The analysis of the BCR-ABL shows 94% in the peripheral blood. The patient was diagnosed with CML. She received a chemotherapy protocol made of hyperalkalinisation, allopurinol, hydroxyurea and a treatment based on imatinib at the dose of 400mg per day. Patient achieved complete hematological remission at three months and complete cytogenetic remission at 12 months. The patient was readmitted into our pediatric department with complains of severe headache, vomiting, pain and bilateral visual loss since three days. On examination, patient was afebrile and appeared pale. Blood pressure was 100/60mm/hg and the heart rate 98 beat/minute. There was no lymphadenopathy and the nervous system examination was normal. Intraocular muscle testing was normal; however, there was an exophthalmia in both eyes. The pupil was sluggish to react to light. Fundoscopy revealed bilateral stade III disc edema and hemorrhages of the retina. She underwent a brain computed tomography (CT) scan with the suspicion of leukemic involvement or any other intracranial event (cerebral edema); however, nothing was found. A subsequent bone marrow exam showed no morphologic or molecular evidence of CML or acute leukemia. Cytological evaluation of cerebrospinal fluid (CSF) was also negative. The patient had no other known pathology that could be held responsible for retina edema. We suggested that it was a side effect of imatinib so its administration was temporary interrupted. The patient was put on an anti-edema therapy (mannitol, dexamethasone). However, few months later, the patient presented in the emergency room with a headache and severe vomiting. She described a recurrence of the same character of headaches accompanied with weakness of extremities and seizures. Nervous system examination revealed neck rigidity, presence of meningeal signs and lower limb paraplegia. CT of the brain revealed subdural chronic hematoma and a serpenginous gyriform enhancement around the contusion in the right parietal and occipital lobes. Analysis of the CSF collected showed lymphoblasts in a WBC count of 11000cells/ml. Flow cytometry of the CSF showed that blast cells were positive for a cluster of differentiation markers (CD) (CD34, CD19, CD10, CD22 and partially positive for CD45) confirming CNS extramedullary lymphoid blast infiltration. A bone marrow aspiration was done to evaluate the status of her chronic myelogenous leukemia and result was consistent with a chronic phase. Fundus examination showed bilateral optic atrophy.
The diagnosis of extramedullary isolated CNS blast crises (lymphoid type) was based on the presence of blasts in CSF (confirmed by flow cytometry).
The patient received a high-dose systemic induction chemotherapy and intrathecal therapy (methotrexate, arabinoside and dexamethasone). The imatinib was replaced by dasatinib at the dose of 100 mg per day. She was treated with 24 Gy of whole-brain radiation therapy.
Allogenic stem cell transplantation was not feasible. We noticed a rapidly progressive amelioration in her neurological status after finishing systemic chemotherapy and physical therapy; however, the patient's visual loss showed no signs of improvement.
| EN100543 |
Flow cytometry of the CSF showed that blast cells were positive for a cluster of differentiation markers (CD) (CD34, CD19, CD10, CD22 and partially positive for CD45) confirming CNS extramedullary lymphoid blast infiltration. | [
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] | A 12-year-old girl presented an abdominal pain, high persistent fever of (40°C) and severe fatigue. The physical exam revealed pallor, hepatomegaly, and grade III splenomegaly. The investigation revealed an elevated white blood cell count (WBC): 545,000/mm³. PNN: 49,050/mm³, hemoglobin: 11.6g/dl, platelets: 328,000/mm³. The patient's peripheral blood smear revealed marked leukocytosis with a significant number of immature myeloid precursors and 21% blasts. The analysis of the BCR-ABL shows 94% in the peripheral blood. The patient was diagnosed with CML. She received a chemotherapy protocol made of hyperalkalinisation, allopurinol, hydroxyurea and a treatment based on imatinib at the dose of 400mg per day. Patient achieved complete hematological remission at three months and complete cytogenetic remission at 12 months. The patient was readmitted into our pediatric department with complains of severe headache, vomiting, pain and bilateral visual loss since three days. On examination, patient was afebrile and appeared pale. Blood pressure was 100/60mm/hg and the heart rate 98 beat/minute. There was no lymphadenopathy and the nervous system examination was normal. Intraocular muscle testing was normal; however, there was an exophthalmia in both eyes. The pupil was sluggish to react to light. Fundoscopy revealed bilateral stade III disc edema and hemorrhages of the retina. She underwent a brain computed tomography (CT) scan with the suspicion of leukemic involvement or any other intracranial event (cerebral edema); however, nothing was found. A subsequent bone marrow exam showed no morphologic or molecular evidence of CML or acute leukemia. Cytological evaluation of cerebrospinal fluid (CSF) was also negative. The patient had no other known pathology that could be held responsible for retina edema. We suggested that it was a side effect of imatinib so its administration was temporary interrupted. The patient was put on an anti-edema therapy (mannitol, dexamethasone). However, few months later, the patient presented in the emergency room with a headache and severe vomiting. She described a recurrence of the same character of headaches accompanied with weakness of extremities and seizures. Nervous system examination revealed neck rigidity, presence of meningeal signs and lower limb paraplegia. CT of the brain revealed subdural chronic hematoma and a serpenginous gyriform enhancement around the contusion in the right parietal and occipital lobes. Analysis of the CSF collected showed lymphoblasts in a WBC count of 11000cells/ml. Flow cytometry of the CSF showed that blast cells were positive for a cluster of differentiation markers (CD) (CD34, CD19, CD10, CD22 and partially positive for CD45) confirming CNS extramedullary lymphoid blast infiltration. A bone marrow aspiration was done to evaluate the status of her chronic myelogenous leukemia and result was consistent with a chronic phase. Fundus examination showed bilateral optic atrophy.
The diagnosis of extramedullary isolated CNS blast crises (lymphoid type) was based on the presence of blasts in CSF (confirmed by flow cytometry).
The patient received a high-dose systemic induction chemotherapy and intrathecal therapy (methotrexate, arabinoside and dexamethasone). The imatinib was replaced by dasatinib at the dose of 100 mg per day. She was treated with 24 Gy of whole-brain radiation therapy.
Allogenic stem cell transplantation was not feasible. We noticed a rapidly progressive amelioration in her neurological status after finishing systemic chemotherapy and physical therapy; however, the patient's visual loss showed no signs of improvement.
| EN100543 |
A bone marrow aspiration was done to evaluate the status of her chronic myelogenous leukemia and result was consistent with a chronic phase. | [
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] | A 12-year-old girl presented an abdominal pain, high persistent fever of (40°C) and severe fatigue. The physical exam revealed pallor, hepatomegaly, and grade III splenomegaly. The investigation revealed an elevated white blood cell count (WBC): 545,000/mm³. PNN: 49,050/mm³, hemoglobin: 11.6g/dl, platelets: 328,000/mm³. The patient's peripheral blood smear revealed marked leukocytosis with a significant number of immature myeloid precursors and 21% blasts. The analysis of the BCR-ABL shows 94% in the peripheral blood. The patient was diagnosed with CML. She received a chemotherapy protocol made of hyperalkalinisation, allopurinol, hydroxyurea and a treatment based on imatinib at the dose of 400mg per day. Patient achieved complete hematological remission at three months and complete cytogenetic remission at 12 months. The patient was readmitted into our pediatric department with complains of severe headache, vomiting, pain and bilateral visual loss since three days. On examination, patient was afebrile and appeared pale. Blood pressure was 100/60mm/hg and the heart rate 98 beat/minute. There was no lymphadenopathy and the nervous system examination was normal. Intraocular muscle testing was normal; however, there was an exophthalmia in both eyes. The pupil was sluggish to react to light. Fundoscopy revealed bilateral stade III disc edema and hemorrhages of the retina. She underwent a brain computed tomography (CT) scan with the suspicion of leukemic involvement or any other intracranial event (cerebral edema); however, nothing was found. A subsequent bone marrow exam showed no morphologic or molecular evidence of CML or acute leukemia. Cytological evaluation of cerebrospinal fluid (CSF) was also negative. The patient had no other known pathology that could be held responsible for retina edema. We suggested that it was a side effect of imatinib so its administration was temporary interrupted. The patient was put on an anti-edema therapy (mannitol, dexamethasone). However, few months later, the patient presented in the emergency room with a headache and severe vomiting. She described a recurrence of the same character of headaches accompanied with weakness of extremities and seizures. Nervous system examination revealed neck rigidity, presence of meningeal signs and lower limb paraplegia. CT of the brain revealed subdural chronic hematoma and a serpenginous gyriform enhancement around the contusion in the right parietal and occipital lobes. Analysis of the CSF collected showed lymphoblasts in a WBC count of 11000cells/ml. Flow cytometry of the CSF showed that blast cells were positive for a cluster of differentiation markers (CD) (CD34, CD19, CD10, CD22 and partially positive for CD45) confirming CNS extramedullary lymphoid blast infiltration. A bone marrow aspiration was done to evaluate the status of her chronic myelogenous leukemia and result was consistent with a chronic phase. Fundus examination showed bilateral optic atrophy.
The diagnosis of extramedullary isolated CNS blast crises (lymphoid type) was based on the presence of blasts in CSF (confirmed by flow cytometry).
The patient received a high-dose systemic induction chemotherapy and intrathecal therapy (methotrexate, arabinoside and dexamethasone). The imatinib was replaced by dasatinib at the dose of 100 mg per day. She was treated with 24 Gy of whole-brain radiation therapy.
