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Red painful nodules in a hospitalized patient
A 58-year-old white man with a history of alcoholism presented to the emergency department with epigastric and right upper quadrant pain radiating to the back, as well as emesis and anorexia. An elevated lipase of 16,609 U/L (reference range, 31–186 U/L) and pathognomonic abdominal computed tomography (CT) findings (FIGURE 1) led to the diagnosis of acute pancreatitis, for which he was admitted.
Fluid resuscitation and pain management were implemented, and over 3 days his diet was advanced from NPO to clear fluids to a full diet. On the sixth day of hospitalization, the patient developed increasing abdominal pain and worsening leukocytosis (white blood cell count, 16.6–22 K/mcL [reference range, 4.5–11 K/mcL]). Repeat CT and blood cultures were obtained, and the patient was started on intravenous meropenem 1 g every 8 hours for presumed necrotizing pancreatitis. The next day he developed acutely tender red to pink patches and nodules on his shins and medial lower legs (FIGURE 2).
WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?
Diagnosis: Pancreatic panniculitis
It’s theorized that the systemic release of trypsin from pancreatic cell destruction causes increased capillary permeability and subsequent escape of lipase from the circulation into the subcutaneous fat. This causes fat necrosis, saponification, and inflammation.3,4 Pancreatic panniculitis is demonstrated histologically as hollowed-out adipocytes with granular basophilic cytoplasm and displaced or absent nuclei—aptly named “ghostlike” adipocytes.3-6
Painful, erythematous nodules most commonly present on the distal lower extremities. Nodules may be found over the shins, posterior calves, and periarticular skin. Rarely, nodules may occur on the buttocks, abdomen, or intramedullary bone.7 In severe cases, nodules spontaneously may ulcerate and drain an oily brown, viscous material formed from necrotic adipocytes.1
Timing of the eruption of skin lesions is varied and may even precede abdominal pain. Lesions can involute and regress several weeks after the underlying etiology improves. With pancreatic carcinoma, there is a greater likelihood of persistence, atypical locations of involvement, ulcerations, and recurrences.7
The histologic features of pancreatic panniculitis and the assessment of the subcutaneous fat are paramount in diagnosis. A deep punch biopsy or incisional biopsy is necessary to reliably reach the depth of the subcutaneous tissue. In our patient, a deep punch biopsy from the lateral calf was performed at the suggestion of Dermatology, and histopathology revealed necrosis of fat lobules with calcium soap around necrotic lipocytes, consistent with pancreatic panniculitis (FIGURE 3).
Continue to: Differential was complicated by antibiotic use
Differential was complicated by antibiotic use
The differential diagnosis was broad due to the confounding factors of recent antibiotic use and worsening pancreatitis.
Cellulitis may present as a red patch and is common on the lower legs; it often is associated with skin pathogens including Staphylococcus and Streptococcus. Usually, symptoms are unilateral and associated with warmth to the touch, expanding borders, leukocytosis, and systemic symptoms.
Vasculitis, which is an inflammation of various sized vessels through immunologic or infectious processes, often manifests on the lower legs. The characteristic sign of small vessel vasculitis is nonblanching purpura or petechiae. There often is a preceding illness or medication that triggers immunoglobulin proliferation and off-target inflammation of the vessels. Associated symptoms include pain and pruritus.
Drug eruptions may present as red patches on the skin. Often the patches are scaly and red and have more widespread distribution than the lower legs. A history of exposure is important, but common inciting drugs include nonsteroidal anti-inflammatory drugs that may be used only occasionally and are challenging to elicit in the history. Our patient did have known drug changes (ie, the introduction of meropenem) while hospitalized, but the morphology was not consistent with this diagnosis.
Treatment is directed to underlying disease
Treatment of pancreatic panniculitis primarily is supportive and directed toward treating the underlying pancreatic disease. Depending upon the underlying pancreatic diagnosis, surgical correction of anatomic or ductal anomalies or pseudocysts may lead to resolution of panniculitis.3,7,8
Continue to: In this case
In this case, our patient had already received fluid resuscitation and pain management, and his diet had been advanced. In addition, his antibiotics were changed to exclude drug eruption as a cause. Over the course of a week, our patient saw a reduction in his pain level and an improvement in the appearance of his legs (FIGURE 4).
His pancreatitis, however, continued to persist and resist increases in his diet. He ultimately required transfer to a tertiary care center for consideration of interventional options including stenting. The patient ultimately recovered, after stenting of the main pancreatic duct, and was discharged home.
CORRESPONDENCE
Jonathan Karnes, MD, 6 East Chestnut Street, Augusta, ME 04330; Jonathan.Karnes@mainegeneral.org
1. Madarasingha NP, Satgurunathan K, Fernando R. Pancreatic panniculitis: a rare form of panniculitis. Dermatol Online J. 2009;15:17.
2. Haber RM, Assaad DM. Panniculitis associated with a pancreas divisum. J Am Acad Dermatol. 1986;14(2 pt 2):331-334.
3. Requena L, Sánchez Yus E. Panniculitis. part II. mostly lobular panniculitis. J Am Acad Dermatol. 2001;45:325-361.
4. Rongioletti F, Caputo V. Pancreatic panniculitis. G Ital Dermatol Venereol. 2013;148:419-425.
5. Förström TL, Winkelmann RK. Acute, generalized panniculitis with amylase and lipase in skin. Arch Dermatol. 1975;111:497-502.
6. Hughes SH, Apisarnthanarax P, Mullins F. Subcutaneous fat necrosis associated with pancreatic disease. Arch Dermatol. 1975;111:506-510.
7. Dahl PR, Su WP, Cullimore KC, et al. Pancreatic panniculitis. J Am Acad Dermatol. 1995;33:413-417.
8. Lambiase P, Seery JP, Taylor-Robinson SD, et al. Resolution of panniculitis after placement of pancreatic duct stent in chro nic pancreatitis. Am J Gastroenterol. 1996;91:1835-1837.
A 58-year-old white man with a history of alcoholism presented to the emergency department with epigastric and right upper quadrant pain radiating to the back, as well as emesis and anorexia. An elevated lipase of 16,609 U/L (reference range, 31–186 U/L) and pathognomonic abdominal computed tomography (CT) findings (FIGURE 1) led to the diagnosis of acute pancreatitis, for which he was admitted.
Fluid resuscitation and pain management were implemented, and over 3 days his diet was advanced from NPO to clear fluids to a full diet. On the sixth day of hospitalization, the patient developed increasing abdominal pain and worsening leukocytosis (white blood cell count, 16.6–22 K/mcL [reference range, 4.5–11 K/mcL]). Repeat CT and blood cultures were obtained, and the patient was started on intravenous meropenem 1 g every 8 hours for presumed necrotizing pancreatitis. The next day he developed acutely tender red to pink patches and nodules on his shins and medial lower legs (FIGURE 2).
WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?
Diagnosis: Pancreatic panniculitis
It’s theorized that the systemic release of trypsin from pancreatic cell destruction causes increased capillary permeability and subsequent escape of lipase from the circulation into the subcutaneous fat. This causes fat necrosis, saponification, and inflammation.3,4 Pancreatic panniculitis is demonstrated histologically as hollowed-out adipocytes with granular basophilic cytoplasm and displaced or absent nuclei—aptly named “ghostlike” adipocytes.3-6
Painful, erythematous nodules most commonly present on the distal lower extremities. Nodules may be found over the shins, posterior calves, and periarticular skin. Rarely, nodules may occur on the buttocks, abdomen, or intramedullary bone.7 In severe cases, nodules spontaneously may ulcerate and drain an oily brown, viscous material formed from necrotic adipocytes.1
Timing of the eruption of skin lesions is varied and may even precede abdominal pain. Lesions can involute and regress several weeks after the underlying etiology improves. With pancreatic carcinoma, there is a greater likelihood of persistence, atypical locations of involvement, ulcerations, and recurrences.7
The histologic features of pancreatic panniculitis and the assessment of the subcutaneous fat are paramount in diagnosis. A deep punch biopsy or incisional biopsy is necessary to reliably reach the depth of the subcutaneous tissue. In our patient, a deep punch biopsy from the lateral calf was performed at the suggestion of Dermatology, and histopathology revealed necrosis of fat lobules with calcium soap around necrotic lipocytes, consistent with pancreatic panniculitis (FIGURE 3).
Continue to: Differential was complicated by antibiotic use
Differential was complicated by antibiotic use
The differential diagnosis was broad due to the confounding factors of recent antibiotic use and worsening pancreatitis.
Cellulitis may present as a red patch and is common on the lower legs; it often is associated with skin pathogens including Staphylococcus and Streptococcus. Usually, symptoms are unilateral and associated with warmth to the touch, expanding borders, leukocytosis, and systemic symptoms.
Vasculitis, which is an inflammation of various sized vessels through immunologic or infectious processes, often manifests on the lower legs. The characteristic sign of small vessel vasculitis is nonblanching purpura or petechiae. There often is a preceding illness or medication that triggers immunoglobulin proliferation and off-target inflammation of the vessels. Associated symptoms include pain and pruritus.
Drug eruptions may present as red patches on the skin. Often the patches are scaly and red and have more widespread distribution than the lower legs. A history of exposure is important, but common inciting drugs include nonsteroidal anti-inflammatory drugs that may be used only occasionally and are challenging to elicit in the history. Our patient did have known drug changes (ie, the introduction of meropenem) while hospitalized, but the morphology was not consistent with this diagnosis.
Treatment is directed to underlying disease
Treatment of pancreatic panniculitis primarily is supportive and directed toward treating the underlying pancreatic disease. Depending upon the underlying pancreatic diagnosis, surgical correction of anatomic or ductal anomalies or pseudocysts may lead to resolution of panniculitis.3,7,8
Continue to: In this case
In this case, our patient had already received fluid resuscitation and pain management, and his diet had been advanced. In addition, his antibiotics were changed to exclude drug eruption as a cause. Over the course of a week, our patient saw a reduction in his pain level and an improvement in the appearance of his legs (FIGURE 4).
His pancreatitis, however, continued to persist and resist increases in his diet. He ultimately required transfer to a tertiary care center for consideration of interventional options including stenting. The patient ultimately recovered, after stenting of the main pancreatic duct, and was discharged home.
CORRESPONDENCE
Jonathan Karnes, MD, 6 East Chestnut Street, Augusta, ME 04330; Jonathan.Karnes@mainegeneral.org
A 58-year-old white man with a history of alcoholism presented to the emergency department with epigastric and right upper quadrant pain radiating to the back, as well as emesis and anorexia. An elevated lipase of 16,609 U/L (reference range, 31–186 U/L) and pathognomonic abdominal computed tomography (CT) findings (FIGURE 1) led to the diagnosis of acute pancreatitis, for which he was admitted.
Fluid resuscitation and pain management were implemented, and over 3 days his diet was advanced from NPO to clear fluids to a full diet. On the sixth day of hospitalization, the patient developed increasing abdominal pain and worsening leukocytosis (white blood cell count, 16.6–22 K/mcL [reference range, 4.5–11 K/mcL]). Repeat CT and blood cultures were obtained, and the patient was started on intravenous meropenem 1 g every 8 hours for presumed necrotizing pancreatitis. The next day he developed acutely tender red to pink patches and nodules on his shins and medial lower legs (FIGURE 2).
WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?
Diagnosis: Pancreatic panniculitis
It’s theorized that the systemic release of trypsin from pancreatic cell destruction causes increased capillary permeability and subsequent escape of lipase from the circulation into the subcutaneous fat. This causes fat necrosis, saponification, and inflammation.3,4 Pancreatic panniculitis is demonstrated histologically as hollowed-out adipocytes with granular basophilic cytoplasm and displaced or absent nuclei—aptly named “ghostlike” adipocytes.3-6
Painful, erythematous nodules most commonly present on the distal lower extremities. Nodules may be found over the shins, posterior calves, and periarticular skin. Rarely, nodules may occur on the buttocks, abdomen, or intramedullary bone.7 In severe cases, nodules spontaneously may ulcerate and drain an oily brown, viscous material formed from necrotic adipocytes.1
Timing of the eruption of skin lesions is varied and may even precede abdominal pain. Lesions can involute and regress several weeks after the underlying etiology improves. With pancreatic carcinoma, there is a greater likelihood of persistence, atypical locations of involvement, ulcerations, and recurrences.7
The histologic features of pancreatic panniculitis and the assessment of the subcutaneous fat are paramount in diagnosis. A deep punch biopsy or incisional biopsy is necessary to reliably reach the depth of the subcutaneous tissue. In our patient, a deep punch biopsy from the lateral calf was performed at the suggestion of Dermatology, and histopathology revealed necrosis of fat lobules with calcium soap around necrotic lipocytes, consistent with pancreatic panniculitis (FIGURE 3).
Continue to: Differential was complicated by antibiotic use
Differential was complicated by antibiotic use
The differential diagnosis was broad due to the confounding factors of recent antibiotic use and worsening pancreatitis.
Cellulitis may present as a red patch and is common on the lower legs; it often is associated with skin pathogens including Staphylococcus and Streptococcus. Usually, symptoms are unilateral and associated with warmth to the touch, expanding borders, leukocytosis, and systemic symptoms.
Vasculitis, which is an inflammation of various sized vessels through immunologic or infectious processes, often manifests on the lower legs. The characteristic sign of small vessel vasculitis is nonblanching purpura or petechiae. There often is a preceding illness or medication that triggers immunoglobulin proliferation and off-target inflammation of the vessels. Associated symptoms include pain and pruritus.
Drug eruptions may present as red patches on the skin. Often the patches are scaly and red and have more widespread distribution than the lower legs. A history of exposure is important, but common inciting drugs include nonsteroidal anti-inflammatory drugs that may be used only occasionally and are challenging to elicit in the history. Our patient did have known drug changes (ie, the introduction of meropenem) while hospitalized, but the morphology was not consistent with this diagnosis.
Treatment is directed to underlying disease
Treatment of pancreatic panniculitis primarily is supportive and directed toward treating the underlying pancreatic disease. Depending upon the underlying pancreatic diagnosis, surgical correction of anatomic or ductal anomalies or pseudocysts may lead to resolution of panniculitis.3,7,8
Continue to: In this case
In this case, our patient had already received fluid resuscitation and pain management, and his diet had been advanced. In addition, his antibiotics were changed to exclude drug eruption as a cause. Over the course of a week, our patient saw a reduction in his pain level and an improvement in the appearance of his legs (FIGURE 4).
His pancreatitis, however, continued to persist and resist increases in his diet. He ultimately required transfer to a tertiary care center for consideration of interventional options including stenting. The patient ultimately recovered, after stenting of the main pancreatic duct, and was discharged home.
CORRESPONDENCE
Jonathan Karnes, MD, 6 East Chestnut Street, Augusta, ME 04330; Jonathan.Karnes@mainegeneral.org
1. Madarasingha NP, Satgurunathan K, Fernando R. Pancreatic panniculitis: a rare form of panniculitis. Dermatol Online J. 2009;15:17.
2. Haber RM, Assaad DM. Panniculitis associated with a pancreas divisum. J Am Acad Dermatol. 1986;14(2 pt 2):331-334.
3. Requena L, Sánchez Yus E. Panniculitis. part II. mostly lobular panniculitis. J Am Acad Dermatol. 2001;45:325-361.
4. Rongioletti F, Caputo V. Pancreatic panniculitis. G Ital Dermatol Venereol. 2013;148:419-425.
5. Förström TL, Winkelmann RK. Acute, generalized panniculitis with amylase and lipase in skin. Arch Dermatol. 1975;111:497-502.
6. Hughes SH, Apisarnthanarax P, Mullins F. Subcutaneous fat necrosis associated with pancreatic disease. Arch Dermatol. 1975;111:506-510.
7. Dahl PR, Su WP, Cullimore KC, et al. Pancreatic panniculitis. J Am Acad Dermatol. 1995;33:413-417.
8. Lambiase P, Seery JP, Taylor-Robinson SD, et al. Resolution of panniculitis after placement of pancreatic duct stent in chro nic pancreatitis. Am J Gastroenterol. 1996;91:1835-1837.
1. Madarasingha NP, Satgurunathan K, Fernando R. Pancreatic panniculitis: a rare form of panniculitis. Dermatol Online J. 2009;15:17.
2. Haber RM, Assaad DM. Panniculitis associated with a pancreas divisum. J Am Acad Dermatol. 1986;14(2 pt 2):331-334.
3. Requena L, Sánchez Yus E. Panniculitis. part II. mostly lobular panniculitis. J Am Acad Dermatol. 2001;45:325-361.
4. Rongioletti F, Caputo V. Pancreatic panniculitis. G Ital Dermatol Venereol. 2013;148:419-425.
5. Förström TL, Winkelmann RK. Acute, generalized panniculitis with amylase and lipase in skin. Arch Dermatol. 1975;111:497-502.
6. Hughes SH, Apisarnthanarax P, Mullins F. Subcutaneous fat necrosis associated with pancreatic disease. Arch Dermatol. 1975;111:506-510.
7. Dahl PR, Su WP, Cullimore KC, et al. Pancreatic panniculitis. J Am Acad Dermatol. 1995;33:413-417.
8. Lambiase P, Seery JP, Taylor-Robinson SD, et al. Resolution of panniculitis after placement of pancreatic duct stent in chro nic pancreatitis. Am J Gastroenterol. 1996;91:1835-1837.
Sharp lower back pain • left-side paraspinal tenderness • anterior thigh sensory loss • Dx?
THE CASE
A 64-year-old woman with a history of late-onset type 1 diabetes mellitus, Hashimoto thyroiditis, and scoliosis presented to the sports medicine clinic with acute-onset, sharp, nonradiating right lower back pain that began when she bent forward to apply lotion. At presentation, she denied fever, chills, numbness, tingling, aggravation of pain with movement, weakness, and incontinence. Her neuromuscular examination was unremarkable except for left-side paraspinal tenderness. She was prescribed cyclobenzaprine for symptomatic relief.
Two days later, she was seen for worsening pain. Her physical exam was unchanged. She was prescribed tramadol and advised to start physical therapy gradually. As the day progressed, however, she developed anterior thigh sensory loss, which gradually extended distally.
The following day, she was brought to the emergency department with severe left-side weakness without urinary incontinence. Her mental status and cranial nerve exams were normal. On examination, strength of the iliopsoas and quadriceps was 1/5 bilaterally, and of the peroneal tendon and gastrocnemius, 3/5 bilaterally. Reflexes of triceps, biceps, knee, and Achilles tendon were symmetric and 3+ with bilateral clonus of the ankle. The Babinski sign was positive bilaterally. The patient had diminished pain sensation bilaterally, extending down from the T11 dermatome (left more than right side) with diminished vibration sensation at the left ankle. Her perianal sensation, bilateral temperature sensation, and cerebellar examination were normal.
Magnetic resonance imaging (MRI) without contrast of the lumbar spine demonstrated ischemia findings corresponding to T12-L1. Degenerative changes from L1-S1 were noted, with multiple osteophytes impinging on the neural foramina without cord compression.
THE DIAGNOSIS
The initial presentation was consistent with mechanical low back pain with signs of anterior spinal artery infarction and medial lemniscus pathway involvement 48 hours after initial presentation. Spinal cord infarction occurs more commonly in women and in the young than does cerebral infarction,1 with better reemployment rates.1,2 Similar to other strokes, long-term prognosis is primarily determined by the initial severity of motor impairment, which is linked to long-term immobility and need for bladder catheterization.3
Neurogenic pain developing years after spinal cord infarction is most often observed in anterior spinal artery infarction4 without functional limitations.
Initial treatment. Our patient was started on aspirin 325 mg/d and clopidogrel 75 mg/d. Her mean arterial blood pressure was maintained above 80 mm Hg. Computed tomography angiography of the abdomen and pelvis was negative for aortic dissection. Lumbar puncture for cerebrospinal fluid analysis was unremarkable. Results of antineutrophil cytoplasmic antibody testing, antinuclear antibody testing, a hepatitis panel, and an antiphospholipid panel were all negative. The patient was started on IV steroids with a plan for gradual tapering. The neurosurgical team agreed with medical management.
Continue to: DISCUSSION
DISCUSSION
Possible etiologies for acute spinal cord infarction include spinal cord ischemia from compression of the vessels, fibrocartilaginous embolism, and arterial thrombosis or atherosclerosis, especially in patients with diabetes.5
The majority (86%) of spinal strokes are due to spontaneous occlusion of the vessels with no identifiable cause; much less frequently (9% of cases), hemorrhage is the causative factor.1 A retrospective study demonstrated that 10 of 27 patients with spinal stroke had an anterior spinal infarct. Of those 10 patients, 6 reported a mechanical triggering movement (similar to this case), indicating potential compression of the radicular arteries due to said movement.4
Fibrocartilaginous embolism (FCE) is worth considering as a possible cause, because it accounts for 5.5% of all cases of acute spinal cord infarction.3 FCE is thought to arise after a precipitating event such as minor trauma, heavy lifting, physical exertion, or Valsalva maneuver causing embolization of the fragments of nucleus pulposus to the arterial system. In a case series of 8 patients, 2 had possible FCE with precipitating events occurring within the prior 24 hours. This was also demonstrated in another case series6 in which 7 of 9 patients had precipitating events.
Although FCE can only definitively be diagnosed postmortem, the researchers6 proposed clinical criteria for its diagnosis in living patients, based on 40 postmortem and 11 suspected antemortem cases of FCE. These criteria include a rapid evolution of symptoms consistent with vascular etiology, with or without preceding minor trauma or Valsalva maneuver; MRI changes consistent with ischemic myelopathy, with or without evidence of disc herniation; and no more than 2 vascular risk factors.
Our patient had no trauma (although there was a triggering movement), no signs of disc herniation, and 2 risk factors (> 60 years and diabetes mellitus). Also, a neurologically symptom-free interval between the painful movement and the onset of neurologic manifestations in our case parallels the clinical picture of FCE.
Continue to: The role of factor V Leiden (FVL) mutation
The role of factor V Leiden (FVL) mutation in arterial thrombosis is questionable. Previous reports demonstrate a risk for venous thrombosis 7 to 10 times higher with heterozygous FVL mutation and 100 times higher with homozygous mutation, with a less established role in arterial thrombosis.7 A retrospective Turkish study compared the incidence of FVL mutation in patients with arterial thrombosis vs healthy subjects; incidence was significantly higher in female patients than female controls (37.5% vs. 2%).7 A meta-analysis of published studies showed an association between arterial ischemic events and FVL mutation to be modest, with an odds ratio of 1.21 (95% CI, 0.99-1.49).8
In contrast, a 3.4-year longitudinal health study of patients ages 65 and older found no significant difference in the occurrence of myocardial infarction, transient ischemic attack, stroke, or angina for more than 5000 patients with heterozygous FVL mutation compared to fewer than 500 controls.9 The case patient’s clinical course did not fit a thrombotic clinical picture.
Evaluating for “red flags” is crucial in any case of low back pain to exclude serious pathologies. Red flag symptoms include signs of myelopathy, signs of infection, history of trauma with focal tenderness to palpation, and steroid or anticoagulant use (to rule out medication adverse effects).10 Our patient lacked these classical signs, but she did have subjective pain out of proportion to the clinical exam findings.
Of note: The above red flags for low back pain are all based on expert opinion,11 and the positive predictive value of a red flag is always low because of the low prevalence of serious spinal pathologies.12
Striking a proper balance. This case emphasizes the necessity to keep uncommon causes—such as nontraumatic spinal stroke, which has a prevalence of about 5% to 8% of all acute myelopathies—in the differential diagnosis.3
Continue to: We recommend watchful...
We recommend watchful waiting coupled with communication with the patient regarding monitoring for changes in symptoms over time.11 Any changes in symptoms concerning for underlying spinal cord injury indicate necessity for transfer to a tertiary care center (if possible), along with immediate evaluation with imaging—including computed tomography angiography of the abdomen to rule out aortic dissection (1%-2% of all spinal cord infarcts), followed by a specialist consultation based on the findings.3
Our patient
Our patient was discharged to rehabilitation on hospital Day 5, after progressive return of lower extremity strength. At the 2-month follow-up visit, she demonstrated grade 4+ strength throughout her lower extremities bilaterally. Weakness was predominant at the hip flexors and ankle dorsiflexors, which was consistent with her status at discharge. She had burning pain in the distribution of the L1 dermatome that responded to ibuprofen.
