Back Clinic Imaging & Diagnostics Team. Dr. Alex Jimenez works with top-rated diagnosticians and imaging specialists. In our association, imaging specialists provide fast, courteous, and top-quality results. In collaboration with our offices, we provide the quality of service our patients’ mandate and deserve. Diagnostic Outpatient Imaging (DOI) is a state-of-the-art Radiology center in El Paso, TX. It is the only center of its kind in El Paso, owned and operated by a Radiologist.
This means when you come to DOI for a radiologic exam, every detail, from the design of the rooms, the choice of the equipment, the hand-picked technologists, and the software which runs the office, is carefully chosen or designed by the Radiologist and not by an accountant. Our market niche is one center of excellence. Our values related to patient care are: We believe in treating patients the way we would treat our family and we will do our best to ensure that you have a good experience at our clinic.
Chiropractors and spine specialists utilize spinal imaging through X-rays, MRIs, or CT scans to figure out what is causing back problems and pain. Imaging is common. Whether chiropractic or spinal surgery, they help immensely discover back issues and allow the individual to see what is happening. Types of cases include back pain that:
X-rays for back pain can be quite helpful. An X-ray is radiation-based and is used to examine the conditions of the bone structures. X-rays are optimal for bone tissue or tissues that are ossified or calcified. They work the best with hard tissues, specifically bones. Soft tissues like muscles, ligaments, or intravertebral discs do not present as well.
Individuals undergoing a back X-ray will be scanned by a machine that generates a beam. A receiver picks registers the beam after it passes through the body and generates an image. It takes around five minutes to complete but could be longer depending on the doctor’s number of images. X-rays are helpful for insurance purposes and rule out bone conditions like compression fractures and/or bone spurs. X-rays are ordered for specific reasons and are often part of a whole-body diagnostic study. This includes MRI and/or CT scan.
CT stands for computed tomography. It is a series of X-rays that are digitized into images using a computer. The advantage of a CT scan to standard X-rays is that it offers different views/angles of the body and can be in 3D. CT scans are most often used in trauma cases or individuals who have had surgery. They take around five minutes. For X-rays, individuals stand up or lay under the X-ray machine as it scans the body. A CT scan has the individual lie down in a circular donut-looking machine that scans while rotating during the imaging. Individuals are recommended to wear casual loose, comfortable clothing. Sometimes a dye, or intravenous contrast, is used to get the vascular tissues to stand out, generating clearer images.
MRI is short for magnetic resonance imaging. MRIs use magnets to generate images. MRI imaging is often used in individuals that have undergone surgery. They take longer, usually around 30 to 45 minutes. No metallic objects are allowed in the MRI. Patients are asked to remove items like belts, jewelry, etc. Contrast dye can be a part of an MRI. The machine is like a tunnel. This can become challenging for individuals that have claustrophobia. Consult with a doctor and find out how to get comfortable during the process.
Other Forms of Spinal Imaging
Other forms of imaging include:
CT navigation shows real-time CT scans during the procedure.
Fluoroscopy involves an X-ray beam that passes directly through the body that shows live, moving images.
Both of these types of spinal imaging are utilized during surgeries. For some cases, intraoperative imaging is used. This type of imaging uses high-tech robotics to help surgeons navigate through tight spaces during the procedure. This increases the surgeon’s accuracy and reduces the size of the incision.
Ultrasound can be used for spinal conditions. This is an imaging test that uses sound waves to generate images. However, the imaging tests which are used in spinal imaging are primarily X-rays and MRIs.
Talk with your doctor or chiropractor ahead of time to understand what to expect during the imaging process. They will let you know how to prepare and any special instructions before the appointment. Along with medical history and a physical examination, spinal imaging is an important part of the diagnostic process to find what is causing the pain and to develop the best treatment plan.
Short-term Effects of Coffee and Blood Pressure
The caffeine in coffee is a stimulant or substance that excites the body’s systems. When caffeine is ingested, individuals experience an increase in excitement, specifically in the cardiovascular system. This excitement causes the heart rate and blood pressure to rise and then lower back to a baseline level for healthy individuals. Coffee slightly increases short-term blood pressure. Moderate coffee consumption is safe for individuals that do not have pre-existing cardiovascular conditions.
United States Nuclear Regulatory Commission. (May 2021) “Doses in Our Daily Lives” https://www.nrc.gov/about-nrc/radiation/around-us/doses-daily-lives.html
X-Ray for Back Pain: Current Reviews in Musculoskeletal Medicine. (April 2009) “What is the role of imaging in acute low back pain?” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2697333/
Gartland classification grades minimally displaced subtle injuries treated with simple immobilization vs. posterior elbow dislocation treated operatively
A potential risk of ischemic compromise if care is delayed (Volkmann contracture)
The Radiological exam is crucial: sail sign & posterior fat pad sign with anterior humeral line failed to intersect mid/2/3 of Capitellum.