Allogenic stem cell transplantation was not feasible. We noticed a rapidly progressive amelioration in her neurological status after finishing systemic chemotherapy and physical therapy; however, the patient's visual loss showed no signs of improvement.
| EN100543 |
Fundus examination showed bilateral optic atrophy. | [
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] | A 12-year-old girl presented an abdominal pain, high persistent fever of (40°C) and severe fatigue. The physical exam revealed pallor, hepatomegaly, and grade III splenomegaly. The investigation revealed an elevated white blood cell count (WBC): 545,000/mm³. PNN: 49,050/mm³, hemoglobin: 11.6g/dl, platelets: 328,000/mm³. The patient's peripheral blood smear revealed marked leukocytosis with a significant number of immature myeloid precursors and 21% blasts. The analysis of the BCR-ABL shows 94% in the peripheral blood. The patient was diagnosed with CML. She received a chemotherapy protocol made of hyperalkalinisation, allopurinol, hydroxyurea and a treatment based on imatinib at the dose of 400mg per day. Patient achieved complete hematological remission at three months and complete cytogenetic remission at 12 months. The patient was readmitted into our pediatric department with complains of severe headache, vomiting, pain and bilateral visual loss since three days. On examination, patient was afebrile and appeared pale. Blood pressure was 100/60mm/hg and the heart rate 98 beat/minute. There was no lymphadenopathy and the nervous system examination was normal. Intraocular muscle testing was normal; however, there was an exophthalmia in both eyes. The pupil was sluggish to react to light. Fundoscopy revealed bilateral stade III disc edema and hemorrhages of the retina. She underwent a brain computed tomography (CT) scan with the suspicion of leukemic involvement or any other intracranial event (cerebral edema); however, nothing was found. A subsequent bone marrow exam showed no morphologic or molecular evidence of CML or acute leukemia. Cytological evaluation of cerebrospinal fluid (CSF) was also negative. The patient had no other known pathology that could be held responsible for retina edema. We suggested that it was a side effect of imatinib so its administration was temporary interrupted. The patient was put on an anti-edema therapy (mannitol, dexamethasone). However, few months later, the patient presented in the emergency room with a headache and severe vomiting. She described a recurrence of the same character of headaches accompanied with weakness of extremities and seizures. Nervous system examination revealed neck rigidity, presence of meningeal signs and lower limb paraplegia. CT of the brain revealed subdural chronic hematoma and a serpenginous gyriform enhancement around the contusion in the right parietal and occipital lobes. Analysis of the CSF collected showed lymphoblasts in a WBC count of 11000cells/ml. Flow cytometry of the CSF showed that blast cells were positive for a cluster of differentiation markers (CD) (CD34, CD19, CD10, CD22 and partially positive for CD45) confirming CNS extramedullary lymphoid blast infiltration. A bone marrow aspiration was done to evaluate the status of her chronic myelogenous leukemia and result was consistent with a chronic phase. Fundus examination showed bilateral optic atrophy.
The diagnosis of extramedullary isolated CNS blast crises (lymphoid type) was based on the presence of blasts in CSF (confirmed by flow cytometry).
The patient received a high-dose systemic induction chemotherapy and intrathecal therapy (methotrexate, arabinoside and dexamethasone). The imatinib was replaced by dasatinib at the dose of 100 mg per day. She was treated with 24 Gy of whole-brain radiation therapy.
Allogenic stem cell transplantation was not feasible. We noticed a rapidly progressive amelioration in her neurological status after finishing systemic chemotherapy and physical therapy; however, the patient's visual loss showed no signs of improvement.
| EN100543 |
The diagnosis of extramedullary isolated CNS blast crises (lymphoid type) was based on the presence of blasts in CSF (confirmed by flow cytometry). | [
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The diagnosis of extramedullary isolated CNS blast crises (lymphoid type) was based on the presence of blasts in CSF (confirmed by flow cytometry).
The patient received a high-dose systemic induction chemotherapy and intrathecal therapy (methotrexate, arabinoside and dexamethasone). The imatinib was replaced by dasatinib at the dose of 100 mg per day. She was treated with 24 Gy of whole-brain radiation therapy.
Allogenic stem cell transplantation was not feasible. We noticed a rapidly progressive amelioration in her neurological status after finishing systemic chemotherapy and physical therapy; however, the patient's visual loss showed no signs of improvement.
| EN100543 |
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The diagnosis of extramedullary isolated CNS blast crises (lymphoid type) was based on the presence of blasts in CSF (confirmed by flow cytometry).
The patient received a high-dose systemic induction chemotherapy and intrathecal therapy (methotrexate, arabinoside and dexamethasone). The imatinib was replaced by dasatinib at the dose of 100 mg per day. She was treated with 24 Gy of whole-brain radiation therapy.
Allogenic stem cell transplantation was not feasible. We noticed a rapidly progressive amelioration in her neurological status after finishing systemic chemotherapy and physical therapy; however, the patient's visual loss showed no signs of improvement.
| EN100543 |
The imatinib was replaced by dasatinib at the dose of 100 mg per day. | [
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The diagnosis of extramedullary isolated CNS blast crises (lymphoid type) was based on the presence of blasts in CSF (confirmed by flow cytometry).
The patient received a high-dose systemic induction chemotherapy and intrathecal therapy (methotrexate, arabinoside and dexamethasone). The imatinib was replaced by dasatinib at the dose of 100 mg per day. She was treated with 24 Gy of whole-brain radiation therapy.
Allogenic stem cell transplantation was not feasible. We noticed a rapidly progressive amelioration in her neurological status after finishing systemic chemotherapy and physical therapy; however, the patient's visual loss showed no signs of improvement.
| EN100543 |
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The patient received a high-dose systemic induction chemotherapy and intrathecal therapy (methotrexate, arabinoside and dexamethasone). The imatinib was replaced by dasatinib at the dose of 100 mg per day. She was treated with 24 Gy of whole-brain radiation therapy.
Allogenic stem cell transplantation was not feasible. We noticed a rapidly progressive amelioration in her neurological status after finishing systemic chemotherapy and physical therapy; however, the patient's visual loss showed no signs of improvement.
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The diagnosis of extramedullary isolated CNS blast crises (lymphoid type) was based on the presence of blasts in CSF (confirmed by flow cytometry).
The patient received a high-dose systemic induction chemotherapy and intrathecal therapy (methotrexate, arabinoside and dexamethasone). The imatinib was replaced by dasatinib at the dose of 100 mg per day. She was treated with 24 Gy of whole-brain radiation therapy.
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| EN100543 |
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The diagnosis of extramedullary isolated CNS blast crises (lymphoid type) was based on the presence of blasts in CSF (confirmed by flow cytometry).
The patient received a high-dose systemic induction chemotherapy and intrathecal therapy (methotrexate, arabinoside and dexamethasone). The imatinib was replaced by dasatinib at the dose of 100 mg per day. She was treated with 24 Gy of whole-brain radiation therapy.
Allogenic stem cell transplantation was not feasible. We noticed a rapidly progressive amelioration in her neurological status after finishing systemic chemotherapy and physical therapy; however, the patient's visual loss showed no signs of improvement.
| EN100543 |
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] | A male patient, born in 1973, fell off the balcony while on holidays in Crete in 1993 and developed complete tetraplegia at C-5 level. In 1996, deafferentation of sacral nerve roots 2, 3 and 4 were carried out bilaterally. Brindley sacral anterior root stimulator was implanted. On eleventh post-operative day, blood stained fluid came out of sacral wound. Microbiology of exudates showed growth of Pseudomonas aeruginosa, sensitive to gentamicin. As discharge of serosanguinous fluid persisted, sacral wound was explored. In March 1997, induration and craggy swelling were noted at the site of receiver. There was discharge from the surgical wound in the back. Wound swab grew Pseudomonas aeruginosa. The receiver was taken out. Cables were retrieved and tunnelled in left flank. Laminectomy wound was left open. In May 1997, cables were removed from left flank through the laminectomy wound. Grommet was sliced down as much as possible without producing leak of cerebrospinal fluid. Histoacryl glue was used over the truncated grommet as a sealing agent. Microbiology of end of S-2 and S-3 cables showed growth of Pseudomonas aeruginosa, which was sensitive to gentamicin. End of S-4 cable showed scanty growth of Pseudomonas aeruginosa and Klebsiella aerogenes. Review of this patient in January 1999 revealed presence of sinuses in dorsal wound exuding purulent material. The wound was explored; grommet and electrodes were removed. The consequences of failed implantation were severe constipation and loss of reflex penile erection and bladder emptying. This patient had to spend increasing amount of time for bowels management. Faecal incontinence limited his mobility. The problem with his bowels was affecting his confidence in doing anything, as the slightest movement could cause his bowels to work. The inconvenience and embarrassment of a bowel accident caused distress to the patient and to his mother.
| EN108254 |
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] | A male patient, born in 1973, fell off the balcony while on holidays in Crete in 1993 and developed complete tetraplegia at C-5 level. In 1996, deafferentation of sacral nerve roots 2, 3 and 4 were carried out bilaterally. Brindley sacral anterior root stimulator was implanted. On eleventh post-operative day, blood stained fluid came out of sacral wound. Microbiology of exudates showed growth of Pseudomonas aeruginosa, sensitive to gentamicin. As discharge of serosanguinous fluid persisted, sacral wound was explored. In March 1997, induration and craggy swelling were noted at the site of receiver. There was discharge from the surgical wound in the back. Wound swab grew Pseudomonas aeruginosa. The receiver was taken out. Cables were retrieved and tunnelled in left flank. Laminectomy wound was left open. In May 1997, cables were removed from left flank through the laminectomy wound. Grommet was sliced down as much as possible without producing leak of cerebrospinal fluid. Histoacryl glue was used over the truncated grommet as a sealing agent. Microbiology of end of S-2 and S-3 cables showed growth of Pseudomonas aeruginosa, which was sensitive to gentamicin. End of S-4 cable showed scanty growth of Pseudomonas aeruginosa and Klebsiella aerogenes. Review of this patient in January 1999 revealed presence of sinuses in dorsal wound exuding purulent material. The wound was explored; grommet and electrodes were removed. The consequences of failed implantation were severe constipation and loss of reflex penile erection and bladder emptying. This patient had to spend increasing amount of time for bowels management. Faecal incontinence limited his mobility. The problem with his bowels was affecting his confidence in doing anything, as the slightest movement could cause his bowels to work. The inconvenience and embarrassment of a bowel accident caused distress to the patient and to his mother.