Hypercoagulability work-up was positive for heterozygous FVL mutation without any previous history of venous thromboembolic disease. She was continued on aspirin 325 mg/d, as per American College of Chest Physicians antithrombotic guidelines.13
One year later, our patient underwent a follow-up MRI of the thoracic spine, which showed an “owl’s eye” hyperintensity in the anterior cord (FIGURE), a sign that’s often seen in bilateral spinal cord infarction
THE TAKEAWAY
Spinal stroke is rare, but a missed diagnosis and lack of treatment can result in long-term morbidity. Therefore, it is prudent to consider this diagnosis in the differential—especially when the patient’s subjective back pain is out of proportion to the clinical examination findings.
CORRESPONDENCE
Srikanth Nithyanandam, MBBS, MS, University of Kentucky Family and Community Medicine, 2195 Harrodsburg Road, Suite 125, Lexington, KY 40504-3504; sri.nisi89@uky.edu.
1. Romi F, Naess H. Spinal cord infarction in clinical neurology: a review of characteristics and long-term prognosis in comparison to cerebral infarction. Eur Neurol. 2016;76:95-98.
2. Hanson SR, Romi F, Rekand T, et al. Long-term outcome after spinal cord infarctions. Acta Neurol Scand. 2015;131:253-257.
3. Rigney L, Cappelen-Smith C, Sebire D, et al. Nontraumatic spinal cord ischaemic syndrome. J Clin Neurosci. 2015;22:1544-1549.
4. Novy J, Carruzzo A, Maeder P, Bogousslavsky J. Spinal cord ischemia: clinical and imaging patterns, pathogenesis, and outcomes in 27 patients. Arch Neurol. 2006;63:1113-1120.
5. Goldstein LB, Adams R, Alberts MJ, et al; American Heart Association; American Stroke Association Stroke Council. Primary prevention of ischemic stroke: a guideline from the American Heart Association/American Stroke Association Stroke Council: cosponsored by the Atherosclerotic Peripheral Vascular Disease Interdisciplinary Working Group; Cardiovascular Nursing Council; Clinical Cardiology Council; Nutrition, Physical Activity, and Metabolism Council; and the Quality of Care and Outcomes Research Interdisciplinary Working Group. Circulation. 2006;113:e873-e923.
6. Mateen FJ, Monrad PA, Hunderfund AN, et al. Clinically suspected fibrocartilaginous embolism: clinical characteristics, treatments, and outcomes. Eur J Neurol. 2011;18:218-225.
7. Ozmen F, Ozmen MM, Ozalp N, et al. The prevalence of factor V (G1691A), MTHFR (C677T) and PT (G20210A) gene mutations in arterial thrombosis. Ulus Travma Acil Cerrahi Derg. 2009;15:113-119.
8. Kim RJ, Becker RC. Association between factor V Leiden, prothrombin G20210A, and methylenetetrahydrofolate reductase C677T mutations and events of the arterial circulatory system: a meta-analysis of published studies. Am Heart J. 2003;146:948-957.
9. Cushman M, Rosendaal FR, Psaty BM, et al. Factor V Leiden is not a risk factor for arterial vascular disease in the elderly: results from the Cardiovascular Health Study. Thromb Haemost. 1998;79:912-915.
10. Strudwick K, McPhee M, Bell A, et al. Review article: best practice management of low back pain in the emergency department (part 1 of the musculoskeletal injuries rapid review series). Emerg Med Australas. 2018;30:18-35.
11. Cook CE, George SZ, Reiman MP. Red flag screening for low back pain: nothing to see here, move along: a narrative review. Br J Sports Med. 2018;52:493-496.
12. Grunau GL, Darlow B, Flynn T, et al. Red flags or red herrings? Redefining the role of red flags in low back pain to reduce overimaging. Br J Sports Med. 2018;52:488-489.
13. Lansberg MG, O’Donnell MJ, Khatri P, et al. Antithrombotic and thrombolytic therapy for ischemic stroke: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest. 2012;141(2 suppl):e601S-e636S.
14. Pikija S, Mutzenbach JS, Kunz AB, et al. Delayed hospital presentation and neuroimaging in non-surgical spinal cord infarction. Front Neurol. 2017;8:143.
THE CASE
A 64-year-old woman with a history of late-onset type 1 diabetes mellitus, Hashimoto thyroiditis, and scoliosis presented to the sports medicine clinic with acute-onset, sharp, nonradiating right lower back pain that began when she bent forward to apply lotion. At presentation, she denied fever, chills, numbness, tingling, aggravation of pain with movement, weakness, and incontinence. Her neuromuscular examination was unremarkable except for left-side paraspinal tenderness. She was prescribed cyclobenzaprine for symptomatic relief.
Two days later, she was seen for worsening pain. Her physical exam was unchanged. She was prescribed tramadol and advised to start physical therapy gradually. As the day progressed, however, she developed anterior thigh sensory loss, which gradually extended distally.
The following day, she was brought to the emergency department with severe left-side weakness without urinary incontinence. Her mental status and cranial nerve exams were normal. On examination, strength of the iliopsoas and quadriceps was 1/5 bilaterally, and of the peroneal tendon and gastrocnemius, 3/5 bilaterally. Reflexes of triceps, biceps, knee, and Achilles tendon were symmetric and 3+ with bilateral clonus of the ankle. The Babinski sign was positive bilaterally. The patient had diminished pain sensation bilaterally, extending down from the T11 dermatome (left more than right side) with diminished vibration sensation at the left ankle. Her perianal sensation, bilateral temperature sensation, and cerebellar examination were normal.
Magnetic resonance imaging (MRI) without contrast of the lumbar spine demonstrated ischemia findings corresponding to T12-L1. Degenerative changes from L1-S1 were noted, with multiple osteophytes impinging on the neural foramina without cord compression.
THE DIAGNOSIS
The initial presentation was consistent with mechanical low back pain with signs of anterior spinal artery infarction and medial lemniscus pathway involvement 48 hours after initial presentation. Spinal cord infarction occurs more commonly in women and in the young than does cerebral infarction,1 with better reemployment rates.1,2 Similar to other strokes, long-term prognosis is primarily determined by the initial severity of motor impairment, which is linked to long-term immobility and need for bladder catheterization.3
Neurogenic pain developing years after spinal cord infarction is most often observed in anterior spinal artery infarction4 without functional limitations.
Initial treatment. Our patient was started on aspirin 325 mg/d and clopidogrel 75 mg/d. Her mean arterial blood pressure was maintained above 80 mm Hg. Computed tomography angiography of the abdomen and pelvis was negative for aortic dissection. Lumbar puncture for cerebrospinal fluid analysis was unremarkable. Results of antineutrophil cytoplasmic antibody testing, antinuclear antibody testing, a hepatitis panel, and an antiphospholipid panel were all negative. The patient was started on IV steroids with a plan for gradual tapering. The neurosurgical team agreed with medical management.
Continue to: DISCUSSION
DISCUSSION
Possible etiologies for acute spinal cord infarction include spinal cord ischemia from compression of the vessels, fibrocartilaginous embolism, and arterial thrombosis or atherosclerosis, especially in patients with diabetes.5
The majority (86%) of spinal strokes are due to spontaneous occlusion of the vessels with no identifiable cause; much less frequently (9% of cases), hemorrhage is the causative factor.1 A retrospective study demonstrated that 10 of 27 patients with spinal stroke had an anterior spinal infarct. Of those 10 patients, 6 reported a mechanical triggering movement (similar to this case), indicating potential compression of the radicular arteries due to said movement.4
Fibrocartilaginous embolism (FCE) is worth considering as a possible cause, because it accounts for 5.5% of all cases of acute spinal cord infarction.3 FCE is thought to arise after a precipitating event such as minor trauma, heavy lifting, physical exertion, or Valsalva maneuver causing embolization of the fragments of nucleus pulposus to the arterial system. In a case series of 8 patients, 2 had possible FCE with precipitating events occurring within the prior 24 hours. This was also demonstrated in another case series6 in which 7 of 9 patients had precipitating events.
Although FCE can only definitively be diagnosed postmortem, the researchers6 proposed clinical criteria for its diagnosis in living patients, based on 40 postmortem and 11 suspected antemortem cases of FCE. These criteria include a rapid evolution of symptoms consistent with vascular etiology, with or without preceding minor trauma or Valsalva maneuver; MRI changes consistent with ischemic myelopathy, with or without evidence of disc herniation; and no more than 2 vascular risk factors.
Our patient had no trauma (although there was a triggering movement), no signs of disc herniation, and 2 risk factors (> 60 years and diabetes mellitus). Also, a neurologically symptom-free interval between the painful movement and the onset of neurologic manifestations in our case parallels the clinical picture of FCE.
Continue to: The role of factor V Leiden (FVL) mutation
The role of factor V Leiden (FVL) mutation in arterial thrombosis is questionable. Previous reports demonstrate a risk for venous thrombosis 7 to 10 times higher with heterozygous FVL mutation and 100 times higher with homozygous mutation, with a less established role in arterial thrombosis.7 A retrospective Turkish study compared the incidence of FVL mutation in patients with arterial thrombosis vs healthy subjects; incidence was significantly higher in female patients than female controls (37.5% vs. 2%).7 A meta-analysis of published studies showed an association between arterial ischemic events and FVL mutation to be modest, with an odds ratio of 1.21 (95% CI, 0.99-1.49).8
In contrast, a 3.4-year longitudinal health study of patients ages 65 and older found no significant difference in the occurrence of myocardial infarction, transient ischemic attack, stroke, or angina for more than 5000 patients with heterozygous FVL mutation compared to fewer than 500 controls.9 The case patient’s clinical course did not fit a thrombotic clinical picture.
Evaluating for “red flags” is crucial in any case of low back pain to exclude serious pathologies. Red flag symptoms include signs of myelopathy, signs of infection, history of trauma with focal tenderness to palpation, and steroid or anticoagulant use (to rule out medication adverse effects).10 Our patient lacked these classical signs, but she did have subjective pain out of proportion to the clinical exam findings.
Of note: The above red flags for low back pain are all based on expert opinion,11 and the positive predictive value of a red flag is always low because of the low prevalence of serious spinal pathologies.12
Striking a proper balance. This case emphasizes the necessity to keep uncommon causes—such as nontraumatic spinal stroke, which has a prevalence of about 5% to 8% of all acute myelopathies—in the differential diagnosis.3
Continue to: We recommend watchful...
We recommend watchful waiting coupled with communication with the patient regarding monitoring for changes in symptoms over time.11 Any changes in symptoms concerning for underlying spinal cord injury indicate necessity for transfer to a tertiary care center (if possible), along with immediate evaluation with imaging—including computed tomography angiography of the abdomen to rule out aortic dissection (1%-2% of all spinal cord infarcts), followed by a specialist consultation based on the findings.3
Our patient
Our patient was discharged to rehabilitation on hospital Day 5, after progressive return of lower extremity strength. At the 2-month follow-up visit, she demonstrated grade 4+ strength throughout her lower extremities bilaterally. Weakness was predominant at the hip flexors and ankle dorsiflexors, which was consistent with her status at discharge. She had burning pain in the distribution of the L1 dermatome that responded to ibuprofen.
Hypercoagulability work-up was positive for heterozygous FVL mutation without any previous history of venous thromboembolic disease. She was continued on aspirin 325 mg/d, as per American College of Chest Physicians antithrombotic guidelines.13
One year later, our patient underwent a follow-up MRI of the thoracic spine, which showed an “owl’s eye” hyperintensity in the anterior cord (FIGURE), a sign that’s often seen in bilateral spinal cord infarction
THE TAKEAWAY
Spinal stroke is rare, but a missed diagnosis and lack of treatment can result in long-term morbidity. Therefore, it is prudent to consider this diagnosis in the differential—especially when the patient’s subjective back pain is out of proportion to the clinical examination findings.
CORRESPONDENCE
Srikanth Nithyanandam, MBBS, MS, University of Kentucky Family and Community Medicine, 2195 Harrodsburg Road, Suite 125, Lexington, KY 40504-3504; sri.nisi89@uky.edu.
THE CASE
A 64-year-old woman with a history of late-onset type 1 diabetes mellitus, Hashimoto thyroiditis, and scoliosis presented to the sports medicine clinic with acute-onset, sharp, nonradiating right lower back pain that began when she bent forward to apply lotion. At presentation, she denied fever, chills, numbness, tingling, aggravation of pain with movement, weakness, and incontinence. Her neuromuscular examination was unremarkable except for left-side paraspinal tenderness. She was prescribed cyclobenzaprine for symptomatic relief.
Two days later, she was seen for worsening pain. Her physical exam was unchanged. She was prescribed tramadol and advised to start physical therapy gradually. As the day progressed, however, she developed anterior thigh sensory loss, which gradually extended distally.
The following day, she was brought to the emergency department with severe left-side weakness without urinary incontinence. Her mental status and cranial nerve exams were normal. On examination, strength of the iliopsoas and quadriceps was 1/5 bilaterally, and of the peroneal tendon and gastrocnemius, 3/5 bilaterally. Reflexes of triceps, biceps, knee, and Achilles tendon were symmetric and 3+ with bilateral clonus of the ankle. The Babinski sign was positive bilaterally. The patient had diminished pain sensation bilaterally, extending down from the T11 dermatome (left more than right side) with diminished vibration sensation at the left ankle. Her perianal sensation, bilateral temperature sensation, and cerebellar examination were normal.
Magnetic resonance imaging (MRI) without contrast of the lumbar spine demonstrated ischemia findings corresponding to T12-L1. Degenerative changes from L1-S1 were noted, with multiple osteophytes impinging on the neural foramina without cord compression.
THE DIAGNOSIS
The initial presentation was consistent with mechanical low back pain with signs of anterior spinal artery infarction and medial lemniscus pathway involvement 48 hours after initial presentation. Spinal cord infarction occurs more commonly in women and in the young than does cerebral infarction,1 with better reemployment rates.1,2 Similar to other strokes, long-term prognosis is primarily determined by the initial severity of motor impairment, which is linked to long-term immobility and need for bladder catheterization.3
Neurogenic pain developing years after spinal cord infarction is most often observed in anterior spinal artery infarction4 without functional limitations.
Initial treatment. Our patient was started on aspirin 325 mg/d and clopidogrel 75 mg/d. Her mean arterial blood pressure was maintained above 80 mm Hg. Computed tomography angiography of the abdomen and pelvis was negative for aortic dissection. Lumbar puncture for cerebrospinal fluid analysis was unremarkable. Results of antineutrophil cytoplasmic antibody testing, antinuclear antibody testing, a hepatitis panel, and an antiphospholipid panel were all negative. The patient was started on IV steroids with a plan for gradual tapering. The neurosurgical team agreed with medical management.
Continue to: DISCUSSION
DISCUSSION
Possible etiologies for acute spinal cord infarction include spinal cord ischemia from compression of the vessels, fibrocartilaginous embolism, and arterial thrombosis or atherosclerosis, especially in patients with diabetes.5
The majority (86%) of spinal strokes are due to spontaneous occlusion of the vessels with no identifiable cause; much less frequently (9% of cases), hemorrhage is the causative factor.1 A retrospective study demonstrated that 10 of 27 patients with spinal stroke had an anterior spinal infarct. Of those 10 patients, 6 reported a mechanical triggering movement (similar to this case), indicating potential compression of the radicular arteries due to said movement.4
Fibrocartilaginous embolism (FCE) is worth considering as a possible cause, because it accounts for 5.5% of all cases of acute spinal cord infarction.3 FCE is thought to arise after a precipitating event such as minor trauma, heavy lifting, physical exertion, or Valsalva maneuver causing embolization of the fragments of nucleus pulposus to the arterial system. In a case series of 8 patients, 2 had possible FCE with precipitating events occurring within the prior 24 hours. This was also demonstrated in another case series6 in which 7 of 9 patients had precipitating events.
Although FCE can only definitively be diagnosed postmortem, the researchers6 proposed clinical criteria for its diagnosis in living patients, based on 40 postmortem and 11 suspected antemortem cases of FCE. These criteria include a rapid evolution of symptoms consistent with vascular etiology, with or without preceding minor trauma or Valsalva maneuver; MRI changes consistent with ischemic myelopathy, with or without evidence of disc herniation; and no more than 2 vascular risk factors.
Our patient had no trauma (although there was a triggering movement), no signs of disc herniation, and 2 risk factors (> 60 years and diabetes mellitus). Also, a neurologically symptom-free interval between the painful movement and the onset of neurologic manifestations in our case parallels the clinical picture of FCE.
Continue to: The role of factor V Leiden (FVL) mutation
The role of factor V Leiden (FVL) mutation in arterial thrombosis is questionable. Previous reports demonstrate a risk for venous thrombosis 7 to 10 times higher with heterozygous FVL mutation and 100 times higher with homozygous mutation, with a less established role in arterial thrombosis.7 A retrospective Turkish study compared the incidence of FVL mutation in patients with arterial thrombosis vs healthy subjects; incidence was significantly higher in female patients than female controls (37.5% vs. 2%).7 A meta-analysis of published studies showed an association between arterial ischemic events and FVL mutation to be modest, with an odds ratio of 1.21 (95% CI, 0.99-1.49).8
In contrast, a 3.4-year longitudinal health study of patients ages 65 and older found no significant difference in the occurrence of myocardial infarction, transient ischemic attack, stroke, or angina for more than 5000 patients with heterozygous FVL mutation compared to fewer than 500 controls.9 The case patient’s clinical course did not fit a thrombotic clinical picture.
Evaluating for “red flags” is crucial in any case of low back pain to exclude serious pathologies. Red flag symptoms include signs of myelopathy, signs of infection, history of trauma with focal tenderness to palpation, and steroid or anticoagulant use (to rule out medication adverse effects).10 Our patient lacked these classical signs, but she did have subjective pain out of proportion to the clinical exam findings.
Of note: The above red flags for low back pain are all based on expert opinion,11 and the positive predictive value of a red flag is always low because of the low prevalence of serious spinal pathologies.12
Striking a proper balance. This case emphasizes the necessity to keep uncommon causes—such as nontraumatic spinal stroke, which has a prevalence of about 5% to 8% of all acute myelopathies—in the differential diagnosis.3
Continue to: We recommend watchful...
We recommend watchful waiting coupled with communication with the patient regarding monitoring for changes in symptoms over time.11 Any changes in symptoms concerning for underlying spinal cord injury indicate necessity for transfer to a tertiary care center (if possible), along with immediate evaluation with imaging—including computed tomography angiography of the abdomen to rule out aortic dissection (1%-2% of all spinal cord infarcts), followed by a specialist consultation based on the findings.3
Our patient
Our patient was discharged to rehabilitation on hospital Day 5, after progressive return of lower extremity strength. At the 2-month follow-up visit, she demonstrated grade 4+ strength throughout her lower extremities bilaterally. Weakness was predominant at the hip flexors and ankle dorsiflexors, which was consistent with her status at discharge. She had burning pain in the distribution of the L1 dermatome that responded to ibuprofen.
Hypercoagulability work-up was positive for heterozygous FVL mutation without any previous history of venous thromboembolic disease. She was continued on aspirin 325 mg/d, as per American College of Chest Physicians antithrombotic guidelines.13
One year later, our patient underwent a follow-up MRI of the thoracic spine, which showed an “owl’s eye” hyperintensity in the anterior cord (FIGURE), a sign that’s often seen in bilateral spinal cord infarction
THE TAKEAWAY
Spinal stroke is rare, but a missed diagnosis and lack of treatment can result in long-term morbidity. Therefore, it is prudent to consider this diagnosis in the differential—especially when the patient’s subjective back pain is out of proportion to the clinical examination findings.
CORRESPONDENCE
Srikanth Nithyanandam, MBBS, MS, University of Kentucky Family and Community Medicine, 2195 Harrodsburg Road, Suite 125, Lexington, KY 40504-3504; sri.nisi89@uky.edu.
1. Romi F, Naess H. Spinal cord infarction in clinical neurology: a review of characteristics and long-term prognosis in comparison to cerebral infarction. Eur Neurol. 2016;76:95-98.
2. Hanson SR, Romi F, Rekand T, et al. Long-term outcome after spinal cord infarctions. Acta Neurol Scand. 2015;131:253-257.
3. Rigney L, Cappelen-Smith C, Sebire D, et al. Nontraumatic spinal cord ischaemic syndrome. J Clin Neurosci. 2015;22:1544-1549.
4. Novy J, Carruzzo A, Maeder P, Bogousslavsky J. Spinal cord ischemia: clinical and imaging patterns, pathogenesis, and outcomes in 27 patients. Arch Neurol. 2006;63:1113-1120.
5. Goldstein LB, Adams R, Alberts MJ, et al; American Heart Association; American Stroke Association Stroke Council. Primary prevention of ischemic stroke: a guideline from the American Heart Association/American Stroke Association Stroke Council: cosponsored by the Atherosclerotic Peripheral Vascular Disease Interdisciplinary Working Group; Cardiovascular Nursing Council; Clinical Cardiology Council; Nutrition, Physical Activity, and Metabolism Council; and the Quality of Care and Outcomes Research Interdisciplinary Working Group. Circulation. 2006;113:e873-e923.
6. Mateen FJ, Monrad PA, Hunderfund AN, et al. Clinically suspected fibrocartilaginous embolism: clinical characteristics, treatments, and outcomes. Eur J Neurol. 2011;18:218-225.
7. Ozmen F, Ozmen MM, Ozalp N, et al. The prevalence of factor V (G1691A), MTHFR (C677T) and PT (G20210A) gene mutations in arterial thrombosis. Ulus Travma Acil Cerrahi Derg. 2009;15:113-119.
8. Kim RJ, Becker RC. Association between factor V Leiden, prothrombin G20210A, and methylenetetrahydrofolate reductase C677T mutations and events of the arterial circulatory system: a meta-analysis of published studies. Am Heart J. 2003;146:948-957.
9. Cushman M, Rosendaal FR, Psaty BM, et al. Factor V Leiden is not a risk factor for arterial vascular disease in the elderly: results from the Cardiovascular Health Study. Thromb Haemost. 1998;79:912-915.
10. Strudwick K, McPhee M, Bell A, et al. Review article: best practice management of low back pain in the emergency department (part 1 of the musculoskeletal injuries rapid review series). Emerg Med Australas. 2018;30:18-35.
11. Cook CE, George SZ, Reiman MP. Red flag screening for low back pain: nothing to see here, move along: a narrative review. Br J Sports Med. 2018;52:493-496.
12. Grunau GL, Darlow B, Flynn T, et al. Red flags or red herrings? Redefining the role of red flags in low back pain to reduce overimaging. Br J Sports Med. 2018;52:488-489.
13. Lansberg MG, O’Donnell MJ, Khatri P, et al. Antithrombotic and thrombolytic therapy for ischemic stroke: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest. 2012;141(2 suppl):e601S-e636S.
14. Pikija S, Mutzenbach JS, Kunz AB, et al. Delayed hospital presentation and neuroimaging in non-surgical spinal cord infarction. Front Neurol. 2017;8:143.
1. Romi F, Naess H. Spinal cord infarction in clinical neurology: a review of characteristics and long-term prognosis in comparison to cerebral infarction. Eur Neurol. 2016;76:95-98.
2. Hanson SR, Romi F, Rekand T, et al. Long-term outcome after spinal cord infarctions. Acta Neurol Scand. 2015;131:253-257.
3. Rigney L, Cappelen-Smith C, Sebire D, et al. Nontraumatic spinal cord ischaemic syndrome. J Clin Neurosci. 2015;22:1544-1549.
4. Novy J, Carruzzo A, Maeder P, Bogousslavsky J. Spinal cord ischemia: clinical and imaging patterns, pathogenesis, and outcomes in 27 patients. Arch Neurol. 2006;63:1113-1120.
5. Goldstein LB, Adams R, Alberts MJ, et al; American Heart Association; American Stroke Association Stroke Council. Primary prevention of ischemic stroke: a guideline from the American Heart Association/American Stroke Association Stroke Council: cosponsored by the Atherosclerotic Peripheral Vascular Disease Interdisciplinary Working Group; Cardiovascular Nursing Council; Clinical Cardiology Council; Nutrition, Physical Activity, and Metabolism Council; and the Quality of Care and Outcomes Research Interdisciplinary Working Group. Circulation. 2006;113:e873-e923.
6. Mateen FJ, Monrad PA, Hunderfund AN, et al. Clinically suspected fibrocartilaginous embolism: clinical characteristics, treatments, and outcomes. Eur J Neurol. 2011;18:218-225.
7. Ozmen F, Ozmen MM, Ozalp N, et al. The prevalence of factor V (G1691A), MTHFR (C677T) and PT (G20210A) gene mutations in arterial thrombosis. Ulus Travma Acil Cerrahi Derg. 2009;15:113-119.