Incomplete pediatric Fx:
Most in <10 y.o. Greenstick, Torus, Plastic aka Bowing deformity
Typically heal well, treated conservatively with immobilization
Plastic deformity if >20-degrees requires closed reduction
Ping pong skull fracture may develop following trauma, forceps delivery and complications of birth trauma. May need to be assessed by the pediatric neurosurgeo.n
Salter-Harris types of physeal growth plate injuries
Type 1-slip. e.g., Slipped Capital Femoral Epiphysis. Typically no bone fracture noted
Type 2-M/C with good prognosis
Type 3- intra-articular, thus carries the risk of premature osteoarthritis and may require operative care d/t being unstable
Type 4- Fx through all regions about the physis. Unfavorable prognosis and limb shortening
Type 5- often no evidence of actual bone fracture. Poor prognosis d/t crush injury and vascular damage with limb shortening
Imaging evaluation is crucial
Non-Accidental Injury (NAI)in Children
There different forms of child abuse. Physical abuse may range from skin injuries to different MSK/systemic injuries affecting bones and soft tissues. Imaging is crucial and may identify definite signs alerting medical providers and informing child protection services and law enforcement agencies about physical abuse.
In an infant: �shaken baby syndrome� may present with CNS signs d/t tearing of immature bridging vein and subdural hematoma which can be fatal. Retinal hemorrhaging often a clue. Head CT is crucial.
MSK Radiological Red Flags:
1) major bone Fx in an un-ambulatory very young child (0-12 m.o.)
2) Posterior ribs Fx: naturally never occur d/t accidents. Most likely mechanisms: grabbing and squeezing a child or direct hit.
3) Multiple Fractures with different chronological healing rates, i.e., bone calluses indicating repeated physical trauma
4) Metaphyseal corner Fx aka Bucket handle Fx, often pathognomonic for NAI in children. Occurs when the affected extremity is held and violently twisted.
5) Spiral fracture of long bones in a young child is another example of NAI.
Other important clues of NAI. Inconsistent history provided by guardians/caregivers. No evidence of congenital/metabolic bone abnormalities like Osteogenesis Imperfecta or Rickets/osteomalacia etc.
N.B. When child�s guardians state a history that reports fall and accidents in the house, It is important to know that apparently most accidents/falls in the house are very rarely or unlikely result in major bone fractures.
Juvenile Idiopathic Arthritis (JIA)-considered M/C chronic disease of childhood. Clinical Dx: joint pain/swelling for 6-weeks or longer in a child <16-y.o. Different forms exist: Early Dx is crucial to prevent delayed complications
Most familiar forms of JIA:
1) Pauciarticular disease (40%)- m/c form of JIA. Girls are at greater risk. Presents as arthritis in <4 joints: knees, ankles, wrist. Elbow. This type shows high association with ocular involvement as iridocyclitis (25%) that may potentially lead to blindness. Labs: RF-ve, ANA positive.
2) Polyarticular disease (25%): RF-ve. Girls are at greater risk. Affects small and large joints often affect Cervical spine
3) Systemic form of JIA (20%): often presents with acute systemic manifestation as spiking fevers, arthralgias, myalgias, lymphadeno[pathy, hepatosplenomegaly, polyserositis (pericardial/pleural effusion). Important Dx features characteristic evanescent salmon pink rash on the extremities and trunk. The Systemic form has a distinct lack of ocular involvement. Joints typically shoe no erosions compared to other types. Thus joint destruction is not typically seen
Imaging in JIA
Joint effusion bone overgrowth squaring of patella cartilage/bone erosion superimposed DJD
Fingers and long bones early physeal closure/limb shortening
Rad DDx knee/ankle: Hemophilic arthropathy Rx: DMARD.
Osteosarcoma (OSA) & Ewing�s sarcoma (ES) are 1 st and 2nd M/C primary malignant bone neoplasms of childhood (peak at 10-20 y.o.) Clinically: bone pain, change in activity, early metastasis especially pulmonary mets may occur. Poor prognosis
Ewing�s may present with bone pain, fever and elevated ESR/CRP mimicking infection. Early Dx with imaging and staging are crucial.
Imaging of OSA & ES: x-ray, followed by MRI, chest CT, PET/CT. On x-rays: OSA may affect any bone but most present as aggressive bone forming neoplasms about the knee (50% cases) especially as osteoid forming an aggressive lesion in the metaphysis with speculated/sunburst periostitis & Codman triangle. Marked soft tissue invasion.
ES may present in the shaft and show very early soft tissue spread. MRI is crucial to reveal the extent of bone and ST invasion, MRI required for surgical planning
OSA & ES Rx: A combination of surgery, radiation, chemo. Limb salvage techniques are performed in some cases. Poor prognosis if detected late.
Imaging of Ewing�s sarcoma
Permeating bone distraction
Early and extensive soft tissue invasion
Aggressive periosteal reaction with laminated (onion skin) response
Saucerisation of cortical bone (orange arrow)
A Lesion is typically diaphyseal with some metaphyseal extension
Known as Round cell tumor along with Multiple Myeloma and Lymphoma
Common Childhood Malignancies
Neuroblastoma (NBL) M/C malignancy of infancy. Derives from neural crest cells aka PNET tumors (e.g., sympathetic ganglia). Most occur in children <24-months. Some show good prognosis but >50% cases present with advanced disease. 70-80% at age 18-months or older present with advanced metastasis. NBL may develop in the adrenal medulla, sympathetic ganglia and other location. Presents as an abdominal mass, vomiting. >50% presents with bone pain d/t metastasis. Clinically: physical exam, labs, imaging: chest and abd x-rays, CT abdomen and chest is crucial to Dx. MRI may help. NBL may metastasize to the skull and infiltrate sutures with a characteristic presentation as pathological sutural diastasis.