| EN108254 |
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] | A male patient, born in 1973, fell off the balcony while on holidays in Crete in 1993 and developed complete tetraplegia at C-5 level. In 1996, deafferentation of sacral nerve roots 2, 3 and 4 were carried out bilaterally. Brindley sacral anterior root stimulator was implanted. On eleventh post-operative day, blood stained fluid came out of sacral wound. Microbiology of exudates showed growth of Pseudomonas aeruginosa, sensitive to gentamicin. As discharge of serosanguinous fluid persisted, sacral wound was explored. In March 1997, induration and craggy swelling were noted at the site of receiver. There was discharge from the surgical wound in the back. Wound swab grew Pseudomonas aeruginosa. The receiver was taken out. Cables were retrieved and tunnelled in left flank. Laminectomy wound was left open. In May 1997, cables were removed from left flank through the laminectomy wound. Grommet was sliced down as much as possible without producing leak of cerebrospinal fluid. Histoacryl glue was used over the truncated grommet as a sealing agent. Microbiology of end of S-2 and S-3 cables showed growth of Pseudomonas aeruginosa, which was sensitive to gentamicin. End of S-4 cable showed scanty growth of Pseudomonas aeruginosa and Klebsiella aerogenes. Review of this patient in January 1999 revealed presence of sinuses in dorsal wound exuding purulent material. The wound was explored; grommet and electrodes were removed. The consequences of failed implantation were severe constipation and loss of reflex penile erection and bladder emptying. This patient had to spend increasing amount of time for bowels management. Faecal incontinence limited his mobility. The problem with his bowels was affecting his confidence in doing anything, as the slightest movement could cause his bowels to work. The inconvenience and embarrassment of a bowel accident caused distress to the patient and to his mother.
| EN108254 |
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] | A male patient, born in 1973, fell off the balcony while on holidays in Crete in 1993 and developed complete tetraplegia at C-5 level. In 1996, deafferentation of sacral nerve roots 2, 3 and 4 were carried out bilaterally. Brindley sacral anterior root stimulator was implanted. On eleventh post-operative day, blood stained fluid came out of sacral wound. Microbiology of exudates showed growth of Pseudomonas aeruginosa, sensitive to gentamicin. As discharge of serosanguinous fluid persisted, sacral wound was explored. In March 1997, induration and craggy swelling were noted at the site of receiver. There was discharge from the surgical wound in the back. Wound swab grew Pseudomonas aeruginosa. The receiver was taken out. Cables were retrieved and tunnelled in left flank. Laminectomy wound was left open. In May 1997, cables were removed from left flank through the laminectomy wound. Grommet was sliced down as much as possible without producing leak of cerebrospinal fluid. Histoacryl glue was used over the truncated grommet as a sealing agent. Microbiology of end of S-2 and S-3 cables showed growth of Pseudomonas aeruginosa, which was sensitive to gentamicin. End of S-4 cable showed scanty growth of Pseudomonas aeruginosa and Klebsiella aerogenes. Review of this patient in January 1999 revealed presence of sinuses in dorsal wound exuding purulent material. The wound was explored; grommet and electrodes were removed. The consequences of failed implantation were severe constipation and loss of reflex penile erection and bladder emptying. This patient had to spend increasing amount of time for bowels management. Faecal incontinence limited his mobility. The problem with his bowels was affecting his confidence in doing anything, as the slightest movement could cause his bowels to work. The inconvenience and embarrassment of a bowel accident caused distress to the patient and to his mother.
| EN108254 |
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] | A male patient, born in 1973, fell off the balcony while on holidays in Crete in 1993 and developed complete tetraplegia at C-5 level. In 1996, deafferentation of sacral nerve roots 2, 3 and 4 were carried out bilaterally. Brindley sacral anterior root stimulator was implanted. On eleventh post-operative day, blood stained fluid came out of sacral wound. Microbiology of exudates showed growth of Pseudomonas aeruginosa, sensitive to gentamicin. As discharge of serosanguinous fluid persisted, sacral wound was explored. In March 1997, induration and craggy swelling were noted at the site of receiver. There was discharge from the surgical wound in the back. Wound swab grew Pseudomonas aeruginosa. The receiver was taken out. Cables were retrieved and tunnelled in left flank. Laminectomy wound was left open. In May 1997, cables were removed from left flank through the laminectomy wound. Grommet was sliced down as much as possible without producing leak of cerebrospinal fluid. Histoacryl glue was used over the truncated grommet as a sealing agent. Microbiology of end of S-2 and S-3 cables showed growth of Pseudomonas aeruginosa, which was sensitive to gentamicin. End of S-4 cable showed scanty growth of Pseudomonas aeruginosa and Klebsiella aerogenes. Review of this patient in January 1999 revealed presence of sinuses in dorsal wound exuding purulent material. The wound was explored; grommet and electrodes were removed. The consequences of failed implantation were severe constipation and loss of reflex penile erection and bladder emptying. This patient had to spend increasing amount of time for bowels management. Faecal incontinence limited his mobility. The problem with his bowels was affecting his confidence in doing anything, as the slightest movement could cause his bowels to work. The inconvenience and embarrassment of a bowel accident caused distress to the patient and to his mother.
| EN108254 |
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] | A male patient, born in 1973, fell off the balcony while on holidays in Crete in 1993 and developed complete tetraplegia at C-5 level. In 1996, deafferentation of sacral nerve roots 2, 3 and 4 were carried out bilaterally. Brindley sacral anterior root stimulator was implanted. On eleventh post-operative day, blood stained fluid came out of sacral wound. Microbiology of exudates showed growth of Pseudomonas aeruginosa, sensitive to gentamicin. As discharge of serosanguinous fluid persisted, sacral wound was explored. In March 1997, induration and craggy swelling were noted at the site of receiver. There was discharge from the surgical wound in the back. Wound swab grew Pseudomonas aeruginosa. The receiver was taken out. Cables were retrieved and tunnelled in left flank. Laminectomy wound was left open. In May 1997, cables were removed from left flank through the laminectomy wound. Grommet was sliced down as much as possible without producing leak of cerebrospinal fluid. Histoacryl glue was used over the truncated grommet as a sealing agent. Microbiology of end of S-2 and S-3 cables showed growth of Pseudomonas aeruginosa, which was sensitive to gentamicin. End of S-4 cable showed scanty growth of Pseudomonas aeruginosa and Klebsiella aerogenes. Review of this patient in January 1999 revealed presence of sinuses in dorsal wound exuding purulent material. The wound was explored; grommet and electrodes were removed. The consequences of failed implantation were severe constipation and loss of reflex penile erection and bladder emptying. This patient had to spend increasing amount of time for bowels management. Faecal incontinence limited his mobility. The problem with his bowels was affecting his confidence in doing anything, as the slightest movement could cause his bowels to work. The inconvenience and embarrassment of a bowel accident caused distress to the patient and to his mother.
| EN108254 |
The receiver was taken out. | [
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] | A male patient, born in 1973, fell off the balcony while on holidays in Crete in 1993 and developed complete tetraplegia at C-5 level. In 1996, deafferentation of sacral nerve roots 2, 3 and 4 were carried out bilaterally. Brindley sacral anterior root stimulator was implanted. On eleventh post-operative day, blood stained fluid came out of sacral wound. Microbiology of exudates showed growth of Pseudomonas aeruginosa, sensitive to gentamicin. As discharge of serosanguinous fluid persisted, sacral wound was explored. In March 1997, induration and craggy swelling were noted at the site of receiver. There was discharge from the surgical wound in the back. Wound swab grew Pseudomonas aeruginosa. The receiver was taken out. Cables were retrieved and tunnelled in left flank. Laminectomy wound was left open. In May 1997, cables were removed from left flank through the laminectomy wound. Grommet was sliced down as much as possible without producing leak of cerebrospinal fluid. Histoacryl glue was used over the truncated grommet as a sealing agent. Microbiology of end of S-2 and S-3 cables showed growth of Pseudomonas aeruginosa, which was sensitive to gentamicin. End of S-4 cable showed scanty growth of Pseudomonas aeruginosa and Klebsiella aerogenes. Review of this patient in January 1999 revealed presence of sinuses in dorsal wound exuding purulent material. The wound was explored; grommet and electrodes were removed. The consequences of failed implantation were severe constipation and loss of reflex penile erection and bladder emptying. This patient had to spend increasing amount of time for bowels management. Faecal incontinence limited his mobility. The problem with his bowels was affecting his confidence in doing anything, as the slightest movement could cause his bowels to work. The inconvenience and embarrassment of a bowel accident caused distress to the patient and to his mother.