8. Kim RJ, Becker RC. Association between factor V Leiden, prothrombin G20210A, and methylenetetrahydrofolate reductase C677T mutations and events of the arterial circulatory system: a meta-analysis of published studies. Am Heart J. 2003;146:948-957.
9. Cushman M, Rosendaal FR, Psaty BM, et al. Factor V Leiden is not a risk factor for arterial vascular disease in the elderly: results from the Cardiovascular Health Study. Thromb Haemost. 1998;79:912-915.
10. Strudwick K, McPhee M, Bell A, et al. Review article: best practice management of low back pain in the emergency department (part 1 of the musculoskeletal injuries rapid review series). Emerg Med Australas. 2018;30:18-35.
11. Cook CE, George SZ, Reiman MP. Red flag screening for low back pain: nothing to see here, move along: a narrative review. Br J Sports Med. 2018;52:493-496.
12. Grunau GL, Darlow B, Flynn T, et al. Red flags or red herrings? Redefining the role of red flags in low back pain to reduce overimaging. Br J Sports Med. 2018;52:488-489.
13. Lansberg MG, O’Donnell MJ, Khatri P, et al. Antithrombotic and thrombolytic therapy for ischemic stroke: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest. 2012;141(2 suppl):e601S-e636S.
14. Pikija S, Mutzenbach JS, Kunz AB, et al. Delayed hospital presentation and neuroimaging in non-surgical spinal cord infarction. Front Neurol. 2017;8:143.
Getting tendinopathy treatment (and terminology) right
The vast majority of patients with tendon problems are successfully treated nonoperatively. But which treatments should you try (and when), and which are not quite ready for prime time? This review presents the evidence for the treatment options available to you. But first, it’s important to get our terminology right.
Tendinitis vs tendinosis vs paratenonitis: Words matter
The term “tendinopathy” encompasses many issues related to tendon pathology including tendinitis, tendinosis, and paratenonitis.1,2 The clinical syndrome consists of pain, swelling, and functional impairment associated with activities of daily living or athletic performance.3 Tendinopathy may be acute or chronic, but most cases result from overuse.1
In healthy tendons, the collagen fibers are packed tightly and organized in a linear pattern (FIGURE 1A). However, tendons that are chronically overused develop cumulative microtrauma that leads to a degenerative process within the tendon that is slow (typically measured in months) to heal. This is due to the relative lack of vasculature and the slow rate of tissue turnover in tendons.2,4,5
Sports and manual labor are the most common causes of tendinopathy, but medical conditions including obesity, high blood pressure, diabetes, and high cholesterol are associated risk factors. Medications, particularly fluoroquinolones and statins, can cause tendon problems, and steroids, particularly those injected intratendinously, have been implicated in tendon rupture.4,6
The term “tendinitis” has long been used for all tendon disorders although it is best reserved for acute inflammatory conditions. For most tendon conditions resulting from overuse, the term “tendinosis” is now more widely recognized and preferred.7,8 Family physicians (FPs) should recognize that tendinitis and tendinosis differ greatly in pathophysiology and treatment.3
Tendinitis: Not as common as you think
Tendinitis is an acute inflammatory condition that accounts for only about 3% of all tendon disorders.3 Patients presenting with tendinitis usually have acute onset of pain and swelling typically either from a new activity or one to which they are unaccustomed (eg, lateral elbow pain after painting a house) or from an acute injury. Partial tearing of the affected tendon is likely, especially following injury.2,3
Tendinosis: A degenerative condition
In contrast to the acute inflammation of tendinitis, tendinosis is a degenerative condition induced by chronic overuse. It is typically encountered in athletes and laborers.2,5,8,9 Tendinotic tissue is generally regarded as noninflammatory, but recent research supports inflammation playing at least a small role, especially in closely associated tissues such as bursae and the paratenon tissue.10
Continue to: Histologically, tendinosis shows...
Histologically, tendinosis shows loss of the typical linear collagen fiber organization, increased mucoid ground substance, hypercellularity, and increased growth of nerves and vessels (FIGURE 1B).
Tendinosis is not always symptomatic.5,11 When pain is present, experts have proposed that it is neurogenically derived rather than from local chemical inflammation. This is supported by evidence of increases in the excitatory neurotransmitter glutamate and its receptor N-methyl-D-aspartate in tendinotic tissue with nerve ingrowth. Tendinotic tissue also contains substance P and calcitonin gene-related peptide, neuropeptides that are associated with pain and nociceptive nerve endings.2,3,6,10
Patients with tendinosis typically present with an insidious onset of a painful, thickened tendon.11 The most common tendons affected include the Achilles, the patellar, the supraspinatus, and the common extensor tendon of the lateral elbow.2 Lower extremity tendinosis is common in athletes, while upper extremity tendinopathies are more often work-related.3
Paratenonitis: Inflammation surrounding the tendon
Occasionally, tendinosis may be associated with paratenonitis, which is inflammation of the paratenon (tissue surrounding some tendons).2,5,10 Paratendinous tissue contains a higher concentration of sensory nerves than the tendon itself and may generate significant discomfort.10,11
The clinical presentation of paratenonitis includes a swollen and erythematous tendon.5 The classic example—de Quervain disease—involves the first dorsal wrist compartment, in which the abductor pollicis longus and extensor pollicis brevis tendons are encased in a synovial sheath. The term tenosynovitis is commonly used to indicate inflammation of both the paratenon and synovial sheath (TABLE 12,3,5,6,9-11).5
Continue to: Treatment demands time and patience
Treatment demands time and patience
Treating tendon conditions is challenging for both the patient and the clinician. Improvement takes time and several different treatment strategies may be required for success. Given the large number of available treatment options and the often weak or limited supporting evidence of their efficacy, designing a treatment plan can be difficult. TABLE 2 summarizes the information detailed below about specific treatment options.
First-line treatments. The vast majority of patients with tendon problems are successfully treated nonoperatively. Reasonable first-line treatments, especially for inflammatory conditions like tendinitis, tenosynovitis, and paratenonitis, include relative rest, activity modification, cryotherapy, and bracing.12-14
Nonsteroidal anti-inflammatory drugs (NSAIDs) for pain control are somewhat controversial. At best, they provide pain relief in the short term (7-14 days); at worst, some studies suggest potential detrimental effects to the tendon.14 If considered, NSAIDs should be used for no longer than 2 weeks. They are ideally reserved for pain control in patients with acute injuries when an inflammatory condition is likely. An alternative for pain control in inflammatory cases is a short course of oral steroids, but the adverse effects of these medications may be challenging for some patients.
Other options. If these more conservative treatments fail, or the patient is experiencing significant and debilitating pain, FPs may consider a corticosteroid injection. If this fails, or the condition is clearly past an inflammatory stage, then physical therapy should be considered. More advanced treatments, such as platelet-rich plasma injections and percutaneous needle tenotomies, are typically reserved for chronic, recalcitrant cases of tendinosis. Various other treatment options are detailed below and can be used on a case-by-case basis. Surgical management should be considered only as a last resort.
Realize that certain barriers may exist to some of these treatments. With extracorporeal shockwave therapy, for example, access to a machine can be challenging, as they are typically only found in major metropolitan areas. Polidocanol, used during sclerotherapy, can be difficult to obtain in the United States. Another challenge is cost. Not all of these procedures are covered by insurance, and they can be expensive when paying out of pocket.
Continue to: Rehabilitation...
Rehabilitation: Eccentric exercises and deep-friction massage
Studies show that eccentric exercises (EEs) help to decrease vascularity and nerve presence in affected tendons, modulate expression of neuronal substances, and may stimulate formation of load-tolerant fibroblasts.2,3
For Achilles tendinosis, EE is a well-established treatment supported by multiple randomized controlled trials (RCTs). Improvements in patient satisfaction and pain range from 60% to 90%; evidence suggests greater success in midsubstance vs insertional Achilles tendinosis.15 The addition of deep-friction massage (DFM), which we’ll discuss in a moment, to EE appears to improve outcomes even more than EE alone.16
EE is also a beneficial treatment for patellar tendinosis,3,14 and it appears to benefit rotator cuff tendinosis,3 but research has shown EE for lateral epicondylosis to be no more effective than stretching alone.17
DFM is for treating tendinosis—not inflammatory conditions. Mechanical stimulation of the tissue being massaged releases cell mediators and growth factors that activate fibroblasts. It is typically performed with plastic or metal tools.16 DFM appears to be a reliable treatment option for the lateral elbow.18
Extracorporeal shockwave therapy appears promising; evidence is limited
Research has shown that extracorporeal shockwave therapy (ESWT) promotes the production of TGF-β1 and IGF-1 in rat models,2 and it is believed to be able to disintegrate calcium deposits and stimulate tissue repair.14 Research is generally supportive of its effectiveness in treating tendinosis; however, evidence is limited by great variability in studies in terms of treatment intensity, frequency, duration, timing, number of treatments, and use of a local anesthetic.14 ESWT appears to be useful in augmenting treatment with EE, particularly with regard to the rotator cuff.19
Continue to: A review of 10 RCTs...
A review of 10 RCTs demonstrated the effectiveness of ESWT for tennis elbow.2 ESWT for greater trochanteric pain syndrome (GTPS, formerly known as trochanteric bursitis) appears to be more effective than corticosteroids and home exercises for outcomes at 4 months and equivalent to home exercises at 15 months.20 In patellar tendinosis, ESWT has been shown to be an effective treatment, especially under ultrasound guidance.12 Studies involving the use of ESWT for Achilles tendinosis have had mixed results for midsubstance tendinosis, and more positive results for insertional tendinosis.15 For a video on how the therapy is administered, see https://www.youtube.com/watch?v=Fq5yqiWByX4.
Glyceryl trinitrate patches: Mixed results
Basic science studies have shown that nitric oxide modulates tendon healing by enhancing fibroblast proliferation and collagen synthesis,2,14 but that it should be used with caution in cardiac patients and in those who take PDE-5 inhibitors. Common adverse effects include rash, headache, and dizziness.
In clinical studies, glyceryl trinitrate (GTN) patches show mixed results. For the upper extremity, GTN appears to be helpful for pain in the short term when combined with physical therapy, but long-term positive outcomes have been absent.21 In one Level 1 study for patellar tendinosis comparing GTN patches with EE to a placebo patch with EE, no significant difference was noted at 24 weeks.22 Benefit for Achilles tendinosis also appears to be lacking.3,23
Corticosteroid injections: Mechanism unknown
The mechanism for the beneficial effects of corticosteroid injections (CSIs) for tendinosis remains controversial. Proposed mechanisms include lysis of peritendinous adhesions, disruption of the nociceptors in the region of the injection, and decreased vascularization.10,15 Given tendinosis is generally regarded as a noninflammatory condition, and the fact that these medications have demonstrated potential negative effects on tendon healing, exercise caution when considering CSIs.2,24
Although steroids can effectively reduce pain in the short term, intermediate- and long-term studies generally show no difference or worse outcomes when they are compared to no treatment, placebo, or other treatment modalities. In fact, strong evidence exists for negative effects of steroids on lateral epicondylosis in both the intermediate (6 months) and long (1 year) term.24 Particular care is required when administering a CSI for medial epicondylosis, as the ulnar nerve is immediately posterior to the medial epicondyle.25
Continue to: In contrast...
In contrast, CSIs appear to be a reliable treatment option for de Quervain disease.26 Landmark-guided injections for GTPS can improve pain in the short term (< 1 month), but are inferior to either home exercises or ESWT beyond a few months. Thus, CSIs are a reasonable option for pain control in GTPS, but should not be the sole treatment modality.20
Studies regarding corticosteroid use for Achilles and patellar tendinosis have had mixed results. Patients can hope for mild improvement in pain at best, and the risk for relapse and tendon rupture is ever present.27 This is especially concerning given the significant load-bearing of the patellar and Achilles tendons.14,15 If you are considering a CSI for these purposes, use imaging guidance to ensure the injection is not placed intratendinously.
Platelet-rich plasma and whole blood: Inducing an anabolic healing response
Platelet-rich plasma (PRP) and whole blood injections both aim to deliver autologous growth factors (eg, VEGF, PDGF, and IGF-1) and bioactive mediators to the site of tendinosis to induce an anabolic healing response. PRP therapy differs from whole blood therapy in that it is withdrawn and then concentrated in a centrifuge before being injected. Patients are typically injected under ultrasound guidance. The great variation in PRP preparation, platelet concentration, use of adjunctive treatments, leukocyte concentration, and number and technique of injections makes it difficult to determine the optimal PRP treatment protocol.10,28,29
In 1 prospective RCT comparing subacromial PRP injections to CSI for the shoulder, the PRP group had better outcomes at 3 months, but similar outcomes at 6 months. The suggestion was made that PRP therapy could be an alternative treatment for individuals with a contraindication to CSIs.30
PRP therapy appears to be an effective treatment option for patellar tendinopathy.28,31 A Level 1 study comparing dry needle tenotomy and EE to dry needle tenotomy with both PRP therapy and EE found faster recovery in the PRP group.32 In another patellar tendon study comparing ESWT to PRP therapy, both were found to be effective, but PRP performed better in terms of pain, function, and satisfaction at 6 and 12 months.12 For Achilles tendons, however, the evidence is mixed; case series have had generally positive outcomes, but the only double-blind RCT found no benefit.28,31
Continue to: In lateral epicondylosis...
In lateral epicondylosis, the use of auto-logous whole blood or PRP injections appears to help both pain and function, with several studies failing to demonstrate superiority of 1 modality over the other.24,25,28,33 This raises the issue of whether PRP therapy is any more effective than whole blood for the treatment of other tendinopathies. Unfortunately, there is a paucity of studies comparing the effectiveness of 1 modality to the other, apart from those for lateral epicondylosis.
Prolotherapy: An option for these 3 conditions
Prolotherapy involves the injection of hypertonic dextrose and local anesthetic, which is believed to lead to an upregulation of inflammatory mediators and growth factors. This treatment usually involves several injections spaced 2 to 6 weeks apart over several months. High-quality studies are not available to clarify the optimal dextrose concentration or number of injections required. The few high-quality studies available support prolotherapy for lateral epicondylosis, rotator cuff tendinopathy, and Osgood Schlatter disease. Lesser-quality studies support its use for refractory pain of the Achilles, hip adductors, and plantar fascia.24,34
Sclerotherapy: Not just for veins
As discussed earlier, tendinotic tissue can have neovascularization that is easily detected on Doppler ultrasound. Sensory nerves typically grow alongside the new vessels. Sclerosing agents, such as polidocanol, can be injected with ultrasound guidance into areas of neovascularization, with the intention of causing denervation and pain relief.15 Neovascularization does not always correlate with pathology, so careful patient selection is necessary.35
Studies of sclerotherapy for patellar tendinopathy are generally favorable. One comparing sclerotherapy to arthroscopic debridement showed improvement in pain from both treatments at 6 and 12 months, but the arthroscopy group had less pain, better satisfaction scores, and a faster return to sport.14 Sclerotherapy is also effective for Achilles tendinosis.15
Stem cells: Not at this time
Stem cell use for tendinosis is based on the theory that these cells possess the capability to differentiate into tenocytes to produce new, healthy tendon tissue. Additionally, stem cell injections are believed to create a local immune response, recruiting local growth factors and cytokines to aide in tendon repair. A recent systematic review failed to identify any high-quality studies (Level 4 data at best) supporting the use of stem cells in tendinopathy, and the researchers did not recommend stem cell use outside of clinical trials at this time.36
Continue to: Percutaneous needle tenotomy...
Percutaneous needle tenotomy: Consider it for difficult cases
Percutaneous needle tenotomy is thought to benefit tendinosis by disrupting the tendinotic tissue via needling, while simultaneously causing bleeding and the release of growth factors to aid in healing. Unlike surgical tenotomy, the procedure is typically performed with ultrasound guidance in the office or other ambulatory setting. After local anesthesia is administered, a needle is passed multiple times through the entire region of abnormality noted on ultrasound. Generally, around 20 to 30 needle fenestrations are performed.37,38
In one retrospective study evaluating 47 patellar tendons, 81% had excellent or good results.38 In a retrospective study for lateral epicondylosis, 80% had good to excellent results.39
CORRESPONDENCE
Kyle Goerl, MD, CAQSM, Lafene Health Center, 1105 Sunset Avenue, Manhattan, KS, 66502-3761; kvg3355@ksu.edu.
1. Andres BM, Murrell GAC. Treatment of tendinopathy: what works, what does not, and what is on the horizon. Clin Orthop Relat Res. 2008;466:1539-1554.
2. Kaeding C, Best TM. Tendinosis: pathophysiology and nonoperative treatment. Sports Health. 2009;1:284-292.
3. Ackermann PW, Renstrom P. Tendinopathy in sport. Sports Health. 2012;4:193-201.
4. Khan KM, Cook JL, Bonar F, et al. Histopathology of common tendinopathies. Update and implications for clinical management. Sports Med. 1999;27:393-408.
5. Maffulli N, Wong J, Almekinders LC. Types and epidemiology of tendinopathy. Clin Sports Med. 2003;22:675-692.
6. Scott A, Backman LJ, Speed C. Tendinopathy: update on pathophysiology. J Orthop Sport Phys Ther. 2015;45:833-841.
7. Puddu G, Ippolito E, Postacchini F. A classification of achilles tendon disease. Am J Sports Med. 1976;4:145-150.
8. Maffulli N, Khan KM, Puddu G. Overuse tendon conditions: time to change a confusing terminology. Arthroscopy. 1998;14:840-843.
9. Kraushaar B, Nirschl R. Current concepts review: tendinosis of the elbow (tennis elbow). J Bone Jt Surg. 1999;81:259-278.
10. Rees JD, Stride M, Scott A. Tendons—time to revisit inflammation. Br J Sports Med. 2014;48:1553-1557.
11. Scott A, Docking S, Vicenzino B, et al. Sports and exercise-related tendinopathies: a review of selected topical issues by participants of the second International Scientific Tendinopathy Symposium (ISTS) Vancouver 2012. Br J Sports Med. 2013;47:536-544.
12. Smith J, Sellon J. Comparing PRP injections with ESWT for athletes with chronic patellar tendinopathy. Clin J Sport Med. 2014;24:88-89.
13. Mallow M, Nazarian LN. Greater trochanteric pain syndrome diagnosis and treatment. Phys Med Rehabil Clin N Am. 2014;25:279-289.
14. Schwartz A, Watson JN, Hutchinson MR. Patellar tendinopathy. Sports Health. 2015;7:415-420.
15. Magnussen RA, Dunn WR, Thomson AB. Nonoperative treatment of midportion Achilles tendinopathy: a systematic review. Clin J Sport Med. 2009;19:54-64.
16. Mccormack JR, Underwood FB, Slaven EJ, et al. Eccentric exercise versus eccentric exercise and soft tissue treatment (Astym) in the management of insertional Achilles tendinopathy: a randomized controlled trial. Sports Health. 2016;8:230-237.
17. Wen DY, Schultz BJ, Schaal B, et al. Eccentric strengthening for chronic lateral epicondylosis: a prospective randomized study. Sports Health. 2011;3:500-503.
18. Yi R, Bratchenko WW, Tan V. Deep friction massage versus steroid injection in the treatment of lateral epicondylitis. Hand (N Y). 2018;13:56-59.
19. Su X, Li Z, Liu Z, et al. Effects of high- and low-energy radial shock waves therapy combined with physiotherapy in the treatment of rotator cuff tendinopathy: a retrospective study. Disabil Rehabil. 2018;40:2488-2494.
20. Barratt PA, Brookes N, Newson A. Conservative treatments for greater trochanteric pain syndrome: a systematic review. Br J Sports Med. 2017;51:97-104.
21. Nguyen L, Kelsberg G, Beecher D, et al. Clinical inquiries: are topical nitrates safe and effective for upper extremity tendinopathies? J Fam Pract. 2014;63:469-470.
22. Steunebrink M, Zwerver J, Brandsema R, et al. Topical glyceryl trinitrate treatment of chronic patellar tendinopathy: a randomised, double-blind, placebo-controlled clinical trial. Br J Sports Med. 2013;47:34-39.
23. Kane TPC, Ismail M, Calder JDF. Topical glyceryl trinitrate and noninsertional Achilles tendinopathy. Am J Sports Med. 2008;36:1160-1163.
24. Coombes BK, Bisset L, Vicenzino B. Efficacy and safety of corticosteroid injections and other injections for management of tendinopathy: a systematic review of randomised controlled trials. Lancet. 2010;376:1751-1767.
25. Taylor SA, Hannafin JA. Evaluation and management of elbow tendinopathy. Sports Health. 2012;4:384-393.
26. Sawaizumi T, Nanno M, Ito H. De Quervain’s disease: efficacy of intra-sheath triamcinolone injection. Int Orthop. 2007;31:265-268.
27. Chen SK, Lu CC, Chou PH, et al. Patellar tendon ruptures in weight lifters after local steroid injections. Arch Orthop Trauma Surg. 2009;129:369-372.
28. Filardo G, Di Matteo B, Kon E, et al. Platelet-rich plasma in tendon-related disorders: results and indications. Knee Surg Sports Traumatol Arthrosc. 2018;26:1984-1999.
29. Cong GT, Carballo C, Camp CL, et al. Platelet-rich plasma in treating patellar tendinopathy. Oper Tech Orthop. 2016;26:110-116.
30. Shams A, El-Sayed M, Gamal O, et al. Subacromial injection of autologous platelet-rich plasma versus corticosteroid for the treatment of symptomatic partial rotator cuff tears. Eur J Orthop Surg Traumatol. 2016;26:837-842.
31. DiMatteo B, Filardo G, Kon E, et al. Platelet-rich plasma: evidence for the treatment of patellar and Achilles tendinopathy — a systematic review. Musculoskelet Surg. 2015;99:1-9.
32. Dragoo JL, Wasterlain AS, Braun HJ, et al. Platelet-rich plasma as a treatment for patellar tendinopathy. Am J Sports Med. 2014;42:610-618.
33. Ellenbecker TS, Nirschl R, Renstrom P. Current concepts in examination and treatment of elbow tendon injury. Sports Health. 2013;5:186-194.
34. Rabago D, Nourani B. Prolotherapy for osteoarthritis and tendinopathy: a descriptive review. Curr Rheumatol Rep. 2017;19:34.
35. Kardouni JR, Seitz AL, Walsworth MK, et al. Neovascularization prevalence in the supraspinatus of patients with rotator cuff tendinopathy. Clin J Sport Med. 2013;23:444-449.
36. Pas HIMFL, Moen MH, Haisma HJ, et al. No evidence for the use of stem cell therapy for tendon disorders: a systematic review. Br J Sports Med. 2017;51:996-1002.
37. Housner JA, Jacobson JA, Misko R. Sonographically guided percutaneous needle tenotomy for the treatment of chronic tendinosis. J Ultrasound Med. 2009;28:1187-1192.
38. Housner JA, Jacobson JA, Morag Y, et al. Should ultrasound-guided needle fenestration be considered as a treatment option for recalcitrant patellar tendinopathy? A retrospective study of 47 cases. Clin J Sport Med. 2010;20:488-490.
39. McShane JM, Nazarian LN, Harwood MI. Sonographically guided percutaneous needle tenotomy for treatment of common extensor tendinosis in the elbow. J Ultrasound Med. 2006;25:1281-1289.
The vast majority of patients with tendon problems are successfully treated nonoperatively. But which treatments should you try (and when), and which are not quite ready for prime time? This review presents the evidence for the treatment options available to you. But first, it’s important to get our terminology right.
Tendinitis vs tendinosis vs paratenonitis: Words matter
The term “tendinopathy” encompasses many issues related to tendon pathology including tendinitis, tendinosis, and paratenonitis.1,2 The clinical syndrome consists of pain, swelling, and functional impairment associated with activities of daily living or athletic performance.3 Tendinopathy may be acute or chronic, but most cases result from overuse.1
In healthy tendons, the collagen fibers are packed tightly and organized in a linear pattern (FIGURE 1A). However, tendons that are chronically overused develop cumulative microtrauma that leads to a degenerative process within the tendon that is slow (typically measured in months) to heal. This is due to the relative lack of vasculature and the slow rate of tissue turnover in tendons.2,4,5
Sports and manual labor are the most common causes of tendinopathy, but medical conditions including obesity, high blood pressure, diabetes, and high cholesterol are associated risk factors. Medications, particularly fluoroquinolones and statins, can cause tendon problems, and steroids, particularly those injected intratendinously, have been implicated in tendon rupture.4,6
The term “tendinitis” has long been used for all tendon disorders although it is best reserved for acute inflammatory conditions. For most tendon conditions resulting from overuse, the term “tendinosis” is now more widely recognized and preferred.7,8 Family physicians (FPs) should recognize that tendinitis and tendinosis differ greatly in pathophysiology and treatment.3
Tendinitis: Not as common as you think
Tendinitis is an acute inflammatory condition that accounts for only about 3% of all tendon disorders.3 Patients presenting with tendinitis usually have acute onset of pain and swelling typically either from a new activity or one to which they are unaccustomed (eg, lateral elbow pain after painting a house) or from an acute injury. Partial tearing of the affected tendon is likely, especially following injury.2,3
Tendinosis: A degenerative condition
In contrast to the acute inflammation of tendinitis, tendinosis is a degenerative condition induced by chronic overuse. It is typically encountered in athletes and laborers.2,5,8,9 Tendinotic tissue is generally regarded as noninflammatory, but recent research supports inflammation playing at least a small role, especially in closely associated tissues such as bursae and the paratenon tissue.10
Continue to: Histologically, tendinosis shows...