Acute Lymphoblastic Leukemia is the m/c malignancy of childhood. Pathology: leukemic cell infiltration of bone marrow leading to bone pain and replacement of other normal marrow cells with anemia, thrombocytopenia, neutropenia and associated complications. Leukemic cells may infiltrate other sites including CNS, spleen, bone and other regions. Dx: CBC, serum lactate dehydrogenase levels, Bone marrow aspiration biopsy is the key. Imaging may help but not essential to diagnosis. On radiography, leukemic infiltration of the bone may typically appear as radiolucent bands along the physeal growth plate. Rx: chemotherapy and treating complications
Medulloblastoma: M/C malignant CNS neoplasm in children
Majority develop before 10-y.o.
M/C location: cerebellum and posterior fossa
Histologically represents a PNET type tumor not a glioma as was originally thought
MBL, as well as Ependymoma and CNS lymphoma, may lead to drop metastasis via CSF and additionally represent a unique that unlike other CNS tumors demonstrate metastatic spread outside CNS, m/c to the bone
50% of MBL may be fully resectable
If Dx and treatment begin before metastasis, 5- year survival is 80%
Imaging is crucial: CT scanning may be used but the imaging modality of choice is MRI that will additionally provide a more superior evaluation of the entire neuraxis for metastasis.
MBL typically appears as heterogenous hypo, iso and hyperintense lesion on T1, T2 and FLAIR scans (top images) if compare to surrounding brain tissue. Often compressing 4th ventricle with obstructive hydrocephalus. The tumor typically shows contrast enhancement on T1+C gad (bottom left image). Drop metastasis from MBL with T1+C enhancing lesion in the cord
Important Pediatric Infections
In the neonate/infant <1month: fever >100.4 (38C) may indicate bacterial and some viral infection. Strep B, Listeria, E. Coli may lead to sepsis, meningitis. Approach: chest x-ray, lumbar puncture with culture, blood culture, CBC, urinalysis.
In young children, Hemophilus influenza type B (HIB) may lead to Epiglottitis a rare but serious complication. The current vaccine helps to reduce the number of cases of Epiglottitis and other HIB related illnesses.
Parainfluenza or RSV virus may lead to Croup or acute Laryngotracheobronchitis.
Epiglottitis and Croup are Dx clinically but AP and lateral soft tissue neck x-rays are very helpful
Epiglottitis presents with a characteristic �thumb sign� that is consistent with thickened epiglottis d/t epiglottic edema. This can be a life-threatening emergency compromising airways (top left)
Croup may show a �steeple sign� or �wine bottle sign� with distended hypopharynx as acute narrowing of subglottic airway on AP and lateral neck soft tissue x-ray (top right)
Respiratory Syncytia Virus (RSV) and influenza may lead to viral pneumonia potentially with life-threatening complications in the immunocompromised, very young and children with comorbidities. CXR is crucial (middle left)
Streptococcal pharyngitis with GABHS infection may lead to some acute or delayed complications (e.g., Rheumatic fever)
Peritonsillar abscess (above middle right) may develop in some cases and be complicated by spreading along soft tissue planes in the neck potentially leading to spread into sublingual/submandibular spaces (Ludwig Angina) when airways need to be controlled d/t base of tongue edema
Development of a retropharyngeal abscess may potentially lead to spread of the infection through freely communicating neck fascia resulting in necrotizing mediastinitis, Lemmier syndrome and invasion of carotid spaces (all are potentially life-threatening complications)
Griesel syndrome- (above bottom left) rare complication of regional tonsillar/pharyngeal oral infections that can spread to prevertebral space leading to C1-2 ligaments laxity and instability
Other important infections in children are typical bacterial (Pneumococcal) pneumonia, Urinary tract infection and Acute Pyelonephritis (especially in girls) and Meningococcal Meningitis
Pediatric Metabolic Disease
Rickets: considered osteomalacia in skeletally immature. Zone of provisional calcification of the epiphyseal growth plate is particularly affected
Clinically presents with growth retardation, extremity bowing, rachitic rosary, pigeon chest, depressed ribs, enlarged and swollen wrists, and ankles, skull deformity
Pathology: Vit D and calcium abnormality is the m/c cause. Lack of sun exposure esp. dark-skinned individual, restrictive clothing to light exposure, prolonged exclusive breastfeeding, veganism, malabsorption syndromes of the gut, renal damage and others
Imaging: frayed metaphysis aka paint brush metaphysis with flaring, widening of the growth plate, bulbous costochondral junction as a rachitic rosary, extremity bowing
Rx: treat underlying causes, correct nutritional deficit, etc.