| EN108254 |
Cables were retrieved and tunnelled in left flank. | [
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| EN108254 |
Laminectomy wound was left open. | [
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] | A male patient, born in 1973, fell off the balcony while on holidays in Crete in 1993 and developed complete tetraplegia at C-5 level. In 1996, deafferentation of sacral nerve roots 2, 3 and 4 were carried out bilaterally. Brindley sacral anterior root stimulator was implanted. On eleventh post-operative day, blood stained fluid came out of sacral wound. Microbiology of exudates showed growth of Pseudomonas aeruginosa, sensitive to gentamicin. As discharge of serosanguinous fluid persisted, sacral wound was explored. In March 1997, induration and craggy swelling were noted at the site of receiver. There was discharge from the surgical wound in the back. Wound swab grew Pseudomonas aeruginosa. The receiver was taken out. Cables were retrieved and tunnelled in left flank. Laminectomy wound was left open. In May 1997, cables were removed from left flank through the laminectomy wound. Grommet was sliced down as much as possible without producing leak of cerebrospinal fluid. Histoacryl glue was used over the truncated grommet as a sealing agent. Microbiology of end of S-2 and S-3 cables showed growth of Pseudomonas aeruginosa, which was sensitive to gentamicin. End of S-4 cable showed scanty growth of Pseudomonas aeruginosa and Klebsiella aerogenes. Review of this patient in January 1999 revealed presence of sinuses in dorsal wound exuding purulent material. The wound was explored; grommet and electrodes were removed. The consequences of failed implantation were severe constipation and loss of reflex penile erection and bladder emptying. This patient had to spend increasing amount of time for bowels management. Faecal incontinence limited his mobility. The problem with his bowels was affecting his confidence in doing anything, as the slightest movement could cause his bowels to work. The inconvenience and embarrassment of a bowel accident caused distress to the patient and to his mother.
| EN108254 |
In May 1997, cables were removed from left flank through the laminectomy wound. | [
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] | A male patient, born in 1973, fell off the balcony while on holidays in Crete in 1993 and developed complete tetraplegia at C-5 level. In 1996, deafferentation of sacral nerve roots 2, 3 and 4 were carried out bilaterally. Brindley sacral anterior root stimulator was implanted. On eleventh post-operative day, blood stained fluid came out of sacral wound. Microbiology of exudates showed growth of Pseudomonas aeruginosa, sensitive to gentamicin. As discharge of serosanguinous fluid persisted, sacral wound was explored. In March 1997, induration and craggy swelling were noted at the site of receiver. There was discharge from the surgical wound in the back. Wound swab grew Pseudomonas aeruginosa. The receiver was taken out. Cables were retrieved and tunnelled in left flank. Laminectomy wound was left open. In May 1997, cables were removed from left flank through the laminectomy wound. Grommet was sliced down as much as possible without producing leak of cerebrospinal fluid. Histoacryl glue was used over the truncated grommet as a sealing agent. Microbiology of end of S-2 and S-3 cables showed growth of Pseudomonas aeruginosa, which was sensitive to gentamicin. End of S-4 cable showed scanty growth of Pseudomonas aeruginosa and Klebsiella aerogenes. Review of this patient in January 1999 revealed presence of sinuses in dorsal wound exuding purulent material. The wound was explored; grommet and electrodes were removed. The consequences of failed implantation were severe constipation and loss of reflex penile erection and bladder emptying. This patient had to spend increasing amount of time for bowels management. Faecal incontinence limited his mobility. The problem with his bowels was affecting his confidence in doing anything, as the slightest movement could cause his bowels to work. The inconvenience and embarrassment of a bowel accident caused distress to the patient and to his mother.
| EN108254 |
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] | A male patient, born in 1973, fell off the balcony while on holidays in Crete in 1993 and developed complete tetraplegia at C-5 level. In 1996, deafferentation of sacral nerve roots 2, 3 and 4 were carried out bilaterally. Brindley sacral anterior root stimulator was implanted. On eleventh post-operative day, blood stained fluid came out of sacral wound. Microbiology of exudates showed growth of Pseudomonas aeruginosa, sensitive to gentamicin. As discharge of serosanguinous fluid persisted, sacral wound was explored. In March 1997, induration and craggy swelling were noted at the site of receiver. There was discharge from the surgical wound in the back. Wound swab grew Pseudomonas aeruginosa. The receiver was taken out. Cables were retrieved and tunnelled in left flank. Laminectomy wound was left open. In May 1997, cables were removed from left flank through the laminectomy wound. Grommet was sliced down as much as possible without producing leak of cerebrospinal fluid. Histoacryl glue was used over the truncated grommet as a sealing agent. Microbiology of end of S-2 and S-3 cables showed growth of Pseudomonas aeruginosa, which was sensitive to gentamicin. End of S-4 cable showed scanty growth of Pseudomonas aeruginosa and Klebsiella aerogenes. Review of this patient in January 1999 revealed presence of sinuses in dorsal wound exuding purulent material. The wound was explored; grommet and electrodes were removed. The consequences of failed implantation were severe constipation and loss of reflex penile erection and bladder emptying. This patient had to spend increasing amount of time for bowels management. Faecal incontinence limited his mobility. The problem with his bowels was affecting his confidence in doing anything, as the slightest movement could cause his bowels to work. The inconvenience and embarrassment of a bowel accident caused distress to the patient and to his mother.
| EN108254 |
Histoacryl glue was used over the truncated grommet as a sealing agent. | [
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| EN108254 |
Microbiology of end of S-2 and S-3 cables showed growth of Pseudomonas aeruginosa, which was sensitive to gentamicin. | [
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] | A male patient, born in 1973, fell off the balcony while on holidays in Crete in 1993 and developed complete tetraplegia at C-5 level. In 1996, deafferentation of sacral nerve roots 2, 3 and 4 were carried out bilaterally. Brindley sacral anterior root stimulator was implanted. On eleventh post-operative day, blood stained fluid came out of sacral wound. Microbiology of exudates showed growth of Pseudomonas aeruginosa, sensitive to gentamicin. As discharge of serosanguinous fluid persisted, sacral wound was explored. In March 1997, induration and craggy swelling were noted at the site of receiver. There was discharge from the surgical wound in the back. Wound swab grew Pseudomonas aeruginosa. The receiver was taken out. Cables were retrieved and tunnelled in left flank. Laminectomy wound was left open. In May 1997, cables were removed from left flank through the laminectomy wound. Grommet was sliced down as much as possible without producing leak of cerebrospinal fluid. Histoacryl glue was used over the truncated grommet as a sealing agent. Microbiology of end of S-2 and S-3 cables showed growth of Pseudomonas aeruginosa, which was sensitive to gentamicin. End of S-4 cable showed scanty growth of Pseudomonas aeruginosa and Klebsiella aerogenes. Review of this patient in January 1999 revealed presence of sinuses in dorsal wound exuding purulent material. The wound was explored; grommet and electrodes were removed. The consequences of failed implantation were severe constipation and loss of reflex penile erection and bladder emptying. This patient had to spend increasing amount of time for bowels management. Faecal incontinence limited his mobility. The problem with his bowels was affecting his confidence in doing anything, as the slightest movement could cause his bowels to work. The inconvenience and embarrassment of a bowel accident caused distress to the patient and to his mother.
| EN108254 |
End of S-4 cable showed scanty growth of Pseudomonas aeruginosa and Klebsiella aerogenes. | [
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] | A male patient, born in 1973, fell off the balcony while on holidays in Crete in 1993 and developed complete tetraplegia at C-5 level. In 1996, deafferentation of sacral nerve roots 2, 3 and 4 were carried out bilaterally. Brindley sacral anterior root stimulator was implanted. On eleventh post-operative day, blood stained fluid came out of sacral wound. Microbiology of exudates showed growth of Pseudomonas aeruginosa, sensitive to gentamicin. As discharge of serosanguinous fluid persisted, sacral wound was explored. In March 1997, induration and craggy swelling were noted at the site of receiver. There was discharge from the surgical wound in the back. Wound swab grew Pseudomonas aeruginosa. The receiver was taken out. Cables were retrieved and tunnelled in left flank. Laminectomy wound was left open. In May 1997, cables were removed from left flank through the laminectomy wound. Grommet was sliced down as much as possible without producing leak of cerebrospinal fluid. Histoacryl glue was used over the truncated grommet as a sealing agent. Microbiology of end of S-2 and S-3 cables showed growth of Pseudomonas aeruginosa, which was sensitive to gentamicin. End of S-4 cable showed scanty growth of Pseudomonas aeruginosa and Klebsiella aerogenes. Review of this patient in January 1999 revealed presence of sinuses in dorsal wound exuding purulent material. The wound was explored; grommet and electrodes were removed. The consequences of failed implantation were severe constipation and loss of reflex penile erection and bladder emptying. This patient had to spend increasing amount of time for bowels management. Faecal incontinence limited his mobility. The problem with his bowels was affecting his confidence in doing anything, as the slightest movement could cause his bowels to work. The inconvenience and embarrassment of a bowel accident caused distress to the patient and to his mother.
| EN108254 |
Review of this patient in January 1999 revealed presence of sinuses in dorsal wound exuding purulent material. | [
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] | A male patient, born in 1973, fell off the balcony while on holidays in Crete in 1993 and developed complete tetraplegia at C-5 level. In 1996, deafferentation of sacral nerve roots 2, 3 and 4 were carried out bilaterally. Brindley sacral anterior root stimulator was implanted. On eleventh post-operative day, blood stained fluid came out of sacral wound. Microbiology of exudates showed growth of Pseudomonas aeruginosa, sensitive to gentamicin. As discharge of serosanguinous fluid persisted, sacral wound was explored. In March 1997, induration and craggy swelling were noted at the site of receiver. There was discharge from the surgical wound in the back. Wound swab grew Pseudomonas aeruginosa. The receiver was taken out. Cables were retrieved and tunnelled in left flank. Laminectomy wound was left open. In May 1997, cables were removed from left flank through the laminectomy wound. Grommet was sliced down as much as possible without producing leak of cerebrospinal fluid. Histoacryl glue was used over the truncated grommet as a sealing agent. Microbiology of end of S-2 and S-3 cables showed growth of Pseudomonas aeruginosa, which was sensitive to gentamicin. End of S-4 cable showed scanty growth of Pseudomonas aeruginosa and Klebsiella aerogenes. Review of this patient in January 1999 revealed presence of sinuses in dorsal wound exuding purulent material. The wound was explored; grommet and electrodes were removed. The consequences of failed implantation were severe constipation and loss of reflex penile erection and bladder emptying. This patient had to spend increasing amount of time for bowels management. Faecal incontinence limited his mobility. The problem with his bowels was affecting his confidence in doing anything, as the slightest movement could cause his bowels to work. The inconvenience and embarrassment of a bowel accident caused distress to the patient and to his mother.