Histologically, tendinosis shows loss of the typical linear collagen fiber organization, increased mucoid ground substance, hypercellularity, and increased growth of nerves and vessels (FIGURE 1B).
Tendinosis is not always symptomatic.5,11 When pain is present, experts have proposed that it is neurogenically derived rather than from local chemical inflammation. This is supported by evidence of increases in the excitatory neurotransmitter glutamate and its receptor N-methyl-D-aspartate in tendinotic tissue with nerve ingrowth. Tendinotic tissue also contains substance P and calcitonin gene-related peptide, neuropeptides that are associated with pain and nociceptive nerve endings.2,3,6,10
Patients with tendinosis typically present with an insidious onset of a painful, thickened tendon.11 The most common tendons affected include the Achilles, the patellar, the supraspinatus, and the common extensor tendon of the lateral elbow.2 Lower extremity tendinosis is common in athletes, while upper extremity tendinopathies are more often work-related.3
Paratenonitis: Inflammation surrounding the tendon
Occasionally, tendinosis may be associated with paratenonitis, which is inflammation of the paratenon (tissue surrounding some tendons).2,5,10 Paratendinous tissue contains a higher concentration of sensory nerves than the tendon itself and may generate significant discomfort.10,11
The clinical presentation of paratenonitis includes a swollen and erythematous tendon.5 The classic example—de Quervain disease—involves the first dorsal wrist compartment, in which the abductor pollicis longus and extensor pollicis brevis tendons are encased in a synovial sheath. The term tenosynovitis is commonly used to indicate inflammation of both the paratenon and synovial sheath (TABLE 12,3,5,6,9-11).5
Continue to: Treatment demands time and patience
Treatment demands time and patience
Treating tendon conditions is challenging for both the patient and the clinician. Improvement takes time and several different treatment strategies may be required for success. Given the large number of available treatment options and the often weak or limited supporting evidence of their efficacy, designing a treatment plan can be difficult. TABLE 2 summarizes the information detailed below about specific treatment options.
First-line treatments. The vast majority of patients with tendon problems are successfully treated nonoperatively. Reasonable first-line treatments, especially for inflammatory conditions like tendinitis, tenosynovitis, and paratenonitis, include relative rest, activity modification, cryotherapy, and bracing.12-14
Nonsteroidal anti-inflammatory drugs (NSAIDs) for pain control are somewhat controversial. At best, they provide pain relief in the short term (7-14 days); at worst, some studies suggest potential detrimental effects to the tendon.14 If considered, NSAIDs should be used for no longer than 2 weeks. They are ideally reserved for pain control in patients with acute injuries when an inflammatory condition is likely. An alternative for pain control in inflammatory cases is a short course of oral steroids, but the adverse effects of these medications may be challenging for some patients.
Other options. If these more conservative treatments fail, or the patient is experiencing significant and debilitating pain, FPs may consider a corticosteroid injection. If this fails, or the condition is clearly past an inflammatory stage, then physical therapy should be considered. More advanced treatments, such as platelet-rich plasma injections and percutaneous needle tenotomies, are typically reserved for chronic, recalcitrant cases of tendinosis. Various other treatment options are detailed below and can be used on a case-by-case basis. Surgical management should be considered only as a last resort.
Realize that certain barriers may exist to some of these treatments. With extracorporeal shockwave therapy, for example, access to a machine can be challenging, as they are typically only found in major metropolitan areas. Polidocanol, used during sclerotherapy, can be difficult to obtain in the United States. Another challenge is cost. Not all of these procedures are covered by insurance, and they can be expensive when paying out of pocket.
Continue to: Rehabilitation...
Rehabilitation: Eccentric exercises and deep-friction massage
Studies show that eccentric exercises (EEs) help to decrease vascularity and nerve presence in affected tendons, modulate expression of neuronal substances, and may stimulate formation of load-tolerant fibroblasts.2,3
For Achilles tendinosis, EE is a well-established treatment supported by multiple randomized controlled trials (RCTs). Improvements in patient satisfaction and pain range from 60% to 90%; evidence suggests greater success in midsubstance vs insertional Achilles tendinosis.15 The addition of deep-friction massage (DFM), which we’ll discuss in a moment, to EE appears to improve outcomes even more than EE alone.16
EE is also a beneficial treatment for patellar tendinosis,3,14 and it appears to benefit rotator cuff tendinosis,3 but research has shown EE for lateral epicondylosis to be no more effective than stretching alone.17
DFM is for treating tendinosis—not inflammatory conditions. Mechanical stimulation of the tissue being massaged releases cell mediators and growth factors that activate fibroblasts. It is typically performed with plastic or metal tools.16 DFM appears to be a reliable treatment option for the lateral elbow.18
Extracorporeal shockwave therapy appears promising; evidence is limited
Research has shown that extracorporeal shockwave therapy (ESWT) promotes the production of TGF-β1 and IGF-1 in rat models,2 and it is believed to be able to disintegrate calcium deposits and stimulate tissue repair.14 Research is generally supportive of its effectiveness in treating tendinosis; however, evidence is limited by great variability in studies in terms of treatment intensity, frequency, duration, timing, number of treatments, and use of a local anesthetic.14 ESWT appears to be useful in augmenting treatment with EE, particularly with regard to the rotator cuff.19
Continue to: A review of 10 RCTs...
A review of 10 RCTs demonstrated the effectiveness of ESWT for tennis elbow.2 ESWT for greater trochanteric pain syndrome (GTPS, formerly known as trochanteric bursitis) appears to be more effective than corticosteroids and home exercises for outcomes at 4 months and equivalent to home exercises at 15 months.20 In patellar tendinosis, ESWT has been shown to be an effective treatment, especially under ultrasound guidance.12 Studies involving the use of ESWT for Achilles tendinosis have had mixed results for midsubstance tendinosis, and more positive results for insertional tendinosis.15 For a video on how the therapy is administered, see https://www.youtube.com/watch?v=Fq5yqiWByX4.
Glyceryl trinitrate patches: Mixed results
Basic science studies have shown that nitric oxide modulates tendon healing by enhancing fibroblast proliferation and collagen synthesis,2,14 but that it should be used with caution in cardiac patients and in those who take PDE-5 inhibitors. Common adverse effects include rash, headache, and dizziness.
In clinical studies, glyceryl trinitrate (GTN) patches show mixed results. For the upper extremity, GTN appears to be helpful for pain in the short term when combined with physical therapy, but long-term positive outcomes have been absent.21 In one Level 1 study for patellar tendinosis comparing GTN patches with EE to a placebo patch with EE, no significant difference was noted at 24 weeks.22 Benefit for Achilles tendinosis also appears to be lacking.3,23
Corticosteroid injections: Mechanism unknown
The mechanism for the beneficial effects of corticosteroid injections (CSIs) for tendinosis remains controversial. Proposed mechanisms include lysis of peritendinous adhesions, disruption of the nociceptors in the region of the injection, and decreased vascularization.10,15 Given tendinosis is generally regarded as a noninflammatory condition, and the fact that these medications have demonstrated potential negative effects on tendon healing, exercise caution when considering CSIs.2,24
Although steroids can effectively reduce pain in the short term, intermediate- and long-term studies generally show no difference or worse outcomes when they are compared to no treatment, placebo, or other treatment modalities. In fact, strong evidence exists for negative effects of steroids on lateral epicondylosis in both the intermediate (6 months) and long (1 year) term.24 Particular care is required when administering a CSI for medial epicondylosis, as the ulnar nerve is immediately posterior to the medial epicondyle.25
Continue to: In contrast...
In contrast, CSIs appear to be a reliable treatment option for de Quervain disease.26 Landmark-guided injections for GTPS can improve pain in the short term (< 1 month), but are inferior to either home exercises or ESWT beyond a few months. Thus, CSIs are a reasonable option for pain control in GTPS, but should not be the sole treatment modality.20
Studies regarding corticosteroid use for Achilles and patellar tendinosis have had mixed results. Patients can hope for mild improvement in pain at best, and the risk for relapse and tendon rupture is ever present.27 This is especially concerning given the significant load-bearing of the patellar and Achilles tendons.14,15 If you are considering a CSI for these purposes, use imaging guidance to ensure the injection is not placed intratendinously.
Platelet-rich plasma and whole blood: Inducing an anabolic healing response
Platelet-rich plasma (PRP) and whole blood injections both aim to deliver autologous growth factors (eg, VEGF, PDGF, and IGF-1) and bioactive mediators to the site of tendinosis to induce an anabolic healing response. PRP therapy differs from whole blood therapy in that it is withdrawn and then concentrated in a centrifuge before being injected. Patients are typically injected under ultrasound guidance. The great variation in PRP preparation, platelet concentration, use of adjunctive treatments, leukocyte concentration, and number and technique of injections makes it difficult to determine the optimal PRP treatment protocol.10,28,29
In 1 prospective RCT comparing subacromial PRP injections to CSI for the shoulder, the PRP group had better outcomes at 3 months, but similar outcomes at 6 months. The suggestion was made that PRP therapy could be an alternative treatment for individuals with a contraindication to CSIs.30
PRP therapy appears to be an effective treatment option for patellar tendinopathy.28,31 A Level 1 study comparing dry needle tenotomy and EE to dry needle tenotomy with both PRP therapy and EE found faster recovery in the PRP group.32 In another patellar tendon study comparing ESWT to PRP therapy, both were found to be effective, but PRP performed better in terms of pain, function, and satisfaction at 6 and 12 months.12 For Achilles tendons, however, the evidence is mixed; case series have had generally positive outcomes, but the only double-blind RCT found no benefit.28,31
Continue to: In lateral epicondylosis...
In lateral epicondylosis, the use of auto-logous whole blood or PRP injections appears to help both pain and function, with several studies failing to demonstrate superiority of 1 modality over the other.24,25,28,33 This raises the issue of whether PRP therapy is any more effective than whole blood for the treatment of other tendinopathies. Unfortunately, there is a paucity of studies comparing the effectiveness of 1 modality to the other, apart from those for lateral epicondylosis.
Prolotherapy: An option for these 3 conditions
Prolotherapy involves the injection of hypertonic dextrose and local anesthetic, which is believed to lead to an upregulation of inflammatory mediators and growth factors. This treatment usually involves several injections spaced 2 to 6 weeks apart over several months. High-quality studies are not available to clarify the optimal dextrose concentration or number of injections required. The few high-quality studies available support prolotherapy for lateral epicondylosis, rotator cuff tendinopathy, and Osgood Schlatter disease. Lesser-quality studies support its use for refractory pain of the Achilles, hip adductors, and plantar fascia.24,34
Sclerotherapy: Not just for veins
As discussed earlier, tendinotic tissue can have neovascularization that is easily detected on Doppler ultrasound. Sensory nerves typically grow alongside the new vessels. Sclerosing agents, such as polidocanol, can be injected with ultrasound guidance into areas of neovascularization, with the intention of causing denervation and pain relief.15 Neovascularization does not always correlate with pathology, so careful patient selection is necessary.35
Studies of sclerotherapy for patellar tendinopathy are generally favorable. One comparing sclerotherapy to arthroscopic debridement showed improvement in pain from both treatments at 6 and 12 months, but the arthroscopy group had less pain, better satisfaction scores, and a faster return to sport.14 Sclerotherapy is also effective for Achilles tendinosis.15
Stem cells: Not at this time
Stem cell use for tendinosis is based on the theory that these cells possess the capability to differentiate into tenocytes to produce new, healthy tendon tissue. Additionally, stem cell injections are believed to create a local immune response, recruiting local growth factors and cytokines to aide in tendon repair. A recent systematic review failed to identify any high-quality studies (Level 4 data at best) supporting the use of stem cells in tendinopathy, and the researchers did not recommend stem cell use outside of clinical trials at this time.36
Continue to: Percutaneous needle tenotomy...
Percutaneous needle tenotomy: Consider it for difficult cases
Percutaneous needle tenotomy is thought to benefit tendinosis by disrupting the tendinotic tissue via needling, while simultaneously causing bleeding and the release of growth factors to aid in healing. Unlike surgical tenotomy, the procedure is typically performed with ultrasound guidance in the office or other ambulatory setting. After local anesthesia is administered, a needle is passed multiple times through the entire region of abnormality noted on ultrasound. Generally, around 20 to 30 needle fenestrations are performed.37,38
In one retrospective study evaluating 47 patellar tendons, 81% had excellent or good results.38 In a retrospective study for lateral epicondylosis, 80% had good to excellent results.39
CORRESPONDENCE
Kyle Goerl, MD, CAQSM, Lafene Health Center, 1105 Sunset Avenue, Manhattan, KS, 66502-3761; kvg3355@ksu.edu.
The vast majority of patients with tendon problems are successfully treated nonoperatively. But which treatments should you try (and when), and which are not quite ready for prime time? This review presents the evidence for the treatment options available to you. But first, it’s important to get our terminology right.
Tendinitis vs tendinosis vs paratenonitis: Words matter
The term “tendinopathy” encompasses many issues related to tendon pathology including tendinitis, tendinosis, and paratenonitis.1,2 The clinical syndrome consists of pain, swelling, and functional impairment associated with activities of daily living or athletic performance.3 Tendinopathy may be acute or chronic, but most cases result from overuse.1
In healthy tendons, the collagen fibers are packed tightly and organized in a linear pattern (FIGURE 1A). However, tendons that are chronically overused develop cumulative microtrauma that leads to a degenerative process within the tendon that is slow (typically measured in months) to heal. This is due to the relative lack of vasculature and the slow rate of tissue turnover in tendons.2,4,5
Sports and manual labor are the most common causes of tendinopathy, but medical conditions including obesity, high blood pressure, diabetes, and high cholesterol are associated risk factors. Medications, particularly fluoroquinolones and statins, can cause tendon problems, and steroids, particularly those injected intratendinously, have been implicated in tendon rupture.4,6
The term “tendinitis” has long been used for all tendon disorders although it is best reserved for acute inflammatory conditions. For most tendon conditions resulting from overuse, the term “tendinosis” is now more widely recognized and preferred.7,8 Family physicians (FPs) should recognize that tendinitis and tendinosis differ greatly in pathophysiology and treatment.3
Tendinitis: Not as common as you think
Tendinitis is an acute inflammatory condition that accounts for only about 3% of all tendon disorders.3 Patients presenting with tendinitis usually have acute onset of pain and swelling typically either from a new activity or one to which they are unaccustomed (eg, lateral elbow pain after painting a house) or from an acute injury. Partial tearing of the affected tendon is likely, especially following injury.2,3
Tendinosis: A degenerative condition
In contrast to the acute inflammation of tendinitis, tendinosis is a degenerative condition induced by chronic overuse. It is typically encountered in athletes and laborers.2,5,8,9 Tendinotic tissue is generally regarded as noninflammatory, but recent research supports inflammation playing at least a small role, especially in closely associated tissues such as bursae and the paratenon tissue.10
Continue to: Histologically, tendinosis shows...
Histologically, tendinosis shows loss of the typical linear collagen fiber organization, increased mucoid ground substance, hypercellularity, and increased growth of nerves and vessels (FIGURE 1B).
Tendinosis is not always symptomatic.5,11 When pain is present, experts have proposed that it is neurogenically derived rather than from local chemical inflammation. This is supported by evidence of increases in the excitatory neurotransmitter glutamate and its receptor N-methyl-D-aspartate in tendinotic tissue with nerve ingrowth. Tendinotic tissue also contains substance P and calcitonin gene-related peptide, neuropeptides that are associated with pain and nociceptive nerve endings.2,3,6,10
Patients with tendinosis typically present with an insidious onset of a painful, thickened tendon.11 The most common tendons affected include the Achilles, the patellar, the supraspinatus, and the common extensor tendon of the lateral elbow.2 Lower extremity tendinosis is common in athletes, while upper extremity tendinopathies are more often work-related.3
Paratenonitis: Inflammation surrounding the tendon
Occasionally, tendinosis may be associated with paratenonitis, which is inflammation of the paratenon (tissue surrounding some tendons).2,5,10 Paratendinous tissue contains a higher concentration of sensory nerves than the tendon itself and may generate significant discomfort.10,11
The clinical presentation of paratenonitis includes a swollen and erythematous tendon.5 The classic example—de Quervain disease—involves the first dorsal wrist compartment, in which the abductor pollicis longus and extensor pollicis brevis tendons are encased in a synovial sheath. The term tenosynovitis is commonly used to indicate inflammation of both the paratenon and synovial sheath (TABLE 12,3,5,6,9-11).5
Continue to: Treatment demands time and patience
Treatment demands time and patience
Treating tendon conditions is challenging for both the patient and the clinician. Improvement takes time and several different treatment strategies may be required for success. Given the large number of available treatment options and the often weak or limited supporting evidence of their efficacy, designing a treatment plan can be difficult. TABLE 2 summarizes the information detailed below about specific treatment options.
First-line treatments. The vast majority of patients with tendon problems are successfully treated nonoperatively. Reasonable first-line treatments, especially for inflammatory conditions like tendinitis, tenosynovitis, and paratenonitis, include relative rest, activity modification, cryotherapy, and bracing.12-14
Nonsteroidal anti-inflammatory drugs (NSAIDs) for pain control are somewhat controversial. At best, they provide pain relief in the short term (7-14 days); at worst, some studies suggest potential detrimental effects to the tendon.14 If considered, NSAIDs should be used for no longer than 2 weeks. They are ideally reserved for pain control in patients with acute injuries when an inflammatory condition is likely. An alternative for pain control in inflammatory cases is a short course of oral steroids, but the adverse effects of these medications may be challenging for some patients.
Other options. If these more conservative treatments fail, or the patient is experiencing significant and debilitating pain, FPs may consider a corticosteroid injection. If this fails, or the condition is clearly past an inflammatory stage, then physical therapy should be considered. More advanced treatments, such as platelet-rich plasma injections and percutaneous needle tenotomies, are typically reserved for chronic, recalcitrant cases of tendinosis. Various other treatment options are detailed below and can be used on a case-by-case basis. Surgical management should be considered only as a last resort.
Realize that certain barriers may exist to some of these treatments. With extracorporeal shockwave therapy, for example, access to a machine can be challenging, as they are typically only found in major metropolitan areas. Polidocanol, used during sclerotherapy, can be difficult to obtain in the United States. Another challenge is cost. Not all of these procedures are covered by insurance, and they can be expensive when paying out of pocket.
Continue to: Rehabilitation...
Rehabilitation: Eccentric exercises and deep-friction massage
Studies show that eccentric exercises (EEs) help to decrease vascularity and nerve presence in affected tendons, modulate expression of neuronal substances, and may stimulate formation of load-tolerant fibroblasts.2,3
For Achilles tendinosis, EE is a well-established treatment supported by multiple randomized controlled trials (RCTs). Improvements in patient satisfaction and pain range from 60% to 90%; evidence suggests greater success in midsubstance vs insertional Achilles tendinosis.15 The addition of deep-friction massage (DFM), which we’ll discuss in a moment, to EE appears to improve outcomes even more than EE alone.16
EE is also a beneficial treatment for patellar tendinosis,3,14 and it appears to benefit rotator cuff tendinosis,3 but research has shown EE for lateral epicondylosis to be no more effective than stretching alone.17
DFM is for treating tendinosis—not inflammatory conditions. Mechanical stimulation of the tissue being massaged releases cell mediators and growth factors that activate fibroblasts. It is typically performed with plastic or metal tools.16 DFM appears to be a reliable treatment option for the lateral elbow.18
Extracorporeal shockwave therapy appears promising; evidence is limited
Research has shown that extracorporeal shockwave therapy (ESWT) promotes the production of TGF-β1 and IGF-1 in rat models,2 and it is believed to be able to disintegrate calcium deposits and stimulate tissue repair.14 Research is generally supportive of its effectiveness in treating tendinosis; however, evidence is limited by great variability in studies in terms of treatment intensity, frequency, duration, timing, number of treatments, and use of a local anesthetic.14 ESWT appears to be useful in augmenting treatment with EE, particularly with regard to the rotator cuff.19
Continue to: A review of 10 RCTs...
A review of 10 RCTs demonstrated the effectiveness of ESWT for tennis elbow.2 ESWT for greater trochanteric pain syndrome (GTPS, formerly known as trochanteric bursitis) appears to be more effective than corticosteroids and home exercises for outcomes at 4 months and equivalent to home exercises at 15 months.20 In patellar tendinosis, ESWT has been shown to be an effective treatment, especially under ultrasound guidance.12 Studies involving the use of ESWT for Achilles tendinosis have had mixed results for midsubstance tendinosis, and more positive results for insertional tendinosis.15 For a video on how the therapy is administered, see https://www.youtube.com/watch?v=Fq5yqiWByX4.
Glyceryl trinitrate patches: Mixed results
Basic science studies have shown that nitric oxide modulates tendon healing by enhancing fibroblast proliferation and collagen synthesis,2,14 but that it should be used with caution in cardiac patients and in those who take PDE-5 inhibitors. Common adverse effects include rash, headache, and dizziness.
In clinical studies, glyceryl trinitrate (GTN) patches show mixed results. For the upper extremity, GTN appears to be helpful for pain in the short term when combined with physical therapy, but long-term positive outcomes have been absent.21 In one Level 1 study for patellar tendinosis comparing GTN patches with EE to a placebo patch with EE, no significant difference was noted at 24 weeks.22 Benefit for Achilles tendinosis also appears to be lacking.3,23
Corticosteroid injections: Mechanism unknown
The mechanism for the beneficial effects of corticosteroid injections (CSIs) for tendinosis remains controversial. Proposed mechanisms include lysis of peritendinous adhesions, disruption of the nociceptors in the region of the injection, and decreased vascularization.10,15 Given tendinosis is generally regarded as a noninflammatory condition, and the fact that these medications have demonstrated potential negative effects on tendon healing, exercise caution when considering CSIs.2,24
Although steroids can effectively reduce pain in the short term, intermediate- and long-term studies generally show no difference or worse outcomes when they are compared to no treatment, placebo, or other treatment modalities. In fact, strong evidence exists for negative effects of steroids on lateral epicondylosis in both the intermediate (6 months) and long (1 year) term.24 Particular care is required when administering a CSI for medial epicondylosis, as the ulnar nerve is immediately posterior to the medial epicondyle.25
Continue to: In contrast...
In contrast, CSIs appear to be a reliable treatment option for de Quervain disease.26 Landmark-guided injections for GTPS can improve pain in the short term (< 1 month), but are inferior to either home exercises or ESWT beyond a few months. Thus, CSIs are a reasonable option for pain control in GTPS, but should not be the sole treatment modality.20
Studies regarding corticosteroid use for Achilles and patellar tendinosis have had mixed results. Patients can hope for mild improvement in pain at best, and the risk for relapse and tendon rupture is ever present.27 This is especially concerning given the significant load-bearing of the patellar and Achilles tendons.14,15 If you are considering a CSI for these purposes, use imaging guidance to ensure the injection is not placed intratendinously.
Platelet-rich plasma and whole blood: Inducing an anabolic healing response
Platelet-rich plasma (PRP) and whole blood injections both aim to deliver autologous growth factors (eg, VEGF, PDGF, and IGF-1) and bioactive mediators to the site of tendinosis to induce an anabolic healing response. PRP therapy differs from whole blood therapy in that it is withdrawn and then concentrated in a centrifuge before being injected. Patients are typically injected under ultrasound guidance. The great variation in PRP preparation, platelet concentration, use of adjunctive treatments, leukocyte concentration, and number and technique of injections makes it difficult to determine the optimal PRP treatment protocol.10,28,29
In 1 prospective RCT comparing subacromial PRP injections to CSI for the shoulder, the PRP group had better outcomes at 3 months, but similar outcomes at 6 months. The suggestion was made that PRP therapy could be an alternative treatment for individuals with a contraindication to CSIs.30
PRP therapy appears to be an effective treatment option for patellar tendinopathy.28,31 A Level 1 study comparing dry needle tenotomy and EE to dry needle tenotomy with both PRP therapy and EE found faster recovery in the PRP group.32 In another patellar tendon study comparing ESWT to PRP therapy, both were found to be effective, but PRP performed better in terms of pain, function, and satisfaction at 6 and 12 months.12 For Achilles tendons, however, the evidence is mixed; case series have had generally positive outcomes, but the only double-blind RCT found no benefit.28,31
Continue to: In lateral epicondylosis...