Diagnosis of the diseases of the abdomen can be classified into:
Abnormalities of the gastrointestinal tract (esophagus, stomach, small & large bowel, and the appendix)
Abnormalities of the accessory digestive organs (Hepatobiliary & pancreatic disorders)
Abnormalities of the genitourinary & reproductive organs
Abnormalities of the abdominal wall and major vessels
This presentation aims to provide the most basic understanding of general diagnostic imaging approach and appropriate clinical management of patients with the most common diseases of the abdomen
Imaging modalities used during an investigation of the abdominal complaints:
AP abdomen (KUB) and upright CXR
Abdominal CT scanning (with oral and I.V. contrast and w/o contrast)
Upper and Lower GI Barium studies
MRI (most used as Liver MRI)
MRI enterography & enteroclysis
Endoscopic Retrograde Cholangiopancreatography (ERCP)- mostly hepatobiliary and pancreatic ductal pathology
Why Order An Abdominal X-ray?
Include a preliminary evaluation of bowel gas in an emergent setting. For example, a negative study in a low probability patient may obviate the need for a CT or other invasive procedures
Evaluation of radiopaque tubes, lines, and radiopaque foreign bodies
Post-procedural evaluation intraperitoneal/retroperitoneal free gas
Monitoring the amount of bowel gas and resolution of postoperative (adynamic) ileus
Monitoring the passage of contrast through the bowel
Colonic transit studies
Monitoring renal calculi
What to Note on AP Abdomen: Supine vs. Upright vs. Decubitus
Free Air (pneumoperitoneum)
Bowel obstruction: Dilated loops: SBO vs LBO (3-6-9 rule) SB-upper limit-3-cm, LB-upper limit-6-cm, Caecum-upper limit-9-cm. Note loss of haustra, note dilation (presence) of valvule conivente (plica semilunaris) in SBO
SBO: note different heights air-fluid levels on upright film step ladder� appearance, typical of SBO
Note paucity of rectal/colonic gas (evacuated) in SBO
Abdominal CT scanning -modality of choice during the investigation of acute and chronic abdominal complaints especially in adults. For example, abdominal malignancy can be successfully diagnosed and staged providing clinical information for care planning
Abdominal, renal and pelvic ultrasound can be performed to help the diagnosis of appendicitis (esp. in children), acute & chronic vascular pathology, hepatobiliary abnormalities, obstetric and gynecological pathology
Use of ionizing radiation (x-rays & CT) should be minimized in children and other vulnerable groups.
Diagnostic Imaging of Major Diseases of the Gastrointestinal System
1) Esophageal disorders
2) Gastric carcinoma
3) Gluten Sensitive Enteropathy
4) Inflammatory Bowel Disease
5) Pancreatic ductal adenocarcinoma
6) Colorectal carcinoma
7) Acute Appendicitis
8) Small bowel obstruction
Achalasia (primary achalasia): failure of organized esophageal peristalsis d/t impaired relaxation of the lower esophageal sphincter (LOS) with marked dilatation of the esophagus and food stasis. Obstruction of the distal esophagus (often due to tumor) has been termed “secondary achalasia” or “pseudoachalasia.� Peristalsis in the distal smooth muscle segment of the esophagus may be lost due to an abnormality of Auerbach plexus (responsible for smooth muscle relaxation). Vagus neurons can also be affected
Primary: 30 -70s, M: F equal
Chagas disease (Trypanosoma Cruzi infection) with the destruction of the Myenteric plexus neurons of the GI system (megacolon & esophagus)
However, the heart is the M/C affected organ
Clinically: Dysphagia for both solids and liquids, in comparison to dysphagia for solids only in cases of esophageal carcinoma. Chest pain and regurgitation. M/C mid esophageal squamous cell carcinoma in approximately 5% due to chronic irritation of the mucosa by stasis of food and secretions. Aspiration pneumonia may develop. Candida esophagitis
Imaging: �Bird -beak� on upper GI barium swallow, dilated esophagus, loss of peristalsis. An endoscopic exam is crucial.
Rx: difficult. Calcium channel blockers (short -term).Pneumatic dilatation, effective in 85% of patients with 3 -5% risk of bleeding/perforation. Botulinum toxin injection lasts only approx. 12 months per treatment. May scar the submucosa leading to increased risk of perforation during subsequent myotomy. Surgical myotomy (Heller myotomy)
10 -30% of patients develop gastroesophageal reflux (GERD)
Presbyesophagus: used to describe the manifestations of degenerating motor function in the aging esophagus >80-y.o. Due to interruption of the reflex arc with decreased sensitivity to distension and alteration in peristalsis.
Patients may complain of dysphagia or chest pain, but most are asymptomatic
Diffuse/distal esophageal spasm (DES) is a motility disorder of the esophagus that may appear as a corkscrew or rosary bead esophagus on barium swallow.
2% of non-cardiac chest pain
Manometry is the gold-standard diagnostic test.