| EN108254 |
The wound was explored; grommet and electrodes were removed. | [
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] | A male patient, born in 1973, fell off the balcony while on holidays in Crete in 1993 and developed complete tetraplegia at C-5 level. In 1996, deafferentation of sacral nerve roots 2, 3 and 4 were carried out bilaterally. Brindley sacral anterior root stimulator was implanted. On eleventh post-operative day, blood stained fluid came out of sacral wound. Microbiology of exudates showed growth of Pseudomonas aeruginosa, sensitive to gentamicin. As discharge of serosanguinous fluid persisted, sacral wound was explored. In March 1997, induration and craggy swelling were noted at the site of receiver. There was discharge from the surgical wound in the back. Wound swab grew Pseudomonas aeruginosa. The receiver was taken out. Cables were retrieved and tunnelled in left flank. Laminectomy wound was left open. In May 1997, cables were removed from left flank through the laminectomy wound. Grommet was sliced down as much as possible without producing leak of cerebrospinal fluid. Histoacryl glue was used over the truncated grommet as a sealing agent. Microbiology of end of S-2 and S-3 cables showed growth of Pseudomonas aeruginosa, which was sensitive to gentamicin. End of S-4 cable showed scanty growth of Pseudomonas aeruginosa and Klebsiella aerogenes. Review of this patient in January 1999 revealed presence of sinuses in dorsal wound exuding purulent material. The wound was explored; grommet and electrodes were removed. The consequences of failed implantation were severe constipation and loss of reflex penile erection and bladder emptying. This patient had to spend increasing amount of time for bowels management. Faecal incontinence limited his mobility. The problem with his bowels was affecting his confidence in doing anything, as the slightest movement could cause his bowels to work. The inconvenience and embarrassment of a bowel accident caused distress to the patient and to his mother.
| EN108254 |
The consequences of failed implantation were severe constipation and loss of reflex penile erection and bladder emptying. | [
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] | A male patient, born in 1973, fell off the balcony while on holidays in Crete in 1993 and developed complete tetraplegia at C-5 level. In 1996, deafferentation of sacral nerve roots 2, 3 and 4 were carried out bilaterally. Brindley sacral anterior root stimulator was implanted. On eleventh post-operative day, blood stained fluid came out of sacral wound. Microbiology of exudates showed growth of Pseudomonas aeruginosa, sensitive to gentamicin. As discharge of serosanguinous fluid persisted, sacral wound was explored. In March 1997, induration and craggy swelling were noted at the site of receiver. There was discharge from the surgical wound in the back. Wound swab grew Pseudomonas aeruginosa. The receiver was taken out. Cables were retrieved and tunnelled in left flank. Laminectomy wound was left open. In May 1997, cables were removed from left flank through the laminectomy wound. Grommet was sliced down as much as possible without producing leak of cerebrospinal fluid. Histoacryl glue was used over the truncated grommet as a sealing agent. Microbiology of end of S-2 and S-3 cables showed growth of Pseudomonas aeruginosa, which was sensitive to gentamicin. End of S-4 cable showed scanty growth of Pseudomonas aeruginosa and Klebsiella aerogenes. Review of this patient in January 1999 revealed presence of sinuses in dorsal wound exuding purulent material. The wound was explored; grommet and electrodes were removed. The consequences of failed implantation were severe constipation and loss of reflex penile erection and bladder emptying. This patient had to spend increasing amount of time for bowels management. Faecal incontinence limited his mobility. The problem with his bowels was affecting his confidence in doing anything, as the slightest movement could cause his bowels to work. The inconvenience and embarrassment of a bowel accident caused distress to the patient and to his mother.
| EN108254 |
This patient had to spend increasing amount of time for bowels management. | [
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] | A male patient, born in 1973, fell off the balcony while on holidays in Crete in 1993 and developed complete tetraplegia at C-5 level. In 1996, deafferentation of sacral nerve roots 2, 3 and 4 were carried out bilaterally. Brindley sacral anterior root stimulator was implanted. On eleventh post-operative day, blood stained fluid came out of sacral wound. Microbiology of exudates showed growth of Pseudomonas aeruginosa, sensitive to gentamicin. As discharge of serosanguinous fluid persisted, sacral wound was explored. In March 1997, induration and craggy swelling were noted at the site of receiver. There was discharge from the surgical wound in the back. Wound swab grew Pseudomonas aeruginosa. The receiver was taken out. Cables were retrieved and tunnelled in left flank. Laminectomy wound was left open. In May 1997, cables were removed from left flank through the laminectomy wound. Grommet was sliced down as much as possible without producing leak of cerebrospinal fluid. Histoacryl glue was used over the truncated grommet as a sealing agent. Microbiology of end of S-2 and S-3 cables showed growth of Pseudomonas aeruginosa, which was sensitive to gentamicin. End of S-4 cable showed scanty growth of Pseudomonas aeruginosa and Klebsiella aerogenes. Review of this patient in January 1999 revealed presence of sinuses in dorsal wound exuding purulent material. The wound was explored; grommet and electrodes were removed. The consequences of failed implantation were severe constipation and loss of reflex penile erection and bladder emptying. This patient had to spend increasing amount of time for bowels management. Faecal incontinence limited his mobility. The problem with his bowels was affecting his confidence in doing anything, as the slightest movement could cause his bowels to work. The inconvenience and embarrassment of a bowel accident caused distress to the patient and to his mother.
| EN108254 |
Faecal incontinence limited his mobility. | [
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] | A male patient, born in 1973, fell off the balcony while on holidays in Crete in 1993 and developed complete tetraplegia at C-5 level. In 1996, deafferentation of sacral nerve roots 2, 3 and 4 were carried out bilaterally. Brindley sacral anterior root stimulator was implanted. On eleventh post-operative day, blood stained fluid came out of sacral wound. Microbiology of exudates showed growth of Pseudomonas aeruginosa, sensitive to gentamicin. As discharge of serosanguinous fluid persisted, sacral wound was explored. In March 1997, induration and craggy swelling were noted at the site of receiver. There was discharge from the surgical wound in the back. Wound swab grew Pseudomonas aeruginosa. The receiver was taken out. Cables were retrieved and tunnelled in left flank. Laminectomy wound was left open. In May 1997, cables were removed from left flank through the laminectomy wound. Grommet was sliced down as much as possible without producing leak of cerebrospinal fluid. Histoacryl glue was used over the truncated grommet as a sealing agent. Microbiology of end of S-2 and S-3 cables showed growth of Pseudomonas aeruginosa, which was sensitive to gentamicin. End of S-4 cable showed scanty growth of Pseudomonas aeruginosa and Klebsiella aerogenes. Review of this patient in January 1999 revealed presence of sinuses in dorsal wound exuding purulent material. The wound was explored; grommet and electrodes were removed. The consequences of failed implantation were severe constipation and loss of reflex penile erection and bladder emptying. This patient had to spend increasing amount of time for bowels management. Faecal incontinence limited his mobility. The problem with his bowels was affecting his confidence in doing anything, as the slightest movement could cause his bowels to work. The inconvenience and embarrassment of a bowel accident caused distress to the patient and to his mother.
| EN108254 |
The problem with his bowels was affecting his confidence in doing anything, as the slightest movement could cause his bowels to work. | [
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] | A male patient, born in 1973, fell off the balcony while on holidays in Crete in 1993 and developed complete tetraplegia at C-5 level. In 1996, deafferentation of sacral nerve roots 2, 3 and 4 were carried out bilaterally. Brindley sacral anterior root stimulator was implanted. On eleventh post-operative day, blood stained fluid came out of sacral wound. Microbiology of exudates showed growth of Pseudomonas aeruginosa, sensitive to gentamicin. As discharge of serosanguinous fluid persisted, sacral wound was explored. In March 1997, induration and craggy swelling were noted at the site of receiver. There was discharge from the surgical wound in the back. Wound swab grew Pseudomonas aeruginosa. The receiver was taken out. Cables were retrieved and tunnelled in left flank. Laminectomy wound was left open. In May 1997, cables were removed from left flank through the laminectomy wound. Grommet was sliced down as much as possible without producing leak of cerebrospinal fluid. Histoacryl glue was used over the truncated grommet as a sealing agent. Microbiology of end of S-2 and S-3 cables showed growth of Pseudomonas aeruginosa, which was sensitive to gentamicin. End of S-4 cable showed scanty growth of Pseudomonas aeruginosa and Klebsiella aerogenes. Review of this patient in January 1999 revealed presence of sinuses in dorsal wound exuding purulent material. The wound was explored; grommet and electrodes were removed. The consequences of failed implantation were severe constipation and loss of reflex penile erection and bladder emptying. This patient had to spend increasing amount of time for bowels management. Faecal incontinence limited his mobility. The problem with his bowels was affecting his confidence in doing anything, as the slightest movement could cause his bowels to work. The inconvenience and embarrassment of a bowel accident caused distress to the patient and to his mother.