In lateral epicondylosis, the use of auto-logous whole blood or PRP injections appears to help both pain and function, with several studies failing to demonstrate superiority of 1 modality over the other.24,25,28,33 This raises the issue of whether PRP therapy is any more effective than whole blood for the treatment of other tendinopathies. Unfortunately, there is a paucity of studies comparing the effectiveness of 1 modality to the other, apart from those for lateral epicondylosis.
Prolotherapy: An option for these 3 conditions
Prolotherapy involves the injection of hypertonic dextrose and local anesthetic, which is believed to lead to an upregulation of inflammatory mediators and growth factors. This treatment usually involves several injections spaced 2 to 6 weeks apart over several months. High-quality studies are not available to clarify the optimal dextrose concentration or number of injections required. The few high-quality studies available support prolotherapy for lateral epicondylosis, rotator cuff tendinopathy, and Osgood Schlatter disease. Lesser-quality studies support its use for refractory pain of the Achilles, hip adductors, and plantar fascia.24,34
Sclerotherapy: Not just for veins
As discussed earlier, tendinotic tissue can have neovascularization that is easily detected on Doppler ultrasound. Sensory nerves typically grow alongside the new vessels. Sclerosing agents, such as polidocanol, can be injected with ultrasound guidance into areas of neovascularization, with the intention of causing denervation and pain relief.15 Neovascularization does not always correlate with pathology, so careful patient selection is necessary.35
Studies of sclerotherapy for patellar tendinopathy are generally favorable. One comparing sclerotherapy to arthroscopic debridement showed improvement in pain from both treatments at 6 and 12 months, but the arthroscopy group had less pain, better satisfaction scores, and a faster return to sport.14 Sclerotherapy is also effective for Achilles tendinosis.15
Stem cells: Not at this time
Stem cell use for tendinosis is based on the theory that these cells possess the capability to differentiate into tenocytes to produce new, healthy tendon tissue. Additionally, stem cell injections are believed to create a local immune response, recruiting local growth factors and cytokines to aide in tendon repair. A recent systematic review failed to identify any high-quality studies (Level 4 data at best) supporting the use of stem cells in tendinopathy, and the researchers did not recommend stem cell use outside of clinical trials at this time.36
Continue to: Percutaneous needle tenotomy...
Percutaneous needle tenotomy: Consider it for difficult cases
Percutaneous needle tenotomy is thought to benefit tendinosis by disrupting the tendinotic tissue via needling, while simultaneously causing bleeding and the release of growth factors to aid in healing. Unlike surgical tenotomy, the procedure is typically performed with ultrasound guidance in the office or other ambulatory setting. After local anesthesia is administered, a needle is passed multiple times through the entire region of abnormality noted on ultrasound. Generally, around 20 to 30 needle fenestrations are performed.37,38
In one retrospective study evaluating 47 patellar tendons, 81% had excellent or good results.38 In a retrospective study for lateral epicondylosis, 80% had good to excellent results.39
CORRESPONDENCE
Kyle Goerl, MD, CAQSM, Lafene Health Center, 1105 Sunset Avenue, Manhattan, KS, 66502-3761; kvg3355@ksu.edu.
1. Andres BM, Murrell GAC. Treatment of tendinopathy: what works, what does not, and what is on the horizon. Clin Orthop Relat Res. 2008;466:1539-1554.
2. Kaeding C, Best TM. Tendinosis: pathophysiology and nonoperative treatment. Sports Health. 2009;1:284-292.
3. Ackermann PW, Renstrom P. Tendinopathy in sport. Sports Health. 2012;4:193-201.
4. Khan KM, Cook JL, Bonar F, et al. Histopathology of common tendinopathies. Update and implications for clinical management. Sports Med. 1999;27:393-408.
5. Maffulli N, Wong J, Almekinders LC. Types and epidemiology of tendinopathy. Clin Sports Med. 2003;22:675-692.
6. Scott A, Backman LJ, Speed C. Tendinopathy: update on pathophysiology. J Orthop Sport Phys Ther. 2015;45:833-841.
7. Puddu G, Ippolito E, Postacchini F. A classification of achilles tendon disease. Am J Sports Med. 1976;4:145-150.
8. Maffulli N, Khan KM, Puddu G. Overuse tendon conditions: time to change a confusing terminology. Arthroscopy. 1998;14:840-843.
9. Kraushaar B, Nirschl R. Current concepts review: tendinosis of the elbow (tennis elbow). J Bone Jt Surg. 1999;81:259-278.
10. Rees JD, Stride M, Scott A. Tendons—time to revisit inflammation. Br J Sports Med. 2014;48:1553-1557.
11. Scott A, Docking S, Vicenzino B, et al. Sports and exercise-related tendinopathies: a review of selected topical issues by participants of the second International Scientific Tendinopathy Symposium (ISTS) Vancouver 2012. Br J Sports Med. 2013;47:536-544.
12. Smith J, Sellon J. Comparing PRP injections with ESWT for athletes with chronic patellar tendinopathy. Clin J Sport Med. 2014;24:88-89.
13. Mallow M, Nazarian LN. Greater trochanteric pain syndrome diagnosis and treatment. Phys Med Rehabil Clin N Am. 2014;25:279-289.
14. Schwartz A, Watson JN, Hutchinson MR. Patellar tendinopathy. Sports Health. 2015;7:415-420.
15. Magnussen RA, Dunn WR, Thomson AB. Nonoperative treatment of midportion Achilles tendinopathy: a systematic review. Clin J Sport Med. 2009;19:54-64.
16. Mccormack JR, Underwood FB, Slaven EJ, et al. Eccentric exercise versus eccentric exercise and soft tissue treatment (Astym) in the management of insertional Achilles tendinopathy: a randomized controlled trial. Sports Health. 2016;8:230-237.
17. Wen DY, Schultz BJ, Schaal B, et al. Eccentric strengthening for chronic lateral epicondylosis: a prospective randomized study. Sports Health. 2011;3:500-503.
18. Yi R, Bratchenko WW, Tan V. Deep friction massage versus steroid injection in the treatment of lateral epicondylitis. Hand (N Y). 2018;13:56-59.
19. Su X, Li Z, Liu Z, et al. Effects of high- and low-energy radial shock waves therapy combined with physiotherapy in the treatment of rotator cuff tendinopathy: a retrospective study. Disabil Rehabil. 2018;40:2488-2494.
20. Barratt PA, Brookes N, Newson A. Conservative treatments for greater trochanteric pain syndrome: a systematic review. Br J Sports Med. 2017;51:97-104.
21. Nguyen L, Kelsberg G, Beecher D, et al. Clinical inquiries: are topical nitrates safe and effective for upper extremity tendinopathies? J Fam Pract. 2014;63:469-470.
22. Steunebrink M, Zwerver J, Brandsema R, et al. Topical glyceryl trinitrate treatment of chronic patellar tendinopathy: a randomised, double-blind, placebo-controlled clinical trial. Br J Sports Med. 2013;47:34-39.
23. Kane TPC, Ismail M, Calder JDF. Topical glyceryl trinitrate and noninsertional Achilles tendinopathy. Am J Sports Med. 2008;36:1160-1163.
24. Coombes BK, Bisset L, Vicenzino B. Efficacy and safety of corticosteroid injections and other injections for management of tendinopathy: a systematic review of randomised controlled trials. Lancet. 2010;376:1751-1767.
25. Taylor SA, Hannafin JA. Evaluation and management of elbow tendinopathy. Sports Health. 2012;4:384-393.
26. Sawaizumi T, Nanno M, Ito H. De Quervain’s disease: efficacy of intra-sheath triamcinolone injection. Int Orthop. 2007;31:265-268.
27. Chen SK, Lu CC, Chou PH, et al. Patellar tendon ruptures in weight lifters after local steroid injections. Arch Orthop Trauma Surg. 2009;129:369-372.
28. Filardo G, Di Matteo B, Kon E, et al. Platelet-rich plasma in tendon-related disorders: results and indications. Knee Surg Sports Traumatol Arthrosc. 2018;26:1984-1999.
29. Cong GT, Carballo C, Camp CL, et al. Platelet-rich plasma in treating patellar tendinopathy. Oper Tech Orthop. 2016;26:110-116.
30. Shams A, El-Sayed M, Gamal O, et al. Subacromial injection of autologous platelet-rich plasma versus corticosteroid for the treatment of symptomatic partial rotator cuff tears. Eur J Orthop Surg Traumatol. 2016;26:837-842.
31. DiMatteo B, Filardo G, Kon E, et al. Platelet-rich plasma: evidence for the treatment of patellar and Achilles tendinopathy — a systematic review. Musculoskelet Surg. 2015;99:1-9.
32. Dragoo JL, Wasterlain AS, Braun HJ, et al. Platelet-rich plasma as a treatment for patellar tendinopathy. Am J Sports Med. 2014;42:610-618.
33. Ellenbecker TS, Nirschl R, Renstrom P. Current concepts in examination and treatment of elbow tendon injury. Sports Health. 2013;5:186-194.
34. Rabago D, Nourani B. Prolotherapy for osteoarthritis and tendinopathy: a descriptive review. Curr Rheumatol Rep. 2017;19:34.
35. Kardouni JR, Seitz AL, Walsworth MK, et al. Neovascularization prevalence in the supraspinatus of patients with rotator cuff tendinopathy. Clin J Sport Med. 2013;23:444-449.
36. Pas HIMFL, Moen MH, Haisma HJ, et al. No evidence for the use of stem cell therapy for tendon disorders: a systematic review. Br J Sports Med. 2017;51:996-1002.
37. Housner JA, Jacobson JA, Misko R. Sonographically guided percutaneous needle tenotomy for the treatment of chronic tendinosis. J Ultrasound Med. 2009;28:1187-1192.
38. Housner JA, Jacobson JA, Morag Y, et al. Should ultrasound-guided needle fenestration be considered as a treatment option for recalcitrant patellar tendinopathy? A retrospective study of 47 cases. Clin J Sport Med. 2010;20:488-490.
39. McShane JM, Nazarian LN, Harwood MI. Sonographically guided percutaneous needle tenotomy for treatment of common extensor tendinosis in the elbow. J Ultrasound Med. 2006;25:1281-1289.
1. Andres BM, Murrell GAC. Treatment of tendinopathy: what works, what does not, and what is on the horizon. Clin Orthop Relat Res. 2008;466:1539-1554.
2. Kaeding C, Best TM. Tendinosis: pathophysiology and nonoperative treatment. Sports Health. 2009;1:284-292.
3. Ackermann PW, Renstrom P. Tendinopathy in sport. Sports Health. 2012;4:193-201.
4. Khan KM, Cook JL, Bonar F, et al. Histopathology of common tendinopathies. Update and implications for clinical management. Sports Med. 1999;27:393-408.
5. Maffulli N, Wong J, Almekinders LC. Types and epidemiology of tendinopathy. Clin Sports Med. 2003;22:675-692.
6. Scott A, Backman LJ, Speed C. Tendinopathy: update on pathophysiology. J Orthop Sport Phys Ther. 2015;45:833-841.
7. Puddu G, Ippolito E, Postacchini F. A classification of achilles tendon disease. Am J Sports Med. 1976;4:145-150.
8. Maffulli N, Khan KM, Puddu G. Overuse tendon conditions: time to change a confusing terminology. Arthroscopy. 1998;14:840-843.
9. Kraushaar B, Nirschl R. Current concepts review: tendinosis of the elbow (tennis elbow). J Bone Jt Surg. 1999;81:259-278.
10. Rees JD, Stride M, Scott A. Tendons—time to revisit inflammation. Br J Sports Med. 2014;48:1553-1557.
11. Scott A, Docking S, Vicenzino B, et al. Sports and exercise-related tendinopathies: a review of selected topical issues by participants of the second International Scientific Tendinopathy Symposium (ISTS) Vancouver 2012. Br J Sports Med. 2013;47:536-544.
12. Smith J, Sellon J. Comparing PRP injections with ESWT for athletes with chronic patellar tendinopathy. Clin J Sport Med. 2014;24:88-89.
13. Mallow M, Nazarian LN. Greater trochanteric pain syndrome diagnosis and treatment. Phys Med Rehabil Clin N Am. 2014;25:279-289.
14. Schwartz A, Watson JN, Hutchinson MR. Patellar tendinopathy. Sports Health. 2015;7:415-420.
15. Magnussen RA, Dunn WR, Thomson AB. Nonoperative treatment of midportion Achilles tendinopathy: a systematic review. Clin J Sport Med. 2009;19:54-64.
16. Mccormack JR, Underwood FB, Slaven EJ, et al. Eccentric exercise versus eccentric exercise and soft tissue treatment (Astym) in the management of insertional Achilles tendinopathy: a randomized controlled trial. Sports Health. 2016;8:230-237.
17. Wen DY, Schultz BJ, Schaal B, et al. Eccentric strengthening for chronic lateral epicondylosis: a prospective randomized study. Sports Health. 2011;3:500-503.
18. Yi R, Bratchenko WW, Tan V. Deep friction massage versus steroid injection in the treatment of lateral epicondylitis. Hand (N Y). 2018;13:56-59.
19. Su X, Li Z, Liu Z, et al. Effects of high- and low-energy radial shock waves therapy combined with physiotherapy in the treatment of rotator cuff tendinopathy: a retrospective study. Disabil Rehabil. 2018;40:2488-2494.
20. Barratt PA, Brookes N, Newson A. Conservative treatments for greater trochanteric pain syndrome: a systematic review. Br J Sports Med. 2017;51:97-104.
21. Nguyen L, Kelsberg G, Beecher D, et al. Clinical inquiries: are topical nitrates safe and effective for upper extremity tendinopathies? J Fam Pract. 2014;63:469-470.
22. Steunebrink M, Zwerver J, Brandsema R, et al. Topical glyceryl trinitrate treatment of chronic patellar tendinopathy: a randomised, double-blind, placebo-controlled clinical trial. Br J Sports Med. 2013;47:34-39.
23. Kane TPC, Ismail M, Calder JDF. Topical glyceryl trinitrate and noninsertional Achilles tendinopathy. Am J Sports Med. 2008;36:1160-1163.
24. Coombes BK, Bisset L, Vicenzino B. Efficacy and safety of corticosteroid injections and other injections for management of tendinopathy: a systematic review of randomised controlled trials. Lancet. 2010;376:1751-1767.
25. Taylor SA, Hannafin JA. Evaluation and management of elbow tendinopathy. Sports Health. 2012;4:384-393.
26. Sawaizumi T, Nanno M, Ito H. De Quervain’s disease: efficacy of intra-sheath triamcinolone injection. Int Orthop. 2007;31:265-268.
27. Chen SK, Lu CC, Chou PH, et al. Patellar tendon ruptures in weight lifters after local steroid injections. Arch Orthop Trauma Surg. 2009;129:369-372.
28. Filardo G, Di Matteo B, Kon E, et al. Platelet-rich plasma in tendon-related disorders: results and indications. Knee Surg Sports Traumatol Arthrosc. 2018;26:1984-1999.
29. Cong GT, Carballo C, Camp CL, et al. Platelet-rich plasma in treating patellar tendinopathy. Oper Tech Orthop. 2016;26:110-116.
30. Shams A, El-Sayed M, Gamal O, et al. Subacromial injection of autologous platelet-rich plasma versus corticosteroid for the treatment of symptomatic partial rotator cuff tears. Eur J Orthop Surg Traumatol. 2016;26:837-842.
31. DiMatteo B, Filardo G, Kon E, et al. Platelet-rich plasma: evidence for the treatment of patellar and Achilles tendinopathy — a systematic review. Musculoskelet Surg. 2015;99:1-9.
32. Dragoo JL, Wasterlain AS, Braun HJ, et al. Platelet-rich plasma as a treatment for patellar tendinopathy. Am J Sports Med. 2014;42:610-618.
33. Ellenbecker TS, Nirschl R, Renstrom P. Current concepts in examination and treatment of elbow tendon injury. Sports Health. 2013;5:186-194.
34. Rabago D, Nourani B. Prolotherapy for osteoarthritis and tendinopathy: a descriptive review. Curr Rheumatol Rep. 2017;19:34.
35. Kardouni JR, Seitz AL, Walsworth MK, et al. Neovascularization prevalence in the supraspinatus of patients with rotator cuff tendinopathy. Clin J Sport Med. 2013;23:444-449.
36. Pas HIMFL, Moen MH, Haisma HJ, et al. No evidence for the use of stem cell therapy for tendon disorders: a systematic review. Br J Sports Med. 2017;51:996-1002.
37. Housner JA, Jacobson JA, Misko R. Sonographically guided percutaneous needle tenotomy for the treatment of chronic tendinosis. J Ultrasound Med. 2009;28:1187-1192.
38. Housner JA, Jacobson JA, Morag Y, et al. Should ultrasound-guided needle fenestration be considered as a treatment option for recalcitrant patellar tendinopathy? A retrospective study of 47 cases. Clin J Sport Med. 2010;20:488-490.
39. McShane JM, Nazarian LN, Harwood MI. Sonographically guided percutaneous needle tenotomy for treatment of common extensor tendinosis in the elbow. J Ultrasound Med. 2006;25:1281-1289.
PRACTICE RECOMMENDATIONS
› Recommend eccentric exercises to treat patients with tendinosis; research has consistently shown them to be an effective and safe treatment for many types of this disorder. A
› Use corticosteroid injections with caution for tendinosis; pain relief is typically short lived, and good evidence exists for long-term relapse and worse outcomes including post-injection tendon rupture, especially in the lower extremity. A
Strength of recommendation (SOR)
A Good-quality patient-oriented evidence
B Inconsistent or limited-quality patient-oriented evidence
C Consensus, usual practice, opinion, disease-oriented evidence, case series
Elderly Americans carry heavier opioid burden
according to the Agency for Healthcare Quality and Research.
Elderly adults with chronic and acute pain obtained an average of 774 morphine milligram equivalents (MMEs) of prescription opioids annually during 2015-2016 from outpatient clinicians, compared with 376 MMEs a year for nonelderly adults, said Asako S. Moriya, PhD, and G. Edward Miller, PhD, of the AHRQ.
Narrowing the age groups shows that opioid MMEs increased with age, starting at 49 MMEs for 18- to 26-year-olds and rising to a high of 856 MMEs in the 65- to 74-year-old group, before dropping off in the oldest adults, the investigators said in a Medical Expenditure Panel Survey (MEPS) research findings report.
The analysis included “all opioid medications that are commonly used to treat pain” and excluded respiratory agents, antitussives, and drugs used for medication-assisted treatment, they noted. The MEPS data cover prescriptions purchased or obtained in outpatient settings but not those administered in inpatient settings or in clinics or physician offices.
according to the Agency for Healthcare Quality and Research.
Elderly adults with chronic and acute pain obtained an average of 774 morphine milligram equivalents (MMEs) of prescription opioids annually during 2015-2016 from outpatient clinicians, compared with 376 MMEs a year for nonelderly adults, said Asako S. Moriya, PhD, and G. Edward Miller, PhD, of the AHRQ.
Narrowing the age groups shows that opioid MMEs increased with age, starting at 49 MMEs for 18- to 26-year-olds and rising to a high of 856 MMEs in the 65- to 74-year-old group, before dropping off in the oldest adults, the investigators said in a Medical Expenditure Panel Survey (MEPS) research findings report.
The analysis included “all opioid medications that are commonly used to treat pain” and excluded respiratory agents, antitussives, and drugs used for medication-assisted treatment, they noted. The MEPS data cover prescriptions purchased or obtained in outpatient settings but not those administered in inpatient settings or in clinics or physician offices.
according to the Agency for Healthcare Quality and Research.
Elderly adults with chronic and acute pain obtained an average of 774 morphine milligram equivalents (MMEs) of prescription opioids annually during 2015-2016 from outpatient clinicians, compared with 376 MMEs a year for nonelderly adults, said Asako S. Moriya, PhD, and G. Edward Miller, PhD, of the AHRQ.
Narrowing the age groups shows that opioid MMEs increased with age, starting at 49 MMEs for 18- to 26-year-olds and rising to a high of 856 MMEs in the 65- to 74-year-old group, before dropping off in the oldest adults, the investigators said in a Medical Expenditure Panel Survey (MEPS) research findings report.
The analysis included “all opioid medications that are commonly used to treat pain” and excluded respiratory agents, antitussives, and drugs used for medication-assisted treatment, they noted. The MEPS data cover prescriptions purchased or obtained in outpatient settings but not those administered in inpatient settings or in clinics or physician offices.
American Headache Society updates guideline on neuroimaging for migraine
Migraine with atypical features may require neuroimaging, according to the guideline. These include an unusual aura; change in clinical features; a first or worst migraine; a migraine that presents with brainstem aura, confusion, or motor manifestation; migraine accompaniments in later life; headaches that are side-locked or posttraumatic; and aura that presents without headache.
Assessing the evidence
The recommendation to avoid MRI or CT in otherwise neurologically normal patients with migraine carried a grade A recommendation from the American Headache Society, while the specific considerations for neuroimaging was based on consensus and carried a grade C recommendation, according to lead author Randolph W. Evans, MD, of the department of neurology at Baylor College of Medicine in Houston, and colleagues.
The recommendations, published in the journal Headache (2020 Feb;60(2):318-36), came from a systematic review of 23 studies of adults at least 18 years old who underwent MRI or CT during outpatient treatment for migraine between 1973 and 2018. Ten studies looked at CT neuroimaging in patients with migraine, nine studies examined MRI neuroimaging alone in patients with migraine, and four studies contained adults with headache or migraine who underwent either MRI or CT. The majority of studies analyzed were retrospective or cross-sectional in nature, while four studies were prospective observational studies.
Dr. Evans and colleagues noted that neuroimaging for patients with suspected migraine is ordered for a variety of reasons, such as excluding conditions that aren’t migraine, diagnostic certainty, cognitive bias, practice workflow, medicolegal concerns, addressing patient and family anxiety, and addressing clinician anxiety. Neuroimaging also can be costly, they said, adding up to an estimated $1 billion annually according to one study, and can lead to additional testing from findings that may not be clinically significant.
Good advice, with caveats
In an interview, Alan M. Rapoport, MD, editor-in-chief of Neurology Reviews, said that while he generally does not like broad guideline recommendations, the recommendation made by the American Headache Society to avoid neuroimaging in patients with a normal neurological examination without any atypical features and red flags “takes most of the important factors into consideration and will work almost all the time.” The recommendation made by consensus for specific considerations of neuroimaging was issued by top headache specialists in the United States who reviewed the data, and it is unlikely a patient with a migraine as diagnosed by the International Classification of Headache Disorders with a normal neurological examination would have a significant abnormality that would appear with imaging, Dr. Rapoport said.
“If everyone caring for migraine patients knew these recommendations, and used them unless the patients fit the exclusions mentioned, we would have more efficient clinical practice and save lots of money on unnecessary scanning,” he said.
However, Dr. Rapoport, clinical professor of neurology at the University of California, Los Angeles, founder of the New England Center for Headache, and past president of The International Headache Society, said that not all clinicians will be convinced by the American Headache Society’s recommendations.
“Various third parties often jump on society recommendations or guidelines and prevent smart clinicians from doing what they need to do when they want to disregard the recommendation or guideline,” he explained. “More importantly, if a physician feels the need to think out of the box and image a patient without a clear reason, and the patient cannot pay for the scan when a medical insurance company refuses to authorize it, there can be a bad result if the patient does not get the study.”
Dr. Rapoport noted that the guideline does not address situations where neuroimaging may not pick up conditions that lead to migraine, such as a subarachnoid or subdural hemorrhage, reversible cerebral vasoconstriction syndrome, or early aspects of low cerebrospinal fluid pressure syndrome. Anxiety on the part of the patient or the clinician is another area that can be addressed by future research, he said.
“If the clinician does a good job of explaining the odds of anything significant being found with a typical migraine history and normal examination, and the patient says [they] need an MRI with contrast to be sure, it will be difficult to dissuade them,” said Dr. Rapoport. “If you don’t order one, they will find a way to get one. If it is abnormal, you could be in trouble. Also, if the clinician has no good reason to do a scan but has anxiety about what is being missed, it will probably get done.”