Zenker diverticulum (ZD) aka pharyngeal pouch
An outpouching at the level of the hypopharynx, just proximal to the upper esophageal sphincter, known as the Killian dehiscence or Killian triangle
Patients are 60-80 y.o and present with dysphagia, regurgitation, halitosis, globus sensation
May complicate with aspiration and pulmonary abnormalities
Patients may accumulate medications
ZD- is a pseudodiverticulum or pulsion diverticulum resulting from herniation of the submucosa through the Killian dehiscence, forming a sac where food and other contents may accumulate.
Mallory-Weiss syndrome refers to mucosal and submucosal tears of the distal oesophageal venous plexus associated with violent retching/vomiting and projection of gastric contents against the lower esophagus. Alcoholics are at particular risk. Cases present with painless hematemesis. Treatment is typically supportive.
Dx: imaging plays little role, but contrast esophagram may demonstrate some mucosal tears filled by contrast (bottom right image). CT scanning may help to exclude other causes of upper GI bleeding
Boerhaave syndrome: esophageal rupture secondary to forceful vomiting
Mechanisms involve forceful expulsion of gastric contents especially with large undigested foods when esophagus forcefully contracts against closed glottis with 90% occurring along left posterolateral wall
Hiatus hernias (HH): herniation of abdominal contents through the esophageal hiatus of the diaphragm into the thoracic cavity.
Many patients with HH are asymptomatic, and it is an incidental finding. However, symptoms may include epigastric/chest pain, postprandial fullness, nausea and vomiting
Sometimes HH is considered synonymous with gastro-oesophageal reflux disease (GORD), but there is a poor correlation between the two conditions!
2-types: sliding hiatus hernia 90% & rolling (paraoesophageal) hernia 10%. The latter may strangulate leading to ischemia and complications.
Esophageal Leiomyoma is the M/C benign esophageal neoplasm. It is often large but yet non-obstructive. Gastrointestinal stromal tumors (GIST) are the least common in the esophagus. Should be differentiated from Esophageal carcinomas.
Imaging: contrast esophagram, upper GI barium swallow, CT scanning. Gastroesophagoscopy is the Dx method of choice.
Esophageal carcinoma: presented with increasing dysphagia, initially to solids and progressing to liquids with obstruction in more advanced cases
<1% of all cancers and 4-10% of all GI malignancies. There is recognized male preponderance with the squamous cell subtype due to smoking and alcohol. Barrett esophagus and adenocarcinoma
M: F 4:1. Black individuals are more susceptible than White individuals 2:1. Poor prognosis!
A barium swallow can be sensitive in identifying esophageal mass. Gastroesophagoscopy (endoscopy) confirms the diagnosis with tissue biopsy
Overall the most common malignancy is 2ndary gastric fundal carcinoma invading distal esophagus
Squamous cell is typically found in the mid esophagus, Adenocarcinoma in the distal region
Gastric carcinoma: primary malignancy of gastric epithelium. Rare before the age of 40. The median age at diagnosis in the United States is 70 years for males and 74 years for females. Japan, South Korea, Chile, and Eastern European countries have one of the highest rates of stomach cancer in the world. Stomach cancer rates are declining worldwide. Gastric cancer is the 5th causes of cancer-related death. Association with Helicobacter pylori infection 60- 80%, but only 2% population with H. Pyloris develop Stomach cancer. 8-10% have an inherited familial component.
Gastric Lymphoma is also linked to H. Pyloris infection. Gastrointestinal Stromal Cell Tumour or GIST is another neoplasm affecting the stomach
Clinically: No symptoms when it is superficial and potentially curable. Up to 50% of patients may have non-specific GI complaints. Patients may present with anorexia and weight loss (95%) as well as vague abdominal pain. Nausea, vomiting, and early satiety d/t obstruction may occur with bulky tumors or infiltrative lesions that impair stomach distension.
Prognosis: Most gastric cancers diagnosed late and may reveal local invasion with regional adenopathy, liver, and mesenteric spread. A 5-year survival rate of 20% or less. In Japan and S. Korea, early screening programmes increased survival to 60%
Imaging: Barium upper GI study, CT scanning. Endoscopic examination is the method of choice for the diagnosis. On imaging, Gastric cancer may appear as an exophytic (polypoid) mass or Fungative type, Ulcerative or Infiltrative/diffuse type (Linitis Plastica). CT scanning is important to evaluate local invasion (nodes, mesentery, liver, etc.)
Celiac disease aka non-tropical sprue aka Gluten-sensitive enteropathy: A T-cell mediated autoimmune chronic gluten-induced mucosal damage resulting in loss of villi in the proximal small bowel and gastrointestinal malabsorption (i.e., sprue). Considered in some cases of iron deficiency anemia of undetermined cause. Common in Caucasians (1 in 200) but rare in Asian and black individuals. Two peaks: a small cluster in early childhood. Typically in 3rd and 4th decades of life.