| EN108254 |
The inconvenience and embarrassment of a bowel accident caused distress to the patient and to his mother. | [
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] | A male patient, born in 1973, fell off the balcony while on holidays in Crete in 1993 and developed complete tetraplegia at C-5 level. In 1996, deafferentation of sacral nerve roots 2, 3 and 4 were carried out bilaterally. Brindley sacral anterior root stimulator was implanted. On eleventh post-operative day, blood stained fluid came out of sacral wound. Microbiology of exudates showed growth of Pseudomonas aeruginosa, sensitive to gentamicin. As discharge of serosanguinous fluid persisted, sacral wound was explored. In March 1997, induration and craggy swelling were noted at the site of receiver. There was discharge from the surgical wound in the back. Wound swab grew Pseudomonas aeruginosa. The receiver was taken out. Cables were retrieved and tunnelled in left flank. Laminectomy wound was left open. In May 1997, cables were removed from left flank through the laminectomy wound. Grommet was sliced down as much as possible without producing leak of cerebrospinal fluid. Histoacryl glue was used over the truncated grommet as a sealing agent. Microbiology of end of S-2 and S-3 cables showed growth of Pseudomonas aeruginosa, which was sensitive to gentamicin. End of S-4 cable showed scanty growth of Pseudomonas aeruginosa and Klebsiella aerogenes. Review of this patient in January 1999 revealed presence of sinuses in dorsal wound exuding purulent material. The wound was explored; grommet and electrodes were removed. The consequences of failed implantation were severe constipation and loss of reflex penile erection and bladder emptying. This patient had to spend increasing amount of time for bowels management. Faecal incontinence limited his mobility. The problem with his bowels was affecting his confidence in doing anything, as the slightest movement could cause his bowels to work. The inconvenience and embarrassment of a bowel accident caused distress to the patient and to his mother.
| EN108254 |
A 38-year-old man presented with a seven month history of progressively worsening bilateral knees pain with associated swelling. | [
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] | A 38-year-old man presented with a seven month history of progressively worsening bilateral knees pain with associated swelling. The pain was present when the patient was at rest, and worsened when the legs was bearing weight, thus restricting his walking to short distances. His knees had become increasingly swollen. He was otherwise fit and well. His medical history was unremarkable and he was only taking a paracetamol, codeine and anti-inflammatory drugs for the pain.
Upon examination, the patient was seen to have visibly swollen popliteal fossa and marked quadriceps wasting of his right lower limb. On palpation, the masses was hard, mobile, well defined, and measured 0.5 - 04 cm. The swelling was non-tender and there were no associated skin changes. He could fully extend his knee, but flexion was restricted to only 110 degrees. There was a McMurray test proved equivocal and no ligamentous instability. An examination of the patient’s hip revealed no abnormality.
A plain radiograph of the patient’s knees revealed multiple calcific densities within the soft tissues surrounding it on the right one. Although some of these appeared to lie within the capsule, the majority appeared to be outside of it, and a solitary image on the left knee. These appearances were thought to be consistent with idiopathic tumoral calcinosis. However, to further scrutinize these calcifications, a magnetic resonance imaging (MRI) scan was recommended. It showed an extensive thickening of the patient’s synovium, multiple intraarticular calcific and ossific loose bodies, and large calcified bursal extensions. These findings were thought to be consistent with very extensive bilateral synovial chondromatosis. The patient’s blood tests were normal: C-reactive protein 5 mg/l and the phosphate calcium balance without errors.
A two-stage procedure was planned following the findings of the MRI scan. The first stage was arthroscopy, which was able to note Grade IV osteoarthritis alongside florid synovial chondromatosis in the lateral compartment of the right knee. There were multiple loose bodies within this compartment and nodules were fixed to the synovium. On the left one, we found an isolated synovial metaplasia in the subvastus quadriceps-sparing. A synovectomy with debridement and excision of these bodies was thus performed.
The second stage involved an open exploration of the patient’s popliteal fossa. Multiple calcified masses were found, all enclosed in bursal sacs. They were lateral to the semimembranosus at the level of the oblique popliteal ligament. All the masses were excised. A histological review confirmed our diagnosis of synovial chondromatosis. The sections showed nests of chondrocytes with focal ossification and focally attenuated synovium overlying the nodules. After the operation, the patient underwent functional rehabilitation sessions focusing on quadriceps strengthening, with a daily exercise regime to supplement this. He recovered well and ten weeks after the operation, has regained his right knee’s full range of movement with flexion increased to 130 degrees, which is equal to that of his left knee.
| EN100156 |
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Upon examination, the patient was seen to have visibly swollen popliteal fossa and marked quadriceps wasting of his right lower limb. On palpation, the masses was hard, mobile, well defined, and measured 0.5 - 04 cm. The swelling was non-tender and there were no associated skin changes. He could fully extend his knee, but flexion was restricted to only 110 degrees. There was a McMurray test proved equivocal and no ligamentous instability. An examination of the patient’s hip revealed no abnormality.
A plain radiograph of the patient’s knees revealed multiple calcific densities within the soft tissues surrounding it on the right one. Although some of these appeared to lie within the capsule, the majority appeared to be outside of it, and a solitary image on the left knee. These appearances were thought to be consistent with idiopathic tumoral calcinosis. However, to further scrutinize these calcifications, a magnetic resonance imaging (MRI) scan was recommended. It showed an extensive thickening of the patient’s synovium, multiple intraarticular calcific and ossific loose bodies, and large calcified bursal extensions. These findings were thought to be consistent with very extensive bilateral synovial chondromatosis. The patient’s blood tests were normal: C-reactive protein 5 mg/l and the phosphate calcium balance without errors.
A two-stage procedure was planned following the findings of the MRI scan. The first stage was arthroscopy, which was able to note Grade IV osteoarthritis alongside florid synovial chondromatosis in the lateral compartment of the right knee. There were multiple loose bodies within this compartment and nodules were fixed to the synovium. On the left one, we found an isolated synovial metaplasia in the subvastus quadriceps-sparing. A synovectomy with debridement and excision of these bodies was thus performed.
The second stage involved an open exploration of the patient’s popliteal fossa. Multiple calcified masses were found, all enclosed in bursal sacs. They were lateral to the semimembranosus at the level of the oblique popliteal ligament. All the masses were excised. A histological review confirmed our diagnosis of synovial chondromatosis. The sections showed nests of chondrocytes with focal ossification and focally attenuated synovium overlying the nodules. After the operation, the patient underwent functional rehabilitation sessions focusing on quadriceps strengthening, with a daily exercise regime to supplement this. He recovered well and ten weeks after the operation, has regained his right knee’s full range of movement with flexion increased to 130 degrees, which is equal to that of his left knee.
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Upon examination, the patient was seen to have visibly swollen popliteal fossa and marked quadriceps wasting of his right lower limb. On palpation, the masses was hard, mobile, well defined, and measured 0.5 - 04 cm. The swelling was non-tender and there were no associated skin changes. He could fully extend his knee, but flexion was restricted to only 110 degrees. There was a McMurray test proved equivocal and no ligamentous instability. An examination of the patient’s hip revealed no abnormality.
A plain radiograph of the patient’s knees revealed multiple calcific densities within the soft tissues surrounding it on the right one. Although some of these appeared to lie within the capsule, the majority appeared to be outside of it, and a solitary image on the left knee. These appearances were thought to be consistent with idiopathic tumoral calcinosis. However, to further scrutinize these calcifications, a magnetic resonance imaging (MRI) scan was recommended. It showed an extensive thickening of the patient’s synovium, multiple intraarticular calcific and ossific loose bodies, and large calcified bursal extensions. These findings were thought to be consistent with very extensive bilateral synovial chondromatosis. The patient’s blood tests were normal: C-reactive protein 5 mg/l and the phosphate calcium balance without errors.
A two-stage procedure was planned following the findings of the MRI scan. The first stage was arthroscopy, which was able to note Grade IV osteoarthritis alongside florid synovial chondromatosis in the lateral compartment of the right knee. There were multiple loose bodies within this compartment and nodules were fixed to the synovium. On the left one, we found an isolated synovial metaplasia in the subvastus quadriceps-sparing. A synovectomy with debridement and excision of these bodies was thus performed.
The second stage involved an open exploration of the patient’s popliteal fossa. Multiple calcified masses were found, all enclosed in bursal sacs. They were lateral to the semimembranosus at the level of the oblique popliteal ligament. All the masses were excised. A histological review confirmed our diagnosis of synovial chondromatosis. The sections showed nests of chondrocytes with focal ossification and focally attenuated synovium overlying the nodules. After the operation, the patient underwent functional rehabilitation sessions focusing on quadriceps strengthening, with a daily exercise regime to supplement this. He recovered well and ten weeks after the operation, has regained his right knee’s full range of movement with flexion increased to 130 degrees, which is equal to that of his left knee.
| EN100156 |
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Upon examination, the patient was seen to have visibly swollen popliteal fossa and marked quadriceps wasting of his right lower limb. On palpation, the masses was hard, mobile, well defined, and measured 0.5 - 04 cm. The swelling was non-tender and there were no associated skin changes. He could fully extend his knee, but flexion was restricted to only 110 degrees. There was a McMurray test proved equivocal and no ligamentous instability. An examination of the patient’s hip revealed no abnormality.
A plain radiograph of the patient’s knees revealed multiple calcific densities within the soft tissues surrounding it on the right one. Although some of these appeared to lie within the capsule, the majority appeared to be outside of it, and a solitary image on the left knee. These appearances were thought to be consistent with idiopathic tumoral calcinosis. However, to further scrutinize these calcifications, a magnetic resonance imaging (MRI) scan was recommended. It showed an extensive thickening of the patient’s synovium, multiple intraarticular calcific and ossific loose bodies, and large calcified bursal extensions. These findings were thought to be consistent with very extensive bilateral synovial chondromatosis. The patient’s blood tests were normal: C-reactive protein 5 mg/l and the phosphate calcium balance without errors.
A two-stage procedure was planned following the findings of the MRI scan. The first stage was arthroscopy, which was able to note Grade IV osteoarthritis alongside florid synovial chondromatosis in the lateral compartment of the right knee. There were multiple loose bodies within this compartment and nodules were fixed to the synovium. On the left one, we found an isolated synovial metaplasia in the subvastus quadriceps-sparing. A synovectomy with debridement and excision of these bodies was thus performed.