There was no funding source for the guidelines. The authors reported personal and institutional relationships in the form of advisory board memberships, investigator appointments, speakers bureau positions, research support, and consultancies for a variety of pharmaceutical companies, agencies, institutions, publishers, and other organizations.
Migraine with atypical features may require neuroimaging, according to the guideline. These include an unusual aura; change in clinical features; a first or worst migraine; a migraine that presents with brainstem aura, confusion, or motor manifestation; migraine accompaniments in later life; headaches that are side-locked or posttraumatic; and aura that presents without headache.
Assessing the evidence
The recommendation to avoid MRI or CT in otherwise neurologically normal patients with migraine carried a grade A recommendation from the American Headache Society, while the specific considerations for neuroimaging was based on consensus and carried a grade C recommendation, according to lead author Randolph W. Evans, MD, of the department of neurology at Baylor College of Medicine in Houston, and colleagues.
The recommendations, published in the journal Headache (2020 Feb;60(2):318-36), came from a systematic review of 23 studies of adults at least 18 years old who underwent MRI or CT during outpatient treatment for migraine between 1973 and 2018. Ten studies looked at CT neuroimaging in patients with migraine, nine studies examined MRI neuroimaging alone in patients with migraine, and four studies contained adults with headache or migraine who underwent either MRI or CT. The majority of studies analyzed were retrospective or cross-sectional in nature, while four studies were prospective observational studies.
Dr. Evans and colleagues noted that neuroimaging for patients with suspected migraine is ordered for a variety of reasons, such as excluding conditions that aren’t migraine, diagnostic certainty, cognitive bias, practice workflow, medicolegal concerns, addressing patient and family anxiety, and addressing clinician anxiety. Neuroimaging also can be costly, they said, adding up to an estimated $1 billion annually according to one study, and can lead to additional testing from findings that may not be clinically significant.
Good advice, with caveats
In an interview, Alan M. Rapoport, MD, editor-in-chief of Neurology Reviews, said that while he generally does not like broad guideline recommendations, the recommendation made by the American Headache Society to avoid neuroimaging in patients with a normal neurological examination without any atypical features and red flags “takes most of the important factors into consideration and will work almost all the time.” The recommendation made by consensus for specific considerations of neuroimaging was issued by top headache specialists in the United States who reviewed the data, and it is unlikely a patient with a migraine as diagnosed by the International Classification of Headache Disorders with a normal neurological examination would have a significant abnormality that would appear with imaging, Dr. Rapoport said.
“If everyone caring for migraine patients knew these recommendations, and used them unless the patients fit the exclusions mentioned, we would have more efficient clinical practice and save lots of money on unnecessary scanning,” he said.
However, Dr. Rapoport, clinical professor of neurology at the University of California, Los Angeles, founder of the New England Center for Headache, and past president of The International Headache Society, said that not all clinicians will be convinced by the American Headache Society’s recommendations.
“Various third parties often jump on society recommendations or guidelines and prevent smart clinicians from doing what they need to do when they want to disregard the recommendation or guideline,” he explained. “More importantly, if a physician feels the need to think out of the box and image a patient without a clear reason, and the patient cannot pay for the scan when a medical insurance company refuses to authorize it, there can be a bad result if the patient does not get the study.”
Dr. Rapoport noted that the guideline does not address situations where neuroimaging may not pick up conditions that lead to migraine, such as a subarachnoid or subdural hemorrhage, reversible cerebral vasoconstriction syndrome, or early aspects of low cerebrospinal fluid pressure syndrome. Anxiety on the part of the patient or the clinician is another area that can be addressed by future research, he said.
“If the clinician does a good job of explaining the odds of anything significant being found with a typical migraine history and normal examination, and the patient says [they] need an MRI with contrast to be sure, it will be difficult to dissuade them,” said Dr. Rapoport. “If you don’t order one, they will find a way to get one. If it is abnormal, you could be in trouble. Also, if the clinician has no good reason to do a scan but has anxiety about what is being missed, it will probably get done.”
There was no funding source for the guidelines. The authors reported personal and institutional relationships in the form of advisory board memberships, investigator appointments, speakers bureau positions, research support, and consultancies for a variety of pharmaceutical companies, agencies, institutions, publishers, and other organizations.
Migraine with atypical features may require neuroimaging, according to the guideline. These include an unusual aura; change in clinical features; a first or worst migraine; a migraine that presents with brainstem aura, confusion, or motor manifestation; migraine accompaniments in later life; headaches that are side-locked or posttraumatic; and aura that presents without headache.
Assessing the evidence
The recommendation to avoid MRI or CT in otherwise neurologically normal patients with migraine carried a grade A recommendation from the American Headache Society, while the specific considerations for neuroimaging was based on consensus and carried a grade C recommendation, according to lead author Randolph W. Evans, MD, of the department of neurology at Baylor College of Medicine in Houston, and colleagues.
The recommendations, published in the journal Headache (2020 Feb;60(2):318-36), came from a systematic review of 23 studies of adults at least 18 years old who underwent MRI or CT during outpatient treatment for migraine between 1973 and 2018. Ten studies looked at CT neuroimaging in patients with migraine, nine studies examined MRI neuroimaging alone in patients with migraine, and four studies contained adults with headache or migraine who underwent either MRI or CT. The majority of studies analyzed were retrospective or cross-sectional in nature, while four studies were prospective observational studies.
Dr. Evans and colleagues noted that neuroimaging for patients with suspected migraine is ordered for a variety of reasons, such as excluding conditions that aren’t migraine, diagnostic certainty, cognitive bias, practice workflow, medicolegal concerns, addressing patient and family anxiety, and addressing clinician anxiety. Neuroimaging also can be costly, they said, adding up to an estimated $1 billion annually according to one study, and can lead to additional testing from findings that may not be clinically significant.
Good advice, with caveats
In an interview, Alan M. Rapoport, MD, editor-in-chief of Neurology Reviews, said that while he generally does not like broad guideline recommendations, the recommendation made by the American Headache Society to avoid neuroimaging in patients with a normal neurological examination without any atypical features and red flags “takes most of the important factors into consideration and will work almost all the time.” The recommendation made by consensus for specific considerations of neuroimaging was issued by top headache specialists in the United States who reviewed the data, and it is unlikely a patient with a migraine as diagnosed by the International Classification of Headache Disorders with a normal neurological examination would have a significant abnormality that would appear with imaging, Dr. Rapoport said.
“If everyone caring for migraine patients knew these recommendations, and used them unless the patients fit the exclusions mentioned, we would have more efficient clinical practice and save lots of money on unnecessary scanning,” he said.
However, Dr. Rapoport, clinical professor of neurology at the University of California, Los Angeles, founder of the New England Center for Headache, and past president of The International Headache Society, said that not all clinicians will be convinced by the American Headache Society’s recommendations.
“Various third parties often jump on society recommendations or guidelines and prevent smart clinicians from doing what they need to do when they want to disregard the recommendation or guideline,” he explained. “More importantly, if a physician feels the need to think out of the box and image a patient without a clear reason, and the patient cannot pay for the scan when a medical insurance company refuses to authorize it, there can be a bad result if the patient does not get the study.”
Dr. Rapoport noted that the guideline does not address situations where neuroimaging may not pick up conditions that lead to migraine, such as a subarachnoid or subdural hemorrhage, reversible cerebral vasoconstriction syndrome, or early aspects of low cerebrospinal fluid pressure syndrome. Anxiety on the part of the patient or the clinician is another area that can be addressed by future research, he said.
“If the clinician does a good job of explaining the odds of anything significant being found with a typical migraine history and normal examination, and the patient says [they] need an MRI with contrast to be sure, it will be difficult to dissuade them,” said Dr. Rapoport. “If you don’t order one, they will find a way to get one. If it is abnormal, you could be in trouble. Also, if the clinician has no good reason to do a scan but has anxiety about what is being missed, it will probably get done.”
There was no funding source for the guidelines. The authors reported personal and institutional relationships in the form of advisory board memberships, investigator appointments, speakers bureau positions, research support, and consultancies for a variety of pharmaceutical companies, agencies, institutions, publishers, and other organizations.
FROM HEADACHE
Implantable stimulator shows promise for chronic knee pain
NATIONAL HARBOR, MD. – Stimulation of the infrapatellar branch of the saphenous nerve with an implantable electrical device is a potentially effective treatment for chronic, intractable knee pain.
In a small case series consisting of five patients with chronic knee pain, pain intensity scores on the visual analog scale (VAS) dropped from an average of 8 out of 10 before the implant to 1.4 out of 10 when measured 6 months afterward.
Pain relief was also long lasting, with an average score at 2 years still significantly reduced from baseline, at 3 out of 10 on the VAS.
“We have a lot of patients with chronic knee pain, and unfortunately, our hands are tied in terms of what we can do for them,” lead author Kwo Wei David Ho, MD, PhD, Stanford University, California, told Medscape Medical News.
“They can use NSAIDs, physical therapy, some get steroid injections, or genicular nerve blocks, but they don’t work that well. Some have knee replacement surgery, and can still have persistent knee pain after the operation, so here we are using an alternative therapy called peripheral nerve stimulation of the saphenous nerve. This provides a way to relieve pain without nerve destruction or motor dysfunction,” Ho said.
The findings were presented here at the American Academy of Pain Medicine (AAPM) 2020 Annual Meeting.
Patient Controlled
For the study, the investigators surgically implanted five patients with intractable knee pain with the StimRouter™ (Bioness, Inc).
The device takes about 15 to 30 minutes to implant, much like a pacemaker, and reduces pain by delivering gentle electrical stimulation directly to a target peripheral nerve, in this case the saphenous nerve, to interrupt the pain signal, Ho said.
“A thin, threadlike lead, or noodle, is implanted below the skin next to the target peripheral nerve responsible for the pain signal under ultrasound guidance, and then a patch or external pulse transmitter (EPT) is worn on top of the skin. This sends electric stimulation through the skin to the lead,” he explained.
The patient can then control the EPT and adjust stimulation with a wireless handheld programmer.
“Some patients turn it on at night for a couple of hours and then turn it off, some leave it on for the entire night, or the whole day if they prefer. What we’ve been noticing in our series is that after a while, patients are using less and less, and the pain gets better and better, and eventually they stop using it entirely because the pain completely resolves,” Ho said.
Good candidates for this treatment are post-knee replacement patients with residual pain, he added.
Durable Effect
Of the five patients in the case series, four had previous knee arthroplasty.
To determine the chances of a good response to the implant, study participants underwent a diagnostic saphenous nerve block, with the rationale that if the block successfully reduced knee pain by 50% or more in the short term, patients would likely respond well to the implant.
Before the peripheral nerve stimulation implant, the average pain intensity was 7.8 out of 10 on the VAS. After stimulator implantation, the average pain intensity was 1.4 at 6 months (P = .019, in 5 patients). At 1 year, the average pain intensity score was virtually the same, at 1.5 on the VAS, (P = .0032, in 4 patients). At 2 years, the average pain intensity score was 2.75 (P = .12, in 2 patients).
“This study provides preliminary evidence that stimulation at the saphenous nerve may be effective for selected patients with chronic knee pain,” Ho said.
Commenting on the findings for Medscape Medical News, Patrick Tighe, MD, MS, University of Florida, Gainesville, said that chronic knee pain continues to present “numerous diagnostic and therapeutic challenges for many patients.”
“It may be surprising, but there is still so much we don’t know about the innervation of the knee, and we are still learning about different ways to alter the behavior of those nerves,” said Tighe, who was not involved with the current study.
“This work points to some exciting opportunities to help patients suffering from chronic knee pain. We certainly need more research in this area to figure out the optimal approach to applying these findings more widely,” he said.
Ho and Tighe have disclosed no relevant financial relationships.
This article first appeared on Medscape.com.
NATIONAL HARBOR, MD. – Stimulation of the infrapatellar branch of the saphenous nerve with an implantable electrical device is a potentially effective treatment for chronic, intractable knee pain.
In a small case series consisting of five patients with chronic knee pain, pain intensity scores on the visual analog scale (VAS) dropped from an average of 8 out of 10 before the implant to 1.4 out of 10 when measured 6 months afterward.
Pain relief was also long lasting, with an average score at 2 years still significantly reduced from baseline, at 3 out of 10 on the VAS.
“We have a lot of patients with chronic knee pain, and unfortunately, our hands are tied in terms of what we can do for them,” lead author Kwo Wei David Ho, MD, PhD, Stanford University, California, told Medscape Medical News.
“They can use NSAIDs, physical therapy, some get steroid injections, or genicular nerve blocks, but they don’t work that well. Some have knee replacement surgery, and can still have persistent knee pain after the operation, so here we are using an alternative therapy called peripheral nerve stimulation of the saphenous nerve. This provides a way to relieve pain without nerve destruction or motor dysfunction,” Ho said.
The findings were presented here at the American Academy of Pain Medicine (AAPM) 2020 Annual Meeting.
Patient Controlled
For the study, the investigators surgically implanted five patients with intractable knee pain with the StimRouter™ (Bioness, Inc).
The device takes about 15 to 30 minutes to implant, much like a pacemaker, and reduces pain by delivering gentle electrical stimulation directly to a target peripheral nerve, in this case the saphenous nerve, to interrupt the pain signal, Ho said.
“A thin, threadlike lead, or noodle, is implanted below the skin next to the target peripheral nerve responsible for the pain signal under ultrasound guidance, and then a patch or external pulse transmitter (EPT) is worn on top of the skin. This sends electric stimulation through the skin to the lead,” he explained.
The patient can then control the EPT and adjust stimulation with a wireless handheld programmer.
“Some patients turn it on at night for a couple of hours and then turn it off, some leave it on for the entire night, or the whole day if they prefer. What we’ve been noticing in our series is that after a while, patients are using less and less, and the pain gets better and better, and eventually they stop using it entirely because the pain completely resolves,” Ho said.
Good candidates for this treatment are post-knee replacement patients with residual pain, he added.
Durable Effect
Of the five patients in the case series, four had previous knee arthroplasty.
To determine the chances of a good response to the implant, study participants underwent a diagnostic saphenous nerve block, with the rationale that if the block successfully reduced knee pain by 50% or more in the short term, patients would likely respond well to the implant.
Before the peripheral nerve stimulation implant, the average pain intensity was 7.8 out of 10 on the VAS. After stimulator implantation, the average pain intensity was 1.4 at 6 months (P = .019, in 5 patients). At 1 year, the average pain intensity score was virtually the same, at 1.5 on the VAS, (P = .0032, in 4 patients). At 2 years, the average pain intensity score was 2.75 (P = .12, in 2 patients).
“This study provides preliminary evidence that stimulation at the saphenous nerve may be effective for selected patients with chronic knee pain,” Ho said.
Commenting on the findings for Medscape Medical News, Patrick Tighe, MD, MS, University of Florida, Gainesville, said that chronic knee pain continues to present “numerous diagnostic and therapeutic challenges for many patients.”
“It may be surprising, but there is still so much we don’t know about the innervation of the knee, and we are still learning about different ways to alter the behavior of those nerves,” said Tighe, who was not involved with the current study.
“This work points to some exciting opportunities to help patients suffering from chronic knee pain. We certainly need more research in this area to figure out the optimal approach to applying these findings more widely,” he said.
Ho and Tighe have disclosed no relevant financial relationships.
This article first appeared on Medscape.com.
NATIONAL HARBOR, MD. – Stimulation of the infrapatellar branch of the saphenous nerve with an implantable electrical device is a potentially effective treatment for chronic, intractable knee pain.
In a small case series consisting of five patients with chronic knee pain, pain intensity scores on the visual analog scale (VAS) dropped from an average of 8 out of 10 before the implant to 1.4 out of 10 when measured 6 months afterward.
Pain relief was also long lasting, with an average score at 2 years still significantly reduced from baseline, at 3 out of 10 on the VAS.
“We have a lot of patients with chronic knee pain, and unfortunately, our hands are tied in terms of what we can do for them,” lead author Kwo Wei David Ho, MD, PhD, Stanford University, California, told Medscape Medical News.
“They can use NSAIDs, physical therapy, some get steroid injections, or genicular nerve blocks, but they don’t work that well. Some have knee replacement surgery, and can still have persistent knee pain after the operation, so here we are using an alternative therapy called peripheral nerve stimulation of the saphenous nerve. This provides a way to relieve pain without nerve destruction or motor dysfunction,” Ho said.
The findings were presented here at the American Academy of Pain Medicine (AAPM) 2020 Annual Meeting.
Patient Controlled
For the study, the investigators surgically implanted five patients with intractable knee pain with the StimRouter™ (Bioness, Inc).
The device takes about 15 to 30 minutes to implant, much like a pacemaker, and reduces pain by delivering gentle electrical stimulation directly to a target peripheral nerve, in this case the saphenous nerve, to interrupt the pain signal, Ho said.
“A thin, threadlike lead, or noodle, is implanted below the skin next to the target peripheral nerve responsible for the pain signal under ultrasound guidance, and then a patch or external pulse transmitter (EPT) is worn on top of the skin. This sends electric stimulation through the skin to the lead,” he explained.
The patient can then control the EPT and adjust stimulation with a wireless handheld programmer.
“Some patients turn it on at night for a couple of hours and then turn it off, some leave it on for the entire night, or the whole day if they prefer. What we’ve been noticing in our series is that after a while, patients are using less and less, and the pain gets better and better, and eventually they stop using it entirely because the pain completely resolves,” Ho said.
Good candidates for this treatment are post-knee replacement patients with residual pain, he added.
Durable Effect
Of the five patients in the case series, four had previous knee arthroplasty.
To determine the chances of a good response to the implant, study participants underwent a diagnostic saphenous nerve block, with the rationale that if the block successfully reduced knee pain by 50% or more in the short term, patients would likely respond well to the implant.
Before the peripheral nerve stimulation implant, the average pain intensity was 7.8 out of 10 on the VAS. After stimulator implantation, the average pain intensity was 1.4 at 6 months (P = .019, in 5 patients). At 1 year, the average pain intensity score was virtually the same, at 1.5 on the VAS, (P = .0032, in 4 patients). At 2 years, the average pain intensity score was 2.75 (P = .12, in 2 patients).
“This study provides preliminary evidence that stimulation at the saphenous nerve may be effective for selected patients with chronic knee pain,” Ho said.
Commenting on the findings for Medscape Medical News, Patrick Tighe, MD, MS, University of Florida, Gainesville, said that chronic knee pain continues to present “numerous diagnostic and therapeutic challenges for many patients.”
“It may be surprising, but there is still so much we don’t know about the innervation of the knee, and we are still learning about different ways to alter the behavior of those nerves,” said Tighe, who was not involved with the current study.
“This work points to some exciting opportunities to help patients suffering from chronic knee pain. We certainly need more research in this area to figure out the optimal approach to applying these findings more widely,” he said.
Ho and Tighe have disclosed no relevant financial relationships.
This article first appeared on Medscape.com.
Chronic anterior knee pain
A 14-year-old girl with an unremarkable medical history presented to the family medicine clinic with a 6-month history of right knee pain (episodic locking and anterior pain). Physical examination of the knee ligaments revealed that the knee was stable and pain-free in the frontal and sagittal planes. There was no intra-articular effusion, the joint spaces were not painful, and range of motion was normal.
Palpation of the knee elicited pain, notably when the physician rolled his fingers over a “cord” above the internal parapatellar compartment. X-rays of the knee were normal. In light of the patient’s chronic pain, magnetic resonance imaging (MRI) was performed (FIGURE 1).
WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?
Diagnosis: Synovial plica
The MRI with fat saturation revealed a symptomatic synovial plica between the patellar facet and the condyle (FIGURE 1, arrow). The normal x-ray findings had already ruled out osteochondritis dissecans of the femoral condyles, patellar abnormalities, and trochlear dysplasia; the MRI ruled out several additional items in the differential, such as damage to the meniscus, ligament, and/or cartilage.
The synovial plica is a normal structure that develops during the embryogenic phase; however, involution is incomplete in up to 50% of the population, resulting in persistent plicae.1 The plica is often located in a medial position but can occur lateral to, above, or below the knee cap. Although usually asymptomatic, the plica can become pathologic when irritation (eg, from repetitive motion) causes an inflammatory response.1
Synovial plica syndrome, as this condition is known, is a common cause of anterior knee pain in adolescents and athletes; incidence ranges from 3.8% to 5.5%.2 The patient often reports trauma (a direct impact to the knee) or participation in sports activities that require repeated flexion-extension of the knee.3
Presenting symptoms and MRI findings can unlock the diagnosis
The combination of anterior knee pain and a painful parapatellar “cord” on palpation is the most frequent diagnostic sign of synovial plica syndrome.1 Quadriceps wasting, intra-articular effusion, and reduced range of motion of the knee may also be observed.1,4 Some patients experience particularly disconcerting symptoms, such as knee locking, clicking, or instability.1
In most cases, MRI confirms the clinical diagnosis while ruling out other possible causes of the symptoms and associated pathologies.5 However, MRI may not reveal the plica if it is attached to the articular capsule or if there is no intra-articular effusion. Dynamic ultrasound might be of diagnostic value but is operator dependent.4
Continue to: If conservative treatment fails, consider surgical repair
If conservative treatment fails, consider surgical repair
Conservative treatment—a combination of analgesics, anti-inflammatories, and physiotherapy with vastus medialis strengthening and stretching—is the preferred first-line treatment, with a success rate of 40% to 60%.1 If conservative treatment fails, surgical treatment can be
Our patient underwent arthroscopic resection of the plica after 6 months of conservative treatment had failed (FIGURE 2). The patient was able to walk immediately after surgery. The outcome was favorable, since physiotherapy was no longer required 2 months after surgery.
CORRESPONDENCE
Céline Klein, MD, Service d’Orthopédie Pédiatrique, CHU Amiens, Groupe Hospitalier Sud, F-80054 Amiens cedex 1, France; celinekleinfr@yahoo.fr.
1. Camanho GL. Treatment of pathological synovial plicae of the knee. Clinics (Sao Paolo). 2010;65:247-250.
2. Ewing JW. Plica: pathologic or not? J Am Acad Orthop Surg. 1993;1:117-121.
3. Patel DR, Villalobos A. Evaluation and management of knee pain in young athletes: overuse injuries of the knee. Transl Pediatr. 2017;6:190-198.
4. Paczesny Ł, Kruczyński J. Medial plica syndrome of the knee: diagnosis with dynamic sonography. Radiology. 2009;251:439-446.
5. Samim M, Smitaman E, Lawrence D, et al. MRI of anterior knee pain. Skeletal Radiol. 2014;43:875-893.
6. Weckström M, Niva MH, Lamminen A, et al. Arthroscopic resection of medial plica of the knee in young adults. Knee. 2010;17:103-107.
7. Kan H, Arai Y, Nakagawa S, et al. Characteristics of medial plica syndrome complicated with cartilage damage. Int Orthop. 2015;39:2489-2494.
A 14-year-old girl with an unremarkable medical history presented to the family medicine clinic with a 6-month history of right knee pain (episodic locking and anterior pain). Physical examination of the knee ligaments revealed that the knee was stable and pain-free in the frontal and sagittal planes. There was no intra-articular effusion, the joint spaces were not painful, and range of motion was normal.
Palpation of the knee elicited pain, notably when the physician rolled his fingers over a “cord” above the internal parapatellar compartment. X-rays of the knee were normal. In light of the patient’s chronic pain, magnetic resonance imaging (MRI) was performed (FIGURE 1).
WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?
Diagnosis: Synovial plica
The MRI with fat saturation revealed a symptomatic synovial plica between the patellar facet and the condyle (FIGURE 1, arrow). The normal x-ray findings had already ruled out osteochondritis dissecans of the femoral condyles, patellar abnormalities, and trochlear dysplasia; the MRI ruled out several additional items in the differential, such as damage to the meniscus, ligament, and/or cartilage.