Clinically: Abdominal pain is the m/c symptom, malabsorption of nutrients/vitamins: IDA and guaiac-positive stools, diarrhea, constipation, steatorrhea, weight loss, osteoporosis/osteomalacia, dermatitis herpetiformis. Increased association with T-cell lymphoma, Increased association with esophageal squamous cell carcinoma, SBO
Dx: Upper GI endoscopy with multiple duodenal biopsies is considered a diagnostic standard for celiac disease. Histology reveals T-cell infiltration and lymphoplasmacytosis, Villi atrophy, Crypts hyperplasia, Submucosa, and Serosa are spared. Rx: elimination of gluten-containing products
Imaging: Not required for Dx but on Barium swallow fluoroscopy: mucosal atrophy and obliteration of mucosal folds (advanced cases only). SB dilation is the most typical finding. Nodularity of the duodenum (bubbly duodenum). Reversal of jejunal and ileal mucosal folds:
�The jejunum looks like ileum, the ileum looks like the jejunum, and the duodenum looks like hell.�
CD: chronic relapsing-remitting autoimmune inflammation that affects any part of the GI tract from the mouth to the anus but at onset most typically involves the terminal ileum. M/C presentation: abdominal pain/cramping and diarrhea. Path: granulomata formation that unlike UC is transmural, potentially leading to strictures. Areas affected by the inflammation are typically patchy
Complications are numerous: malabsorption of nutrients/vitamins (anemia, osteoporosis, developmental delay in children, susceptibility to GI malignancy, bowel obstruction, fistula formation, extra-abdominal manifestations: uveitis, arthritis, AS, erythema nodosum and others. 10- 20% may require abdominal surgery after 10-years of CD usually for strictures, fistiluzation, BO.
Dx: clinical, CBC, CMP, CRP, ESR, serological tests: DDx of IBD: anti-Saccharomyces cerevisiae antibodies (ASCA), perinuclear antineutrophil cytoplasmic antibody (p-ANCA) histologically or in serum. Fecal Calprotectin test helps to DDx IBS and evaluate response to treatment, disease activity/relapses.
Dx of choice: endoscopy, ileoscopy, and multiple biopsies may reveal endoscopic and histological changes. Video capsule endoscopy (VCE), Imaging may help with Dx of complications. Rx: immunomodulatory drugs, complementary medicine, diet, probiotics, operative. No cure but the aim is to induce remission, control symptoms and prevent/treat complications
Imaging Dx: KUB to DDx SBO, Barium enema (single and double contrast), small bowel follow through. Findings: skip lesions, aphthous/deep ulcerations, fistula/sinus tracts, String sign, creeping fat pushed loops of LB, cobblestone appearance d/t fissures/ulcers pushing mucosa, CT scanning with oral and IV contrast.
Imaging from a Crohn’s patient who had a small bowel resection for obstruction.
(B) MRE of the same area shows a fibrostenotic stricture
UC: characteristically involves only the colon but backwash ileitis may develop. Onset is typically at 15-40s and is more prevalent in males, but the onset after the age of 50 is also common. More common in North America and Europe (hygiene hypothesis). Etiology: A combination of environmental, genetic and gut microbiome changes are involved. Smoking and early appendectomy tend to show a negative association with UC, unlike in CD considered some of the risk factors.
Clinical Features: Rectal bleeding (common), diarrhea, rectal mucous discharge, tenesmus (occasionally), lower abdominal pain and severe dehydration from purulent rectal discharge (in severe cases, especially in the elderly), fulminant colitis and toxic megacolon can be fetal but are rare complications. Pathology: No granulomata. Ulcerations affect mucosa and submucosa. Pseudopolyps present as elevated spared mucosa.
An initial process always affects the rectum and remain a local disease (proctitis) in (25%). 30% Proximal disease extension may occur. UC may present as left-sided (55%) and pancolitis (10%). Majority of cases are mild to moderate
Imaging: not required for Dx but barium enema may reveal ulcerations, thumbprinting, in advanced cases loss of haustra and narrowing of the colon producing �lead-pipe colon.� CT scanning may help with Dx seen as mucosal thickening detected only in moderate and severe cases. CT may help with of Dx of complications. Plain film image reveals �lead-pipe colon� and sacroiliitis as Enteropathic arthritis (AS)
Colorectal carcinoma (CRC) m/c cancer of the GI tract and the 2nd most frequent malignancy in adults. Dx: endoscopy and biopsy. CT is the modalities most frequently used for staging. Surgical resection may be curative although the five-year survival rate is 40- 50% depending on staging. Risk factors: low fiber and high fat and animal protein diet, obesity (especially in men), chronic ulcerative colitis. Colonic adenomas (polyps). Familial adenomatous polyposis syndromes (Gardener syndrome) and Lynch syndrome as non-familial polyposis.
Clinically: insidious onset with altered bowel habits, fresh blood or melena, iron deficiency anemia from chronic occult blood loss especially in the right-sided tumors. Bowel obstruction, intussusception, heavy bleeding and metastatic disease especially to the Liver may be initial presentation. Path: 98% are adenocarcinomas, arise from pre-existing colonic adenomas (neoplastic polyps) with malignant transformation. The five-year survival rate is 40-50%, with stage at operation the single most important factor affecting prognosis. M/C rectosigmoid tumors (55%),
N.B. Some adenocarcinomas esp. mucinous types typically presented late and usually carry poor prognosis due to late presentation and mucin secretion and local/distant spread
Imaging: Barium enema is sensitivities for polyps >1 cm, single contrast: 77-94%, double contrast: 82-98%. Colonoscopy is a modality of choice for prevention, detection, and identification of colorectal carcinoma. Contrast-enhanced CT scanning is used for staging and prognosis evaluation of mets.