The second stage involved an open exploration of the patient’s popliteal fossa. Multiple calcified masses were found, all enclosed in bursal sacs. They were lateral to the semimembranosus at the level of the oblique popliteal ligament. All the masses were excised. A histological review confirmed our diagnosis of synovial chondromatosis. The sections showed nests of chondrocytes with focal ossification and focally attenuated synovium overlying the nodules. After the operation, the patient underwent functional rehabilitation sessions focusing on quadriceps strengthening, with a daily exercise regime to supplement this. He recovered well and ten weeks after the operation, has regained his right knee’s full range of movement with flexion increased to 130 degrees, which is equal to that of his left knee.
| EN100156 |
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Upon examination, the patient was seen to have visibly swollen popliteal fossa and marked quadriceps wasting of his right lower limb. On palpation, the masses was hard, mobile, well defined, and measured 0.5 - 04 cm. The swelling was non-tender and there were no associated skin changes. He could fully extend his knee, but flexion was restricted to only 110 degrees. There was a McMurray test proved equivocal and no ligamentous instability. An examination of the patient’s hip revealed no abnormality.
A plain radiograph of the patient’s knees revealed multiple calcific densities within the soft tissues surrounding it on the right one. Although some of these appeared to lie within the capsule, the majority appeared to be outside of it, and a solitary image on the left knee. These appearances were thought to be consistent with idiopathic tumoral calcinosis. However, to further scrutinize these calcifications, a magnetic resonance imaging (MRI) scan was recommended. It showed an extensive thickening of the patient’s synovium, multiple intraarticular calcific and ossific loose bodies, and large calcified bursal extensions. These findings were thought to be consistent with very extensive bilateral synovial chondromatosis. The patient’s blood tests were normal: C-reactive protein 5 mg/l and the phosphate calcium balance without errors.
A two-stage procedure was planned following the findings of the MRI scan. The first stage was arthroscopy, which was able to note Grade IV osteoarthritis alongside florid synovial chondromatosis in the lateral compartment of the right knee. There were multiple loose bodies within this compartment and nodules were fixed to the synovium. On the left one, we found an isolated synovial metaplasia in the subvastus quadriceps-sparing. A synovectomy with debridement and excision of these bodies was thus performed.
The second stage involved an open exploration of the patient’s popliteal fossa. Multiple calcified masses were found, all enclosed in bursal sacs. They were lateral to the semimembranosus at the level of the oblique popliteal ligament. All the masses were excised. A histological review confirmed our diagnosis of synovial chondromatosis. The sections showed nests of chondrocytes with focal ossification and focally attenuated synovium overlying the nodules. After the operation, the patient underwent functional rehabilitation sessions focusing on quadriceps strengthening, with a daily exercise regime to supplement this. He recovered well and ten weeks after the operation, has regained his right knee’s full range of movement with flexion increased to 130 degrees, which is equal to that of his left knee.
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Upon examination, the patient was seen to have visibly swollen popliteal fossa and marked quadriceps wasting of his right lower limb. On palpation, the masses was hard, mobile, well defined, and measured 0.5 - 04 cm. The swelling was non-tender and there were no associated skin changes. He could fully extend his knee, but flexion was restricted to only 110 degrees. There was a McMurray test proved equivocal and no ligamentous instability. An examination of the patient’s hip revealed no abnormality.
A plain radiograph of the patient’s knees revealed multiple calcific densities within the soft tissues surrounding it on the right one. Although some of these appeared to lie within the capsule, the majority appeared to be outside of it, and a solitary image on the left knee. These appearances were thought to be consistent with idiopathic tumoral calcinosis. However, to further scrutinize these calcifications, a magnetic resonance imaging (MRI) scan was recommended. It showed an extensive thickening of the patient’s synovium, multiple intraarticular calcific and ossific loose bodies, and large calcified bursal extensions. These findings were thought to be consistent with very extensive bilateral synovial chondromatosis. The patient’s blood tests were normal: C-reactive protein 5 mg/l and the phosphate calcium balance without errors.
A two-stage procedure was planned following the findings of the MRI scan. The first stage was arthroscopy, which was able to note Grade IV osteoarthritis alongside florid synovial chondromatosis in the lateral compartment of the right knee. There were multiple loose bodies within this compartment and nodules were fixed to the synovium. On the left one, we found an isolated synovial metaplasia in the subvastus quadriceps-sparing. A synovectomy with debridement and excision of these bodies was thus performed.
The second stage involved an open exploration of the patient’s popliteal fossa. Multiple calcified masses were found, all enclosed in bursal sacs. They were lateral to the semimembranosus at the level of the oblique popliteal ligament. All the masses were excised. A histological review confirmed our diagnosis of synovial chondromatosis. The sections showed nests of chondrocytes with focal ossification and focally attenuated synovium overlying the nodules. After the operation, the patient underwent functional rehabilitation sessions focusing on quadriceps strengthening, with a daily exercise regime to supplement this. He recovered well and ten weeks after the operation, has regained his right knee’s full range of movement with flexion increased to 130 degrees, which is equal to that of his left knee.
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Upon examination, the patient was seen to have visibly swollen popliteal fossa and marked quadriceps wasting of his right lower limb. On palpation, the masses was hard, mobile, well defined, and measured 0.5 - 04 cm. The swelling was non-tender and there were no associated skin changes. He could fully extend his knee, but flexion was restricted to only 110 degrees. There was a McMurray test proved equivocal and no ligamentous instability. An examination of the patient’s hip revealed no abnormality.
A plain radiograph of the patient’s knees revealed multiple calcific densities within the soft tissues surrounding it on the right one. Although some of these appeared to lie within the capsule, the majority appeared to be outside of it, and a solitary image on the left knee. These appearances were thought to be consistent with idiopathic tumoral calcinosis. However, to further scrutinize these calcifications, a magnetic resonance imaging (MRI) scan was recommended. It showed an extensive thickening of the patient’s synovium, multiple intraarticular calcific and ossific loose bodies, and large calcified bursal extensions. These findings were thought to be consistent with very extensive bilateral synovial chondromatosis. The patient’s blood tests were normal: C-reactive protein 5 mg/l and the phosphate calcium balance without errors.
A two-stage procedure was planned following the findings of the MRI scan. The first stage was arthroscopy, which was able to note Grade IV osteoarthritis alongside florid synovial chondromatosis in the lateral compartment of the right knee. There were multiple loose bodies within this compartment and nodules were fixed to the synovium. On the left one, we found an isolated synovial metaplasia in the subvastus quadriceps-sparing. A synovectomy with debridement and excision of these bodies was thus performed.
The second stage involved an open exploration of the patient’s popliteal fossa. Multiple calcified masses were found, all enclosed in bursal sacs. They were lateral to the semimembranosus at the level of the oblique popliteal ligament. All the masses were excised. A histological review confirmed our diagnosis of synovial chondromatosis. The sections showed nests of chondrocytes with focal ossification and focally attenuated synovium overlying the nodules. After the operation, the patient underwent functional rehabilitation sessions focusing on quadriceps strengthening, with a daily exercise regime to supplement this. He recovered well and ten weeks after the operation, has regained his right knee’s full range of movement with flexion increased to 130 degrees, which is equal to that of his left knee.
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Upon examination, the patient was seen to have visibly swollen popliteal fossa and marked quadriceps wasting of his right lower limb. On palpation, the masses was hard, mobile, well defined, and measured 0.5 - 04 cm. The swelling was non-tender and there were no associated skin changes. He could fully extend his knee, but flexion was restricted to only 110 degrees. There was a McMurray test proved equivocal and no ligamentous instability. An examination of the patient’s hip revealed no abnormality.
A plain radiograph of the patient’s knees revealed multiple calcific densities within the soft tissues surrounding it on the right one. Although some of these appeared to lie within the capsule, the majority appeared to be outside of it, and a solitary image on the left knee. These appearances were thought to be consistent with idiopathic tumoral calcinosis. However, to further scrutinize these calcifications, a magnetic resonance imaging (MRI) scan was recommended. It showed an extensive thickening of the patient’s synovium, multiple intraarticular calcific and ossific loose bodies, and large calcified bursal extensions. These findings were thought to be consistent with very extensive bilateral synovial chondromatosis. The patient’s blood tests were normal: C-reactive protein 5 mg/l and the phosphate calcium balance without errors.
A two-stage procedure was planned following the findings of the MRI scan. The first stage was arthroscopy, which was able to note Grade IV osteoarthritis alongside florid synovial chondromatosis in the lateral compartment of the right knee. There were multiple loose bodies within this compartment and nodules were fixed to the synovium. On the left one, we found an isolated synovial metaplasia in the subvastus quadriceps-sparing. A synovectomy with debridement and excision of these bodies was thus performed.
The second stage involved an open exploration of the patient’s popliteal fossa. Multiple calcified masses were found, all enclosed in bursal sacs. They were lateral to the semimembranosus at the level of the oblique popliteal ligament. All the masses were excised. A histological review confirmed our diagnosis of synovial chondromatosis. The sections showed nests of chondrocytes with focal ossification and focally attenuated synovium overlying the nodules. After the operation, the patient underwent functional rehabilitation sessions focusing on quadriceps strengthening, with a daily exercise regime to supplement this. He recovered well and ten weeks after the operation, has regained his right knee’s full range of movement with flexion increased to 130 degrees, which is equal to that of his left knee.
| EN100156 |
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] | A 38-year-old man presented with a seven month history of progressively worsening bilateral knees pain with associated swelling. The pain was present when the patient was at rest, and worsened when the legs was bearing weight, thus restricting his walking to short distances. His knees had become increasingly swollen. He was otherwise fit and well. His medical history was unremarkable and he was only taking a paracetamol, codeine and anti-inflammatory drugs for the pain.