The synovial plica is a normal structure that develops during the embryogenic phase; however, involution is incomplete in up to 50% of the population, resulting in persistent plicae.1 The plica is often located in a medial position but can occur lateral to, above, or below the knee cap. Although usually asymptomatic, the plica can become pathologic when irritation (eg, from repetitive motion) causes an inflammatory response.1
Synovial plica syndrome, as this condition is known, is a common cause of anterior knee pain in adolescents and athletes; incidence ranges from 3.8% to 5.5%.2 The patient often reports trauma (a direct impact to the knee) or participation in sports activities that require repeated flexion-extension of the knee.3
Presenting symptoms and MRI findings can unlock the diagnosis
The combination of anterior knee pain and a painful parapatellar “cord” on palpation is the most frequent diagnostic sign of synovial plica syndrome.1 Quadriceps wasting, intra-articular effusion, and reduced range of motion of the knee may also be observed.1,4 Some patients experience particularly disconcerting symptoms, such as knee locking, clicking, or instability.1
In most cases, MRI confirms the clinical diagnosis while ruling out other possible causes of the symptoms and associated pathologies.5 However, MRI may not reveal the plica if it is attached to the articular capsule or if there is no intra-articular effusion. Dynamic ultrasound might be of diagnostic value but is operator dependent.4
Continue to: If conservative treatment fails, consider surgical repair
If conservative treatment fails, consider surgical repair
Conservative treatment—a combination of analgesics, anti-inflammatories, and physiotherapy with vastus medialis strengthening and stretching—is the preferred first-line treatment, with a success rate of 40% to 60%.1 If conservative treatment fails, surgical treatment can be
Our patient underwent arthroscopic resection of the plica after 6 months of conservative treatment had failed (FIGURE 2). The patient was able to walk immediately after surgery. The outcome was favorable, since physiotherapy was no longer required 2 months after surgery.
CORRESPONDENCE
Céline Klein, MD, Service d’Orthopédie Pédiatrique, CHU Amiens, Groupe Hospitalier Sud, F-80054 Amiens cedex 1, France; celinekleinfr@yahoo.fr.
A 14-year-old girl with an unremarkable medical history presented to the family medicine clinic with a 6-month history of right knee pain (episodic locking and anterior pain). Physical examination of the knee ligaments revealed that the knee was stable and pain-free in the frontal and sagittal planes. There was no intra-articular effusion, the joint spaces were not painful, and range of motion was normal.
Palpation of the knee elicited pain, notably when the physician rolled his fingers over a “cord” above the internal parapatellar compartment. X-rays of the knee were normal. In light of the patient’s chronic pain, magnetic resonance imaging (MRI) was performed (FIGURE 1).
WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?
Diagnosis: Synovial plica
The MRI with fat saturation revealed a symptomatic synovial plica between the patellar facet and the condyle (FIGURE 1, arrow). The normal x-ray findings had already ruled out osteochondritis dissecans of the femoral condyles, patellar abnormalities, and trochlear dysplasia; the MRI ruled out several additional items in the differential, such as damage to the meniscus, ligament, and/or cartilage.
The synovial plica is a normal structure that develops during the embryogenic phase; however, involution is incomplete in up to 50% of the population, resulting in persistent plicae.1 The plica is often located in a medial position but can occur lateral to, above, or below the knee cap. Although usually asymptomatic, the plica can become pathologic when irritation (eg, from repetitive motion) causes an inflammatory response.1
Synovial plica syndrome, as this condition is known, is a common cause of anterior knee pain in adolescents and athletes; incidence ranges from 3.8% to 5.5%.2 The patient often reports trauma (a direct impact to the knee) or participation in sports activities that require repeated flexion-extension of the knee.3
Presenting symptoms and MRI findings can unlock the diagnosis
The combination of anterior knee pain and a painful parapatellar “cord” on palpation is the most frequent diagnostic sign of synovial plica syndrome.1 Quadriceps wasting, intra-articular effusion, and reduced range of motion of the knee may also be observed.1,4 Some patients experience particularly disconcerting symptoms, such as knee locking, clicking, or instability.1
In most cases, MRI confirms the clinical diagnosis while ruling out other possible causes of the symptoms and associated pathologies.5 However, MRI may not reveal the plica if it is attached to the articular capsule or if there is no intra-articular effusion. Dynamic ultrasound might be of diagnostic value but is operator dependent.4
Continue to: If conservative treatment fails, consider surgical repair
If conservative treatment fails, consider surgical repair
Conservative treatment—a combination of analgesics, anti-inflammatories, and physiotherapy with vastus medialis strengthening and stretching—is the preferred first-line treatment, with a success rate of 40% to 60%.1 If conservative treatment fails, surgical treatment can be
Our patient underwent arthroscopic resection of the plica after 6 months of conservative treatment had failed (FIGURE 2). The patient was able to walk immediately after surgery. The outcome was favorable, since physiotherapy was no longer required 2 months after surgery.
CORRESPONDENCE
Céline Klein, MD, Service d’Orthopédie Pédiatrique, CHU Amiens, Groupe Hospitalier Sud, F-80054 Amiens cedex 1, France; celinekleinfr@yahoo.fr.
1. Camanho GL. Treatment of pathological synovial plicae of the knee. Clinics (Sao Paolo). 2010;65:247-250.
2. Ewing JW. Plica: pathologic or not? J Am Acad Orthop Surg. 1993;1:117-121.
3. Patel DR, Villalobos A. Evaluation and management of knee pain in young athletes: overuse injuries of the knee. Transl Pediatr. 2017;6:190-198.
4. Paczesny Ł, Kruczyński J. Medial plica syndrome of the knee: diagnosis with dynamic sonography. Radiology. 2009;251:439-446.
5. Samim M, Smitaman E, Lawrence D, et al. MRI of anterior knee pain. Skeletal Radiol. 2014;43:875-893.
6. Weckström M, Niva MH, Lamminen A, et al. Arthroscopic resection of medial plica of the knee in young adults. Knee. 2010;17:103-107.
7. Kan H, Arai Y, Nakagawa S, et al. Characteristics of medial plica syndrome complicated with cartilage damage. Int Orthop. 2015;39:2489-2494.
1. Camanho GL. Treatment of pathological synovial plicae of the knee. Clinics (Sao Paolo). 2010;65:247-250.
2. Ewing JW. Plica: pathologic or not? J Am Acad Orthop Surg. 1993;1:117-121.
3. Patel DR, Villalobos A. Evaluation and management of knee pain in young athletes: overuse injuries of the knee. Transl Pediatr. 2017;6:190-198.
4. Paczesny Ł, Kruczyński J. Medial plica syndrome of the knee: diagnosis with dynamic sonography. Radiology. 2009;251:439-446.
5. Samim M, Smitaman E, Lawrence D, et al. MRI of anterior knee pain. Skeletal Radiol. 2014;43:875-893.
6. Weckström M, Niva MH, Lamminen A, et al. Arthroscopic resection of medial plica of the knee in young adults. Knee. 2010;17:103-107.
7. Kan H, Arai Y, Nakagawa S, et al. Characteristics of medial plica syndrome complicated with cartilage damage. Int Orthop. 2015;39:2489-2494.
Surgery for shoulder pain? Think twice
Shoulder pain is a very common presenting complaint in family physicians’ offices. Typically, a patient will have had minor trauma, such as a fall, or overuse from work or a recreational activity. Most of these patients have rotator cuff injuries, so we refer them to physical therapy or we prescribe a self-directed home exercise program and the problem gradually resolves. If the patient does not improve, however, should s(he) be referred for arthroscopic surgery? This answer, of course, is “it depends.”
In this issue of JFP, Onks et al provide an excellent review of conservative vs surgical management of rotator cuff tears. For complete or near complete tears in young people—especially athletes—arthroscopic surgery is the preferred approach. For partial tears, chronic tears, and for older folks like me, nonoperative management is the preferred approach. Surgery is reserved for those who do not improve with prolonged conservative management.
But what approach is best for the majority of people in whom shoulder pain is due to impingement syndrome, with or without a small rotator cuff tear? This question has been studied extensively and summarized in a recent Cochrane meta-analysis.1
The meta-analysis included 8 trials, with a total of 1062 participants with rotator cuff disease, all with subacromial impingement. “Compared with placebo, high-certainty evidence indicates that subacromial decompression provides no improvement in pain, shoulder function, or health-related quality of life up to one year, and probably no improvement in global success (moderate-certainty evidence).”1
A recently published guideline developed by doctors and patients for the treatment of shoulder pain gives a strong recommendation to avoid surgery for chronic shoulder pain due to impingement syndrome.2
Interestingly, research has shown that arthroscopic surgery for knee osteoarthritis and chronic meniscus tears is no better that conservative therapy.3,4 Similarly, surgery for chronic back pain due to degenerative disease (in the absence of spondylolisthesis) provides minimal, if any, improvement in pain and function.5 I see a pattern here.
When we talk to our patients who are contemplating these surgical procedures for these indications (except complete rotator cuff tears), we should advise them to have limited expectations or to avoid surgery altogether.
1. Karjalainen TV, Jain NB, Page CM, et al. Subacromial decompression surgery for rotator cuff disease. Cochrane Database Syst Rev. 2019;(1):CD005619. Epub January 17, 2019.
2. Vandvik PO, Lahdeoja T, Ardern C, et al. Subacromial decompression surgery for adults with shoulder pain: a clinical practice guideline. BMJ. 2019;364:1294.
3. Monk P, Garfjeld Roberts P, Palmer AJ, et al. The urgent need for evidence in arthroscopic meniscal surgery. Am J Sports Med. 2017;45:965-973.
4. Kirkley A, Birmingham TB, Litchfield RB, et al. A randomized trial of arthroscopic surgery for osteoarthritis of the knee. N Engl J Med. 2008;359:1097-1107.
5. Yavin D, Casha S, Wiebe S, et al. Lumbar fusion for degenerative disease: a systematic review and meta-analysis. Neurosurgery. 2017;80:701-715.
Editor-in-Chief
Editor-in-Chief
Editor-in-Chief
Shoulder pain is a very common presenting complaint in family physicians’ offices. Typically, a patient will have had minor trauma, such as a fall, or overuse from work or a recreational activity. Most of these patients have rotator cuff injuries, so we refer them to physical therapy or we prescribe a self-directed home exercise program and the problem gradually resolves. If the patient does not improve, however, should s(he) be referred for arthroscopic surgery? This answer, of course, is “it depends.”
In this issue of JFP, Onks et al provide an excellent review of conservative vs surgical management of rotator cuff tears. For complete or near complete tears in young people—especially athletes—arthroscopic surgery is the preferred approach. For partial tears, chronic tears, and for older folks like me, nonoperative management is the preferred approach. Surgery is reserved for those who do not improve with prolonged conservative management.
But what approach is best for the majority of people in whom shoulder pain is due to impingement syndrome, with or without a small rotator cuff tear? This question has been studied extensively and summarized in a recent Cochrane meta-analysis.1
The meta-analysis included 8 trials, with a total of 1062 participants with rotator cuff disease, all with subacromial impingement. “Compared with placebo, high-certainty evidence indicates that subacromial decompression provides no improvement in pain, shoulder function, or health-related quality of life up to one year, and probably no improvement in global success (moderate-certainty evidence).”1
A recently published guideline developed by doctors and patients for the treatment of shoulder pain gives a strong recommendation to avoid surgery for chronic shoulder pain due to impingement syndrome.2
Interestingly, research has shown that arthroscopic surgery for knee osteoarthritis and chronic meniscus tears is no better that conservative therapy.3,4 Similarly, surgery for chronic back pain due to degenerative disease (in the absence of spondylolisthesis) provides minimal, if any, improvement in pain and function.5 I see a pattern here.
When we talk to our patients who are contemplating these surgical procedures for these indications (except complete rotator cuff tears), we should advise them to have limited expectations or to avoid surgery altogether.
Shoulder pain is a very common presenting complaint in family physicians’ offices. Typically, a patient will have had minor trauma, such as a fall, or overuse from work or a recreational activity. Most of these patients have rotator cuff injuries, so we refer them to physical therapy or we prescribe a self-directed home exercise program and the problem gradually resolves. If the patient does not improve, however, should s(he) be referred for arthroscopic surgery? This answer, of course, is “it depends.”
In this issue of JFP, Onks et al provide an excellent review of conservative vs surgical management of rotator cuff tears. For complete or near complete tears in young people—especially athletes—arthroscopic surgery is the preferred approach. For partial tears, chronic tears, and for older folks like me, nonoperative management is the preferred approach. Surgery is reserved for those who do not improve with prolonged conservative management.
But what approach is best for the majority of people in whom shoulder pain is due to impingement syndrome, with or without a small rotator cuff tear? This question has been studied extensively and summarized in a recent Cochrane meta-analysis.1
The meta-analysis included 8 trials, with a total of 1062 participants with rotator cuff disease, all with subacromial impingement. “Compared with placebo, high-certainty evidence indicates that subacromial decompression provides no improvement in pain, shoulder function, or health-related quality of life up to one year, and probably no improvement in global success (moderate-certainty evidence).”1
A recently published guideline developed by doctors and patients for the treatment of shoulder pain gives a strong recommendation to avoid surgery for chronic shoulder pain due to impingement syndrome.2
Interestingly, research has shown that arthroscopic surgery for knee osteoarthritis and chronic meniscus tears is no better that conservative therapy.3,4 Similarly, surgery for chronic back pain due to degenerative disease (in the absence of spondylolisthesis) provides minimal, if any, improvement in pain and function.5 I see a pattern here.
When we talk to our patients who are contemplating these surgical procedures for these indications (except complete rotator cuff tears), we should advise them to have limited expectations or to avoid surgery altogether.
1. Karjalainen TV, Jain NB, Page CM, et al. Subacromial decompression surgery for rotator cuff disease. Cochrane Database Syst Rev. 2019;(1):CD005619. Epub January 17, 2019.
2. Vandvik PO, Lahdeoja T, Ardern C, et al. Subacromial decompression surgery for adults with shoulder pain: a clinical practice guideline. BMJ. 2019;364:1294.
3. Monk P, Garfjeld Roberts P, Palmer AJ, et al. The urgent need for evidence in arthroscopic meniscal surgery. Am J Sports Med. 2017;45:965-973.
4. Kirkley A, Birmingham TB, Litchfield RB, et al. A randomized trial of arthroscopic surgery for osteoarthritis of the knee. N Engl J Med. 2008;359:1097-1107.
5. Yavin D, Casha S, Wiebe S, et al. Lumbar fusion for degenerative disease: a systematic review and meta-analysis. Neurosurgery. 2017;80:701-715.
1. Karjalainen TV, Jain NB, Page CM, et al. Subacromial decompression surgery for rotator cuff disease. Cochrane Database Syst Rev. 2019;(1):CD005619. Epub January 17, 2019.
2. Vandvik PO, Lahdeoja T, Ardern C, et al. Subacromial decompression surgery for adults with shoulder pain: a clinical practice guideline. BMJ. 2019;364:1294.
3. Monk P, Garfjeld Roberts P, Palmer AJ, et al. The urgent need for evidence in arthroscopic meniscal surgery. Am J Sports Med. 2017;45:965-973.
4. Kirkley A, Birmingham TB, Litchfield RB, et al. A randomized trial of arthroscopic surgery for osteoarthritis of the knee. N Engl J Med. 2008;359:1097-1107.
5. Yavin D, Casha S, Wiebe S, et al. Lumbar fusion for degenerative disease: a systematic review and meta-analysis. Neurosurgery. 2017;80:701-715.
Borderline personality disorder common in chronic pain patients
NATIONAL HARBOR, MD. – A significant proportion of patients who suffer from chronic pain also have features of borderline personality disorder (BPD), new research shows.
Results of a systematic literature review showed 23% of patients with chronic noncancer pain (CNCP) had some features of BPD, including difficulty maintaining relationships, as well as affect and mood instability.
“The fact that one-fourth of individuals with CNCP could have co-occurring BPD underscores the need for improved access to good psychological care,” lead investigator Fei Cao, MD, PhD, University of Missouri at Kansas City, said in an interview.
“If we treat the borderline personality disorder and address the psychiatric needs as well as the pain needs of the patient, then we will be able to treat their pain more successfully,” Cao said.
The findings were presented at the American Academy of Pain Medicine (AAPM) 2020 Annual Meeting.
Treatment resistance
Cao noted that a “significant number” of CNCP patients have at least some resistance to any type of pain treatment and speculated that BPD may increase treatment-resistant chronic pain.
Initially an anesthesiologist and pain medicine specialist, Cao later became a psychiatrist after recognizing the importance of addressing the underlying psychological needs of patients with chronic pain.
He noted that there is a strong psychological component to chronic pain and that many patients with chronic pain have suffered psychological trauma.
“You have to think about what may have happened to these patients. That is most important. I would not say these are difficult patients. I would say we just don’t know what happened to them,” he said.
To gain a better understanding of the prevalence of BPD in patients suffering from chronic pain and potentially provide some unexploited targets for chronic pain management, the investigators analyzed data from 11 studies published between 1994 and 2019. They found the prevalence of BPD among CNCP patients was 23.3%. Pain types included chronic headache (11.3%), arthritis (27.5%), and chronic spinal cord pain (24.3%).
We also have to treat their BPD. This can then make pain easier to control. Chronic pain management is often long-term and requires good compliance. A diagnosis of BPD might suggest poor compliance,” said Cao.
Screen for BPD
The study findings, he added, indicate a need to screen for BPD in patients with chronic pain. Interventions that are effective in the treatment of BPD and CNCP include cognitive-behavioral therapy, dialectical behavior therapy, antidepressants, and anticonvulsants.
“These should be considered as the first-line treatment in persons with comorbid pain and BPD,” Cao said.
Commenting on the findings, Ann E. Hansen, DVM, MD, Chronic Pain Wellness Center, Phoenix VA Health Care System, Arizona, said the study illustrates the multifactorial nature of chronic pain syndromes, and underscores the importance of a multidisciplinary approach to evaluation and treatment.
“The authors present data showing that BPD is a common diagnosis in patients with chronic pain, thus raising provider awareness to consider BPD and to involve behavioral health colleagues in comanaging these complex patients to achieve optimal outcomes,” Hansen said.
Cao and Hansen have disclosed no relevant financial relationships.
This article first appeared on Medscape.com.
SOURCE: Cao F et al. American Academy of Pain Medicine (AAPM) 2020 Annual Meeting, Abstract 505.
NATIONAL HARBOR, MD. – A significant proportion of patients who suffer from chronic pain also have features of borderline personality disorder (BPD), new research shows.
Results of a systematic literature review showed 23% of patients with chronic noncancer pain (CNCP) had some features of BPD, including difficulty maintaining relationships, as well as affect and mood instability.
“The fact that one-fourth of individuals with CNCP could have co-occurring BPD underscores the need for improved access to good psychological care,” lead investigator Fei Cao, MD, PhD, University of Missouri at Kansas City, said in an interview.
“If we treat the borderline personality disorder and address the psychiatric needs as well as the pain needs of the patient, then we will be able to treat their pain more successfully,” Cao said.
The findings were presented at the American Academy of Pain Medicine (AAPM) 2020 Annual Meeting.
Treatment resistance
Cao noted that a “significant number” of CNCP patients have at least some resistance to any type of pain treatment and speculated that BPD may increase treatment-resistant chronic pain.
Initially an anesthesiologist and pain medicine specialist, Cao later became a psychiatrist after recognizing the importance of addressing the underlying psychological needs of patients with chronic pain.
He noted that there is a strong psychological component to chronic pain and that many patients with chronic pain have suffered psychological trauma.
“You have to think about what may have happened to these patients. That is most important. I would not say these are difficult patients. I would say we just don’t know what happened to them,” he said.
To gain a better understanding of the prevalence of BPD in patients suffering from chronic pain and potentially provide some unexploited targets for chronic pain management, the investigators analyzed data from 11 studies published between 1994 and 2019. They found the prevalence of BPD among CNCP patients was 23.3%. Pain types included chronic headache (11.3%), arthritis (27.5%), and chronic spinal cord pain (24.3%).
We also have to treat their BPD. This can then make pain easier to control. Chronic pain management is often long-term and requires good compliance. A diagnosis of BPD might suggest poor compliance,” said Cao.
Screen for BPD
The study findings, he added, indicate a need to screen for BPD in patients with chronic pain. Interventions that are effective in the treatment of BPD and CNCP include cognitive-behavioral therapy, dialectical behavior therapy, antidepressants, and anticonvulsants.
“These should be considered as the first-line treatment in persons with comorbid pain and BPD,” Cao said.
Commenting on the findings, Ann E. Hansen, DVM, MD, Chronic Pain Wellness Center, Phoenix VA Health Care System, Arizona, said the study illustrates the multifactorial nature of chronic pain syndromes, and underscores the importance of a multidisciplinary approach to evaluation and treatment.
“The authors present data showing that BPD is a common diagnosis in patients with chronic pain, thus raising provider awareness to consider BPD and to involve behavioral health colleagues in comanaging these complex patients to achieve optimal outcomes,” Hansen said.
Cao and Hansen have disclosed no relevant financial relationships.
This article first appeared on Medscape.com.
SOURCE: Cao F et al. American Academy of Pain Medicine (AAPM) 2020 Annual Meeting, Abstract 505.
NATIONAL HARBOR, MD. – A significant proportion of patients who suffer from chronic pain also have features of borderline personality disorder (BPD), new research shows.
Results of a systematic literature review showed 23% of patients with chronic noncancer pain (CNCP) had some features of BPD, including difficulty maintaining relationships, as well as affect and mood instability.
“The fact that one-fourth of individuals with CNCP could have co-occurring BPD underscores the need for improved access to good psychological care,” lead investigator Fei Cao, MD, PhD, University of Missouri at Kansas City, said in an interview.
“If we treat the borderline personality disorder and address the psychiatric needs as well as the pain needs of the patient, then we will be able to treat their pain more successfully,” Cao said.
The findings were presented at the American Academy of Pain Medicine (AAPM) 2020 Annual Meeting.
Treatment resistance
Cao noted that a “significant number” of CNCP patients have at least some resistance to any type of pain treatment and speculated that BPD may increase treatment-resistant chronic pain.
Initially an anesthesiologist and pain medicine specialist, Cao later became a psychiatrist after recognizing the importance of addressing the underlying psychological needs of patients with chronic pain.
He noted that there is a strong psychological component to chronic pain and that many patients with chronic pain have suffered psychological trauma.
“You have to think about what may have happened to these patients. That is most important. I would not say these are difficult patients. I would say we just don’t know what happened to them,” he said.
To gain a better understanding of the prevalence of BPD in patients suffering from chronic pain and potentially provide some unexploited targets for chronic pain management, the investigators analyzed data from 11 studies published between 1994 and 2019. They found the prevalence of BPD among CNCP patients was 23.3%. Pain types included chronic headache (11.3%), arthritis (27.5%), and chronic spinal cord pain (24.3%).
We also have to treat their BPD. This can then make pain easier to control. Chronic pain management is often long-term and requires good compliance. A diagnosis of BPD might suggest poor compliance,” said Cao.
Screen for BPD
The study findings, he added, indicate a need to screen for BPD in patients with chronic pain. Interventions that are effective in the treatment of BPD and CNCP include cognitive-behavioral therapy, dialectical behavior therapy, antidepressants, and anticonvulsants.
“These should be considered as the first-line treatment in persons with comorbid pain and BPD,” Cao said.
Commenting on the findings, Ann E. Hansen, DVM, MD, Chronic Pain Wellness Center, Phoenix VA Health Care System, Arizona, said the study illustrates the multifactorial nature of chronic pain syndromes, and underscores the importance of a multidisciplinary approach to evaluation and treatment.
“The authors present data showing that BPD is a common diagnosis in patients with chronic pain, thus raising provider awareness to consider BPD and to involve behavioral health colleagues in comanaging these complex patients to achieve optimal outcomes,” Hansen said.
Cao and Hansen have disclosed no relevant financial relationships.
This article first appeared on Medscape.com.
SOURCE: Cao F et al. American Academy of Pain Medicine (AAPM) 2020 Annual Meeting, Abstract 505.
REPORTING FROM THE AAPM 2020 ANNUAL MEETING
Fever, abdominal pain, and adnexal mass
At the recommendation of her primary care physician, a 53-year-old perimenopausal woman sought care at the emergency department for the fever, abdominal pain, and pyuria that had persisted for 4 days despite outpatient treatment for pyelonephritis. On physical examination, she was febrile and tachycardic with abdominal tenderness of the left lower quadrant. Genitourinary examination revealed copious brown vaginal discharge, left adnexal tenderness, and no cervical motion tenderness.
Laboratory testing revealed leukocytosis but otherwise normal electrolytes, liver function tests, and lactate levels. Urine culture obtained when she presented to an urgent care facility 3 days earlier had been negative. Computed tomography (CT) was performed and was read by Radiology as “closed loop small bowel obstruction in the left lower abdomen” (FIGURE 1). The patient was taken emergently to the operating room where her entire length of bowel was run without any obstruction found. Instead, the surgeons identified a mass in the left iliac fossa originating from the left ovary and fallopian tube (FIGURE 2).
WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?