Screening: colonoscopy: men 50 y.o.-10-years if normal, 5-years if polypectomy, FOB, 1st degree relative with CA begin surveillance at 40 y.o
Pancreatic Cancer: ductal epithelial adenocarcinoma (90%), very poor prognosis with high mortality. 3rd M/C abdominal cancer. Colon is #1, stomach #2. Pancreatic cancer accounts for 22% of all deaths due to gastrointestinal malignancy, and 5% of all cancer deaths. 80% of cases in 60+. Cigarette smoking is the strongest environmental risk factor, a diet rich in animal fats and protein. Obesity. Family history. M/C detected in the head and uncinate process.
Dx: CT scanning is crucial. Invasion of Superior Mesenteric Artery (SMA) indicates unresectable disease. 90% of pancreatic adenocarcinomas are unresectable at Dx. Most patients die within 1-year of Dx. Clinically: painless jaundice, abd. Pain, Courvoisier�s gallbladder: painless jaundice and enlarged gallbladder, Trousseau�s syndrome: migratory thrombophlebitis, new onset diabetes mellitus, regional and distant metastasis.
CT Dx: pancreatic mass with strong desmoplastic reaction, poor enhancement, and slightly lower attenuation compared to the adjacent normal gland, SMA invasion.
Appendicitis: very common condition in general radiology practice and is a major cause of abdominal surgery in young patients
CT is the most sensitive modality to detect appendicitis
Ultrasound should be employed in younger patients and children
KUB Radiographs should play no role in the diagnosis of appendicitis
On imaging, appendicitis reveals inflamed appendix with wall thickening, enlargement, and periappendiceal fat stranding. Similar findings of wall thickening and enlargement are noted on US. Typical �target sign� is noted on short axis US probe position.
If the appendix is retro-caecal than US may fail to provide accurate Dx and CT scanning may be required
Rx: operative to avoid complications
Small bowel obstruction (SBO)-80% of all mechanical intestinal obstruction; the remaining 20% result from large bowel obstruction. It has a mortality rate of 5.5%
M/C cause: any Hx of previous abdominal surgery and adhesions
Classical presentation is constipation, increasing abdominal distension with nausea and vomiting
Radiographs are only 50% sensitive for SBO
CT will demonstrate the cause of SBO in 80% of cases
There are variable criteria for maximal small bowel obstruction, but 3.5 cm is a conservative estimate of dilated bowel
On Abd x-ray: supine vs. upright. Dilated bowel, stretched valvulae conivente (mucosal folds), alternative air-fluid levels �step ladder.� Absent gas in the rectum/colon
Rx: operative as �acute abdomen.�
Volvulus-m/c in the Sigmoid colon esp. in elderly. The main reason: chronic constipation with redundant sigmoid twisting on sigmoid mesocolon. Leads to Large bowel obstruction (LBO). Other common causes: a colon tumor. Sigmoid vs. Caecum volvulus
Clinically: signs of LBO with constipation, abdominal bloating, pain, nausea, and vomiting. Onset may be acute or chronic
Radiographically: loss of haustra in the LB, LB distension (>6-cm), �coffee bean sign� next slide, the lower end of volvulus points to the pelvis
N.B: Rule of thumb for dilated bowel should be 3-6-9 where 3-cm SB, 6-cm LB & 9-cm Coecum
Note generations of the tracheal-bronchial tree, lobes, segments, and fissures. Note secondary pulmonary lobule (1.5-2-cm)-the basic functional unit of lungs observed on HRCT. Note important structural organization of the alveolar spaces with communications in between (pores of Kohn & canals of Lambert) that permit air drift and by the same mechanism allow exudative or transudative fluid to spread through the lung and stopped at the fissure. Note the anatomy of the pleura: parietal that is a part of the endothoracic fascia and the visceral that forms a lung edge � pleural space in between.
Mediastinum: surrounded by the pleura and the lung. Accommodates major structures contains numerous lymph nodes (see diagramme showing mediastinal nodes and their involvement in Lymphoma
General Approach to Investigating Chest Complaints
Decubitus views right and left: help to evaluate subtle pleural effusion, pneumothorax and other pathology
Normal CXR PA & Lateral views. Ensure good exposure: T-spine discs and vessels through the heart are visualized on PA view. Count 9-10 right posterior ribs to confirm adequate inspiratory effort. Begin a thorough survey using the following approach: Are There Many Lung Lesions A-abdomen/diaphragm, T-thorax wall, M-mediastinum, L-lungs individually, Lungs-both. Develop a good search pattern
1) Airspace disease aka alveolar lung disease? Filling of the lung’s alveoli, acini and subsequently the entire lobe with fluid or substance of any composition (blood, pus, water, proteinaceous material or even cells) Radiographically: lobar or segmental distribution, airspace nodules may be noted, tendency to coalesce, air bronchograms and silhouette sign present. Batwing (butterfly) distribution noted as in (CHF). Rapidly changing over time, i.e., increase or decrease (days)
2) Interstitial disease: infiltration of pulmonary interstitium (alveoli septum, lung parenchyma, vessel walls, etc.) by for example by viruses, small bacteria, protozoans. Also infiltration by cells such as inflammatory/malignant cells (e.g., lymphocytes) Presented as an accentuation of lung interstitium with a reticular, nodular, mixed reticulonodular pattern. Different etiologies: inflammatory autoimmune diseases, fibrosing lung disease, occupational lung disease, viral/mycoplasma infection, TB, sarcoidosis lymphoma/leukemia and many other.