Upon examination, the patient was seen to have visibly swollen popliteal fossa and marked quadriceps wasting of his right lower limb. On palpation, the masses was hard, mobile, well defined, and measured 0.5 - 04 cm. The swelling was non-tender and there were no associated skin changes. He could fully extend his knee, but flexion was restricted to only 110 degrees. There was a McMurray test proved equivocal and no ligamentous instability. An examination of the patient’s hip revealed no abnormality.
A plain radiograph of the patient’s knees revealed multiple calcific densities within the soft tissues surrounding it on the right one. Although some of these appeared to lie within the capsule, the majority appeared to be outside of it, and a solitary image on the left knee. These appearances were thought to be consistent with idiopathic tumoral calcinosis. However, to further scrutinize these calcifications, a magnetic resonance imaging (MRI) scan was recommended. It showed an extensive thickening of the patient’s synovium, multiple intraarticular calcific and ossific loose bodies, and large calcified bursal extensions. These findings were thought to be consistent with very extensive bilateral synovial chondromatosis. The patient’s blood tests were normal: C-reactive protein 5 mg/l and the phosphate calcium balance without errors.
A two-stage procedure was planned following the findings of the MRI scan. The first stage was arthroscopy, which was able to note Grade IV osteoarthritis alongside florid synovial chondromatosis in the lateral compartment of the right knee. There were multiple loose bodies within this compartment and nodules were fixed to the synovium. On the left one, we found an isolated synovial metaplasia in the subvastus quadriceps-sparing. A synovectomy with debridement and excision of these bodies was thus performed.
The second stage involved an open exploration of the patient’s popliteal fossa. Multiple calcified masses were found, all enclosed in bursal sacs. They were lateral to the semimembranosus at the level of the oblique popliteal ligament. All the masses were excised. A histological review confirmed our diagnosis of synovial chondromatosis. The sections showed nests of chondrocytes with focal ossification and focally attenuated synovium overlying the nodules. After the operation, the patient underwent functional rehabilitation sessions focusing on quadriceps strengthening, with a daily exercise regime to supplement this. He recovered well and ten weeks after the operation, has regained his right knee’s full range of movement with flexion increased to 130 degrees, which is equal to that of his left knee.
| EN100156 |
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] | A 38-year-old man presented with a seven month history of progressively worsening bilateral knees pain with associated swelling. The pain was present when the patient was at rest, and worsened when the legs was bearing weight, thus restricting his walking to short distances. His knees had become increasingly swollen. He was otherwise fit and well. His medical history was unremarkable and he was only taking a paracetamol, codeine and anti-inflammatory drugs for the pain.
Upon examination, the patient was seen to have visibly swollen popliteal fossa and marked quadriceps wasting of his right lower limb. On palpation, the masses was hard, mobile, well defined, and measured 0.5 - 04 cm. The swelling was non-tender and there were no associated skin changes. He could fully extend his knee, but flexion was restricted to only 110 degrees. There was a McMurray test proved equivocal and no ligamentous instability. An examination of the patient’s hip revealed no abnormality.
A plain radiograph of the patient’s knees revealed multiple calcific densities within the soft tissues surrounding it on the right one. Although some of these appeared to lie within the capsule, the majority appeared to be outside of it, and a solitary image on the left knee. These appearances were thought to be consistent with idiopathic tumoral calcinosis. However, to further scrutinize these calcifications, a magnetic resonance imaging (MRI) scan was recommended. It showed an extensive thickening of the patient’s synovium, multiple intraarticular calcific and ossific loose bodies, and large calcified bursal extensions. These findings were thought to be consistent with very extensive bilateral synovial chondromatosis. The patient’s blood tests were normal: C-reactive protein 5 mg/l and the phosphate calcium balance without errors.
A two-stage procedure was planned following the findings of the MRI scan. The first stage was arthroscopy, which was able to note Grade IV osteoarthritis alongside florid synovial chondromatosis in the lateral compartment of the right knee. There were multiple loose bodies within this compartment and nodules were fixed to the synovium. On the left one, we found an isolated synovial metaplasia in the subvastus quadriceps-sparing. A synovectomy with debridement and excision of these bodies was thus performed.
The second stage involved an open exploration of the patient’s popliteal fossa. Multiple calcified masses were found, all enclosed in bursal sacs. They were lateral to the semimembranosus at the level of the oblique popliteal ligament. All the masses were excised. A histological review confirmed our diagnosis of synovial chondromatosis. The sections showed nests of chondrocytes with focal ossification and focally attenuated synovium overlying the nodules. After the operation, the patient underwent functional rehabilitation sessions focusing on quadriceps strengthening, with a daily exercise regime to supplement this. He recovered well and ten weeks after the operation, has regained his right knee’s full range of movement with flexion increased to 130 degrees, which is equal to that of his left knee.
| EN100156 |
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] | A 38-year-old man presented with a seven month history of progressively worsening bilateral knees pain with associated swelling. The pain was present when the patient was at rest, and worsened when the legs was bearing weight, thus restricting his walking to short distances. His knees had become increasingly swollen. He was otherwise fit and well. His medical history was unremarkable and he was only taking a paracetamol, codeine and anti-inflammatory drugs for the pain.
Upon examination, the patient was seen to have visibly swollen popliteal fossa and marked quadriceps wasting of his right lower limb. On palpation, the masses was hard, mobile, well defined, and measured 0.5 - 04 cm. The swelling was non-tender and there were no associated skin changes. He could fully extend his knee, but flexion was restricted to only 110 degrees. There was a McMurray test proved equivocal and no ligamentous instability. An examination of the patient’s hip revealed no abnormality.
A plain radiograph of the patient’s knees revealed multiple calcific densities within the soft tissues surrounding it on the right one. Although some of these appeared to lie within the capsule, the majority appeared to be outside of it, and a solitary image on the left knee. These appearances were thought to be consistent with idiopathic tumoral calcinosis. However, to further scrutinize these calcifications, a magnetic resonance imaging (MRI) scan was recommended. It showed an extensive thickening of the patient’s synovium, multiple intraarticular calcific and ossific loose bodies, and large calcified bursal extensions. These findings were thought to be consistent with very extensive bilateral synovial chondromatosis. The patient’s blood tests were normal: C-reactive protein 5 mg/l and the phosphate calcium balance without errors.
A two-stage procedure was planned following the findings of the MRI scan. The first stage was arthroscopy, which was able to note Grade IV osteoarthritis alongside florid synovial chondromatosis in the lateral compartment of the right knee. There were multiple loose bodies within this compartment and nodules were fixed to the synovium. On the left one, we found an isolated synovial metaplasia in the subvastus quadriceps-sparing. A synovectomy with debridement and excision of these bodies was thus performed.
The second stage involved an open exploration of the patient’s popliteal fossa. Multiple calcified masses were found, all enclosed in bursal sacs. They were lateral to the semimembranosus at the level of the oblique popliteal ligament. All the masses were excised. A histological review confirmed our diagnosis of synovial chondromatosis. The sections showed nests of chondrocytes with focal ossification and focally attenuated synovium overlying the nodules. After the operation, the patient underwent functional rehabilitation sessions focusing on quadriceps strengthening, with a daily exercise regime to supplement this. He recovered well and ten weeks after the operation, has regained his right knee’s full range of movement with flexion increased to 130 degrees, which is equal to that of his left knee.
| EN100156 |
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] | A 38-year-old man presented with a seven month history of progressively worsening bilateral knees pain with associated swelling. The pain was present when the patient was at rest, and worsened when the legs was bearing weight, thus restricting his walking to short distances. His knees had become increasingly swollen. He was otherwise fit and well. His medical history was unremarkable and he was only taking a paracetamol, codeine and anti-inflammatory drugs for the pain.
Upon examination, the patient was seen to have visibly swollen popliteal fossa and marked quadriceps wasting of his right lower limb. On palpation, the masses was hard, mobile, well defined, and measured 0.5 - 04 cm. The swelling was non-tender and there were no associated skin changes. He could fully extend his knee, but flexion was restricted to only 110 degrees. There was a McMurray test proved equivocal and no ligamentous instability. An examination of the patient’s hip revealed no abnormality.
A plain radiograph of the patient’s knees revealed multiple calcific densities within the soft tissues surrounding it on the right one. Although some of these appeared to lie within the capsule, the majority appeared to be outside of it, and a solitary image on the left knee. These appearances were thought to be consistent with idiopathic tumoral calcinosis. However, to further scrutinize these calcifications, a magnetic resonance imaging (MRI) scan was recommended. It showed an extensive thickening of the patient’s synovium, multiple intraarticular calcific and ossific loose bodies, and large calcified bursal extensions. These findings were thought to be consistent with very extensive bilateral synovial chondromatosis. The patient’s blood tests were normal: C-reactive protein 5 mg/l and the phosphate calcium balance without errors.
A two-stage procedure was planned following the findings of the MRI scan. The first stage was arthroscopy, which was able to note Grade IV osteoarthritis alongside florid synovial chondromatosis in the lateral compartment of the right knee. There were multiple loose bodies within this compartment and nodules were fixed to the synovium. On the left one, we found an isolated synovial metaplasia in the subvastus quadriceps-sparing. A synovectomy with debridement and excision of these bodies was thus performed.
The second stage involved an open exploration of the patient’s popliteal fossa. Multiple calcified masses were found, all enclosed in bursal sacs. They were lateral to the semimembranosus at the level of the oblique popliteal ligament. All the masses were excised. A histological review confirmed our diagnosis of synovial chondromatosis. The sections showed nests of chondrocytes with focal ossification and focally attenuated synovium overlying the nodules. After the operation, the patient underwent functional rehabilitation sessions focusing on quadriceps strengthening, with a daily exercise regime to supplement this. He recovered well and ten weeks after the operation, has regained his right knee’s full range of movement with flexion increased to 130 degrees, which is equal to that of his left knee.
| EN100156 |
Subsets and Splits