Dx: Pelvic inflammatory disease with tubo-ovarian abscess
The presence and location of this mass, paired with the patient’s symptoms, led to the diagnosis of pelvic inflammatory disease. PID is an acute infection of the upper genital tract in women thought to be due to ascending infection from the lower genital tract. The prevalence of PID in reproductive-aged women in the United States is estimated to be 4.4%.1
Diagnosis of PID in middle-aged women is a challenge given the broad differential diagnosis of nonspecific presenting symptoms, lower index of suspicion in this age group, and unknown exact incidence of PID in postmenopausal women. While delay in diagnosis of PID in women of reproductive age is associated with increased infertility and ectopic pregnancy,2 delay in diagnosis in postmenopausal women also poses serious potential complications such as tubo-ovarian abscess (TOA)—as was seen with this patient—and concurrent gynecologic malignancy found on pathology of TOA specimens.3,4
Risk factors for PID in the postmenopausal population include recent uterine instrumentation, history of prior PID, and structural abnormalities such as cervical stenosis, uterine anatomic abnormalities, or tubal disease. The microbiology of PID in postmenopausal women differs from that of women of reproductive age. While sexually transmitted pathogens such as Neisseria gonorrhoeae and Chlamydia trachomatis most commonly are implicated in PID among premenopausal patients, aerobic gram-negative bacteria including Escherichia coli and Klebsiella pneumoniae most frequently are associated in postmenopausal cases.
Differential diagnosis for abdominal pain is broad
The differential diagnosis for a patient with fever and abdominal pain includes PID, as well as the following:
Diverticulitis classically presents with left lower abdominal pain and a low-grade fever. Complications may include bowel obstruction, abscess, fistula, or perforation. Abdominal imaging such as a CT scan is required to establish the diagnosis.
Continue to: Urinary tract infection
Urinary tract infection should be suspected in a patient with dysuria, urinary frequency or urgency, and abdominal or flank pain. Urinalysis and culture should be performed and imaging may be considered for suspected obstruction, complication, or failure to improve on appropriate therapy.
Appendicitis may present as right lower quadrant pain with anorexia, fever, and nausea. Imaging studies such as CT or ultrasound can help support the diagnosis and rule out alternate etiologies of the presenting symptoms.
Ectopic pregnancy—while not considered in this case—should be suspected in a patient presenting with pelvic pain, missed menses or vaginal bleeding, and a positive pregnancy test. Further evaluation may be performed with a transvaginal ultrasound and serial measurement of serum quantitative human chorionic gonadotropin level.
Diagnosing PID is a clinical process
PID often is difficult to diagnose because of an absence of symptoms or the presence of symptoms that are subtle or nonspecific. Laparoscopy or endometrial biopsy can be useful but may not be justifiable due to their invasive nature when symptoms are mild or vague.5 Thus, a diagnosis of PID usually is based on clinical findings.
Clinical criteria to look for. Although PID commonly is attributed to N gonorrhoeae and C trachomatis, fewer than 50% of those with a diagnosis of acute PID test positive for either of these organisms.5 As such, the Centers for Disease Control and Prevention (CDC) 2015 Sexually Transmitted Diseases Treatment Guidelines recommend presumptive treatment for PID in women with pelvic or lower abdominal pain with 1 or more of the following clinical criteria: cervical motion tenderness, uterine tenderness, or adnexal tenderness.
Continue to: The following criteria...
The following criteria enhance specificity and support the diagnosis5:
- oral temperature > 101°F (> 38.3°C),
- abnormal cervical mucopurulent discharge or cervical friability,
- presence of “abundant numbers of white blood cells on saline microscopy of vaginal fluid,”
- elevated erythrocyte sedimentation rate (reference range, 0–20 mm/hr),
- elevated C-reactive protein (reference range, 0.08-3.1 mg/L), and
- laboratory documentation of cervical infection with N gonorrhoeae or C trachomatis.
The CDC also suggests that the most specific criteria for PID include5
- endometrial biopsy consistent with endometritis,
- imaging (transvaginal ultrasound or magnetic resonance imaging) demonstrating fluid-filled tubes, or
- laparoscopic findings consistent with PID.
Treatment of PID includes IV antibiotics
Due to the polymicrobial nature of PID, antibiotics should cover not only gonorrhea and chlamydia but also anaerobic pathogens. CDC guidelines recommend the following treatment5,6:
- intravenous (IV) cefotetan (2 g bid) plus doxycycline (100 mg PO or IV bid),
- IV cefoxitin (2 g qid) plus doxycycline (100 mg PO or IV bid), or
- IV clindamycin (900 mg tid) plus IV or intramuscular (IM) gentamicin loading dose (2 mg/kg) followed by a maintenance dose (1.5 mg/kg tid).
In mild-to-moderate PID cases deemed appropriate for outpatient therapy, the following regimens have been shown to have similar outcomes to IV therapy5,6:
- IM ceftriaxone (250 mg, single dose) plus PO doxycycline (100 mg bid) for 14 days with/without PO metronidazole (500 mg bid) for 14 days,
- IM cefoxitin (2 g, single dose) and PO probenecid (1 g, single dose) plus PO doxycycline (100 mg bid) for 14 days with/without PO metronidazole (500 mg bid) for 14 days, or
- other parenteral third-generation cephalosporin plus PO doxycycline (100 mg bid) for 14 days with/without PO metronidazole (500 mg bid) for 14 days.
Management in older women may be more intensive
Due to the increased risk of malignancy in postmenopausal women with TOA, surgical intervention may be needed.3,4
Continue to: Our patient
Our patient underwent diagnostic laparoscopy, hysterectomy, left salpingo-oophorectomy, and right salpingectomy (with her right ovary left in place due to her perimenopausal status). Intraoperatively, she was found to have cervical stenosis. Postoperatively, she improved on IV cefoxitin (2 g qid) and IV doxycycline (100 mg bid), which was eventually transitioned to oral doxycycline (100 mg bid) and metronidazole (500 mg bid) on discharge.
Her final microbiology was negative for gonorrhea/chlamydia but the bacterial culture of peritoneal fluid grew E coli. Pathology was consistent with acute salpingitis, TOA, and acute cervicitis. She made a full recovery and is doing well.
CORRESPONDENCE
Catherine Peony Khoo, MD, 1920 Colorado Avenue, Santa Monica, CA 90404; Ckhoo@mednet.ucla.edu
1. Kreisel K, Torrone E, Bernstein K, et al. Prevalence of pelvic inflammatory disease in sexually experienced women of reproductive age—United States, 2013-2014. MMWR Morb Mortal Wkly Rep. 2017;66:80-83.
2. Weström L, Joesoef R, Reynolds G, et al. Pelvic inflammatory disease and fertility: a cohort study of 1,844 women with laparoscopically verified disease and 657 control women with normal laparoscopic results. Sex Transm Dis. 1992;19:185-192.
3. Jackson SL, Soper DE. Pelvic inflammatory disease in the postmenopausal woman. Infect Dis Obstet Gynecol. 1999;7:248-252.
4. Protopas AG, Diakomanolis ES, Milingos SD, et al. Tubo-ovarian abscesses in postmenopausal women: gynecological malignancy until proven otherwise? Eur J Obstet Gynecol Reprod Biol. 2004;114:203-209.
5. Workowski KA, Bolan GA; Centers for Disease Control and Prevention. Sexually transmitted diseases treatment guidelines, 2015. MMWR Recomm Rep. 2015;64:1-137.
6. Ness RB, Soper DE, Holley RL, et al. Effectiveness of inpatient and outpatient treatment strategies for women with pelvic inflammatory disease: results from the Pelvic Inflammatory Disease Evaluation and Clinical Health (PEACH) randomized trial. Am J Obstet Gynecol. 2002;186:929-937 .
At the recommendation of her primary care physician, a 53-year-old perimenopausal woman sought care at the emergency department for the fever, abdominal pain, and pyuria that had persisted for 4 days despite outpatient treatment for pyelonephritis. On physical examination, she was febrile and tachycardic with abdominal tenderness of the left lower quadrant. Genitourinary examination revealed copious brown vaginal discharge, left adnexal tenderness, and no cervical motion tenderness.
Laboratory testing revealed leukocytosis but otherwise normal electrolytes, liver function tests, and lactate levels. Urine culture obtained when she presented to an urgent care facility 3 days earlier had been negative. Computed tomography (CT) was performed and was read by Radiology as “closed loop small bowel obstruction in the left lower abdomen” (FIGURE 1). The patient was taken emergently to the operating room where her entire length of bowel was run without any obstruction found. Instead, the surgeons identified a mass in the left iliac fossa originating from the left ovary and fallopian tube (FIGURE 2).
WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?
Dx: Pelvic inflammatory disease with tubo-ovarian abscess
The presence and location of this mass, paired with the patient’s symptoms, led to the diagnosis of pelvic inflammatory disease. PID is an acute infection of the upper genital tract in women thought to be due to ascending infection from the lower genital tract. The prevalence of PID in reproductive-aged women in the United States is estimated to be 4.4%.1
Diagnosis of PID in middle-aged women is a challenge given the broad differential diagnosis of nonspecific presenting symptoms, lower index of suspicion in this age group, and unknown exact incidence of PID in postmenopausal women. While delay in diagnosis of PID in women of reproductive age is associated with increased infertility and ectopic pregnancy,2 delay in diagnosis in postmenopausal women also poses serious potential complications such as tubo-ovarian abscess (TOA)—as was seen with this patient—and concurrent gynecologic malignancy found on pathology of TOA specimens.3,4
Risk factors for PID in the postmenopausal population include recent uterine instrumentation, history of prior PID, and structural abnormalities such as cervical stenosis, uterine anatomic abnormalities, or tubal disease. The microbiology of PID in postmenopausal women differs from that of women of reproductive age. While sexually transmitted pathogens such as Neisseria gonorrhoeae and Chlamydia trachomatis most commonly are implicated in PID among premenopausal patients, aerobic gram-negative bacteria including Escherichia coli and Klebsiella pneumoniae most frequently are associated in postmenopausal cases.
Differential diagnosis for abdominal pain is broad
The differential diagnosis for a patient with fever and abdominal pain includes PID, as well as the following:
Diverticulitis classically presents with left lower abdominal pain and a low-grade fever. Complications may include bowel obstruction, abscess, fistula, or perforation. Abdominal imaging such as a CT scan is required to establish the diagnosis.
Continue to: Urinary tract infection
Urinary tract infection should be suspected in a patient with dysuria, urinary frequency or urgency, and abdominal or flank pain. Urinalysis and culture should be performed and imaging may be considered for suspected obstruction, complication, or failure to improve on appropriate therapy.
Appendicitis may present as right lower quadrant pain with anorexia, fever, and nausea. Imaging studies such as CT or ultrasound can help support the diagnosis and rule out alternate etiologies of the presenting symptoms.
Ectopic pregnancy—while not considered in this case—should be suspected in a patient presenting with pelvic pain, missed menses or vaginal bleeding, and a positive pregnancy test. Further evaluation may be performed with a transvaginal ultrasound and serial measurement of serum quantitative human chorionic gonadotropin level.
Diagnosing PID is a clinical process
PID often is difficult to diagnose because of an absence of symptoms or the presence of symptoms that are subtle or nonspecific. Laparoscopy or endometrial biopsy can be useful but may not be justifiable due to their invasive nature when symptoms are mild or vague.5 Thus, a diagnosis of PID usually is based on clinical findings.
Clinical criteria to look for. Although PID commonly is attributed to N gonorrhoeae and C trachomatis, fewer than 50% of those with a diagnosis of acute PID test positive for either of these organisms.5 As such, the Centers for Disease Control and Prevention (CDC) 2015 Sexually Transmitted Diseases Treatment Guidelines recommend presumptive treatment for PID in women with pelvic or lower abdominal pain with 1 or more of the following clinical criteria: cervical motion tenderness, uterine tenderness, or adnexal tenderness.
Continue to: The following criteria...
The following criteria enhance specificity and support the diagnosis5:
- oral temperature > 101°F (> 38.3°C),
- abnormal cervical mucopurulent discharge or cervical friability,
- presence of “abundant numbers of white blood cells on saline microscopy of vaginal fluid,”
- elevated erythrocyte sedimentation rate (reference range, 0–20 mm/hr),
- elevated C-reactive protein (reference range, 0.08-3.1 mg/L), and
- laboratory documentation of cervical infection with N gonorrhoeae or C trachomatis.
The CDC also suggests that the most specific criteria for PID include5
- endometrial biopsy consistent with endometritis,
- imaging (transvaginal ultrasound or magnetic resonance imaging) demonstrating fluid-filled tubes, or
- laparoscopic findings consistent with PID.
Treatment of PID includes IV antibiotics
Due to the polymicrobial nature of PID, antibiotics should cover not only gonorrhea and chlamydia but also anaerobic pathogens. CDC guidelines recommend the following treatment5,6:
- intravenous (IV) cefotetan (2 g bid) plus doxycycline (100 mg PO or IV bid),
- IV cefoxitin (2 g qid) plus doxycycline (100 mg PO or IV bid), or
- IV clindamycin (900 mg tid) plus IV or intramuscular (IM) gentamicin loading dose (2 mg/kg) followed by a maintenance dose (1.5 mg/kg tid).
In mild-to-moderate PID cases deemed appropriate for outpatient therapy, the following regimens have been shown to have similar outcomes to IV therapy5,6:
- IM ceftriaxone (250 mg, single dose) plus PO doxycycline (100 mg bid) for 14 days with/without PO metronidazole (500 mg bid) for 14 days,
- IM cefoxitin (2 g, single dose) and PO probenecid (1 g, single dose) plus PO doxycycline (100 mg bid) for 14 days with/without PO metronidazole (500 mg bid) for 14 days, or
- other parenteral third-generation cephalosporin plus PO doxycycline (100 mg bid) for 14 days with/without PO metronidazole (500 mg bid) for 14 days.
Management in older women may be more intensive
Due to the increased risk of malignancy in postmenopausal women with TOA, surgical intervention may be needed.3,4
Continue to: Our patient
Our patient underwent diagnostic laparoscopy, hysterectomy, left salpingo-oophorectomy, and right salpingectomy (with her right ovary left in place due to her perimenopausal status). Intraoperatively, she was found to have cervical stenosis. Postoperatively, she improved on IV cefoxitin (2 g qid) and IV doxycycline (100 mg bid), which was eventually transitioned to oral doxycycline (100 mg bid) and metronidazole (500 mg bid) on discharge.
Her final microbiology was negative for gonorrhea/chlamydia but the bacterial culture of peritoneal fluid grew E coli. Pathology was consistent with acute salpingitis, TOA, and acute cervicitis. She made a full recovery and is doing well.
CORRESPONDENCE
Catherine Peony Khoo, MD, 1920 Colorado Avenue, Santa Monica, CA 90404; Ckhoo@mednet.ucla.edu
At the recommendation of her primary care physician, a 53-year-old perimenopausal woman sought care at the emergency department for the fever, abdominal pain, and pyuria that had persisted for 4 days despite outpatient treatment for pyelonephritis. On physical examination, she was febrile and tachycardic with abdominal tenderness of the left lower quadrant. Genitourinary examination revealed copious brown vaginal discharge, left adnexal tenderness, and no cervical motion tenderness.
Laboratory testing revealed leukocytosis but otherwise normal electrolytes, liver function tests, and lactate levels. Urine culture obtained when she presented to an urgent care facility 3 days earlier had been negative. Computed tomography (CT) was performed and was read by Radiology as “closed loop small bowel obstruction in the left lower abdomen” (FIGURE 1). The patient was taken emergently to the operating room where her entire length of bowel was run without any obstruction found. Instead, the surgeons identified a mass in the left iliac fossa originating from the left ovary and fallopian tube (FIGURE 2).
WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?
Dx: Pelvic inflammatory disease with tubo-ovarian abscess
The presence and location of this mass, paired with the patient’s symptoms, led to the diagnosis of pelvic inflammatory disease. PID is an acute infection of the upper genital tract in women thought to be due to ascending infection from the lower genital tract. The prevalence of PID in reproductive-aged women in the United States is estimated to be 4.4%.1
Diagnosis of PID in middle-aged women is a challenge given the broad differential diagnosis of nonspecific presenting symptoms, lower index of suspicion in this age group, and unknown exact incidence of PID in postmenopausal women. While delay in diagnosis of PID in women of reproductive age is associated with increased infertility and ectopic pregnancy,2 delay in diagnosis in postmenopausal women also poses serious potential complications such as tubo-ovarian abscess (TOA)—as was seen with this patient—and concurrent gynecologic malignancy found on pathology of TOA specimens.3,4
Risk factors for PID in the postmenopausal population include recent uterine instrumentation, history of prior PID, and structural abnormalities such as cervical stenosis, uterine anatomic abnormalities, or tubal disease. The microbiology of PID in postmenopausal women differs from that of women of reproductive age. While sexually transmitted pathogens such as Neisseria gonorrhoeae and Chlamydia trachomatis most commonly are implicated in PID among premenopausal patients, aerobic gram-negative bacteria including Escherichia coli and Klebsiella pneumoniae most frequently are associated in postmenopausal cases.
Differential diagnosis for abdominal pain is broad
The differential diagnosis for a patient with fever and abdominal pain includes PID, as well as the following:
Diverticulitis classically presents with left lower abdominal pain and a low-grade fever. Complications may include bowel obstruction, abscess, fistula, or perforation. Abdominal imaging such as a CT scan is required to establish the diagnosis.
Continue to: Urinary tract infection
Urinary tract infection should be suspected in a patient with dysuria, urinary frequency or urgency, and abdominal or flank pain. Urinalysis and culture should be performed and imaging may be considered for suspected obstruction, complication, or failure to improve on appropriate therapy.
Appendicitis may present as right lower quadrant pain with anorexia, fever, and nausea. Imaging studies such as CT or ultrasound can help support the diagnosis and rule out alternate etiologies of the presenting symptoms.
Ectopic pregnancy—while not considered in this case—should be suspected in a patient presenting with pelvic pain, missed menses or vaginal bleeding, and a positive pregnancy test. Further evaluation may be performed with a transvaginal ultrasound and serial measurement of serum quantitative human chorionic gonadotropin level.
Diagnosing PID is a clinical process
PID often is difficult to diagnose because of an absence of symptoms or the presence of symptoms that are subtle or nonspecific. Laparoscopy or endometrial biopsy can be useful but may not be justifiable due to their invasive nature when symptoms are mild or vague.5 Thus, a diagnosis of PID usually is based on clinical findings.
Clinical criteria to look for. Although PID commonly is attributed to N gonorrhoeae and C trachomatis, fewer than 50% of those with a diagnosis of acute PID test positive for either of these organisms.5 As such, the Centers for Disease Control and Prevention (CDC) 2015 Sexually Transmitted Diseases Treatment Guidelines recommend presumptive treatment for PID in women with pelvic or lower abdominal pain with 1 or more of the following clinical criteria: cervical motion tenderness, uterine tenderness, or adnexal tenderness.
Continue to: The following criteria...
The following criteria enhance specificity and support the diagnosis5:
- oral temperature > 101°F (> 38.3°C),
- abnormal cervical mucopurulent discharge or cervical friability,
- presence of “abundant numbers of white blood cells on saline microscopy of vaginal fluid,”
- elevated erythrocyte sedimentation rate (reference range, 0–20 mm/hr),
- elevated C-reactive protein (reference range, 0.08-3.1 mg/L), and
- laboratory documentation of cervical infection with N gonorrhoeae or C trachomatis.
The CDC also suggests that the most specific criteria for PID include5
- endometrial biopsy consistent with endometritis,
- imaging (transvaginal ultrasound or magnetic resonance imaging) demonstrating fluid-filled tubes, or
- laparoscopic findings consistent with PID.
Treatment of PID includes IV antibiotics
Due to the polymicrobial nature of PID, antibiotics should cover not only gonorrhea and chlamydia but also anaerobic pathogens. CDC guidelines recommend the following treatment5,6:
- intravenous (IV) cefotetan (2 g bid) plus doxycycline (100 mg PO or IV bid),
- IV cefoxitin (2 g qid) plus doxycycline (100 mg PO or IV bid), or
- IV clindamycin (900 mg tid) plus IV or intramuscular (IM) gentamicin loading dose (2 mg/kg) followed by a maintenance dose (1.5 mg/kg tid).
In mild-to-moderate PID cases deemed appropriate for outpatient therapy, the following regimens have been shown to have similar outcomes to IV therapy5,6:
- IM ceftriaxone (250 mg, single dose) plus PO doxycycline (100 mg bid) for 14 days with/without PO metronidazole (500 mg bid) for 14 days,
- IM cefoxitin (2 g, single dose) and PO probenecid (1 g, single dose) plus PO doxycycline (100 mg bid) for 14 days with/without PO metronidazole (500 mg bid) for 14 days, or
- other parenteral third-generation cephalosporin plus PO doxycycline (100 mg bid) for 14 days with/without PO metronidazole (500 mg bid) for 14 days.
Management in older women may be more intensive
Due to the increased risk of malignancy in postmenopausal women with TOA, surgical intervention may be needed.3,4
Continue to: Our patient
Our patient underwent diagnostic laparoscopy, hysterectomy, left salpingo-oophorectomy, and right salpingectomy (with her right ovary left in place due to her perimenopausal status). Intraoperatively, she was found to have cervical stenosis. Postoperatively, she improved on IV cefoxitin (2 g qid) and IV doxycycline (100 mg bid), which was eventually transitioned to oral doxycycline (100 mg bid) and metronidazole (500 mg bid) on discharge.
Her final microbiology was negative for gonorrhea/chlamydia but the bacterial culture of peritoneal fluid grew E coli. Pathology was consistent with acute salpingitis, TOA, and acute cervicitis. She made a full recovery and is doing well.
CORRESPONDENCE
Catherine Peony Khoo, MD, 1920 Colorado Avenue, Santa Monica, CA 90404; Ckhoo@mednet.ucla.edu
1. Kreisel K, Torrone E, Bernstein K, et al. Prevalence of pelvic inflammatory disease in sexually experienced women of reproductive age—United States, 2013-2014. MMWR Morb Mortal Wkly Rep. 2017;66:80-83.
2. Weström L, Joesoef R, Reynolds G, et al. Pelvic inflammatory disease and fertility: a cohort study of 1,844 women with laparoscopically verified disease and 657 control women with normal laparoscopic results. Sex Transm Dis. 1992;19:185-192.
3. Jackson SL, Soper DE. Pelvic inflammatory disease in the postmenopausal woman. Infect Dis Obstet Gynecol. 1999;7:248-252.
4. Protopas AG, Diakomanolis ES, Milingos SD, et al. Tubo-ovarian abscesses in postmenopausal women: gynecological malignancy until proven otherwise? Eur J Obstet Gynecol Reprod Biol. 2004;114:203-209.
5. Workowski KA, Bolan GA; Centers for Disease Control and Prevention. Sexually transmitted diseases treatment guidelines, 2015. MMWR Recomm Rep. 2015;64:1-137.
6. Ness RB, Soper DE, Holley RL, et al. Effectiveness of inpatient and outpatient treatment strategies for women with pelvic inflammatory disease: results from the Pelvic Inflammatory Disease Evaluation and Clinical Health (PEACH) randomized trial. Am J Obstet Gynecol. 2002;186:929-937 .
1. Kreisel K, Torrone E, Bernstein K, et al. Prevalence of pelvic inflammatory disease in sexually experienced women of reproductive age—United States, 2013-2014. MMWR Morb Mortal Wkly Rep. 2017;66:80-83.
2. Weström L, Joesoef R, Reynolds G, et al. Pelvic inflammatory disease and fertility: a cohort study of 1,844 women with laparoscopically verified disease and 657 control women with normal laparoscopic results. Sex Transm Dis. 1992;19:185-192.
3. Jackson SL, Soper DE. Pelvic inflammatory disease in the postmenopausal woman. Infect Dis Obstet Gynecol. 1999;7:248-252.
4. Protopas AG, Diakomanolis ES, Milingos SD, et al. Tubo-ovarian abscesses in postmenopausal women: gynecological malignancy until proven otherwise? Eur J Obstet Gynecol Reprod Biol. 2004;114:203-209.
5. Workowski KA, Bolan GA; Centers for Disease Control and Prevention. Sexually transmitted diseases treatment guidelines, 2015. MMWR Recomm Rep. 2015;64:1-137.
6. Ness RB, Soper DE, Holley RL, et al. Effectiveness of inpatient and outpatient treatment strategies for women with pelvic inflammatory disease: results from the Pelvic Inflammatory Disease Evaluation and Clinical Health (PEACH) randomized trial. Am J Obstet Gynecol. 2002;186:929-937 .