Recognizing different patterns of pulmonary disease can help with DDx. Mass vs. Consolidation (left). Note different patterns of pulmonary disease: airspace disease as lobar consolidation indicative of pneumonia, diffuse consolidation indicative of pulmonary edema. Atelectasis (collapse and volume loss). Interstitial patterns of pulmonary disease: reticular, nodular or mixed. SPN vs. Multiple focal consolidations (nodules) likely representing mets infiltrates vs. septic infiltrates
A = intraparenchymal
B = pleural
C = extrapleura
Recognize important location of chest lesions
Important signs: Silhouette sign: help with localization and DDx. Example: Bottom left image: radiopacity in the right lung, where is it located? Right MM because the right heart border that is adjacent to right middle lobe is not seen (silhouetted) Air bronchograms: air containing bronchi/bronchioles surrounded by fluid
Pneumothorax (PTX): air (gas) in the pleural space. Many causes. Complications:
Tension PTX: continuous increase of air in the pleural space that rapidly compresses mediastinum and lung rapidly reducing venous return to the heart. It can be fatal if not treated rapidly
Spontaneous PTX: primary (young adults (30 -40) especially tall, thin men. Additional causes: Marfan�s syndrome, EDS, Homocystinuria, a – 1 -antitrypsin deficiency. Secondary: older pts with parenchymal disease: neoplasms, abscess, emphysema, lung fibrosis and honeycombing, catamenial PTX d/t endometriosis and others.
CXR: note visceral pleural line aka lung edge. An Absence of pulmonary tissue/vessels beyond the visceral pleural line. Subtle pneumothorax can be missed. On erect position, air rises and PTX should be sought at the top.
Rib fractures: v.common. Traumatic or pathological (e.g., mets, MM) Rib series x – rays are not very useful because CXR and/or CT scanning are more important to evaluate posttraumatic PTX (bottom left) lung laceration and another major path
Pneumonia: bacterial vs. viral or fungal or in the immunocompromised host (e.g., Cryptococcus in HIV/AIDS) Pulmonary TB
Pneumonia: community-acquired vs. hospital-acquired. Typical bacterial pneumonia or Lobar (non-segmental) pneumonia with purulent material filling the alveoli and spreading to the entire lobe. M/C organismStreptococcus Pneumonia or the Pneumococcus
Others: (Staph, Pseudomonas, Klebsiella esp. in alcoholics potentially leading to necroSIS/lung gangrene) Mycoplasma (20-30s) aka walking pneumonia, etc.
Clinically: a productive cough, fever, pleuritic chest pain sometimes hemoptysis.
CXR: confluent airspace opacity confined to the entire lobe. Air bronchograms. Silhouette sign help with location.
Viral: Influenza, VZV, HSV, EBV, RSV, etc. presents as interstitial lung disease that can be bilateral. May lead to respiratory compromise
Atypical pneumonia and Fungal Pneumonia: Mycoplasma, Legionnaire’s disease, and some fungal/Cryptococcus pneumonia may present with interstitial lung disease.
Pulmonary abscess: an infectious collection of purulent material in the lungs that often necrotizes. May lead to significant pulmonary and system complications/life-threatening.
On CXR or CT: round collection with thick borders and central necrosis containing air-fluid level. DDx from empyema that distorts the lung and pleural-based
Rx: antibiotics, antifungal, antiviral agents.
Pneumonia needs to be followed up with repeat CXR to ensure complete resolution
Lack of radiographic improvement of pneumonia may represent declined immunity, antibiotic resistance, underlying lung carcinoma or other complicating factors
Common infection worldwide (3rd world countries). 1 in 3 persons worldwide is affected by TB. TB is caused by Mycobacterium TB or Mycobacterium Bovis. Intracellular bacillus. Macrophage plays a key role.
Primary Pulmonary TB & Post-primary TB. Requires repeated exposure through inhalation. In most immunocompetent hosts, the active infection does not develop
TB presents as 1) cleared by the host, 2) suppressed into Latent Tuberculosis Infection (LTBI) 3) cause active disease TB. Patients with LTBI are not spreading TB.
Imaging: CXR, HRCT. Primary TB: pulmonary airspace consolidation (60%) lower lobes, lymphadenopathy (95%- hilar & paratracheal), pleural effusion (10%). The Spread of primary TB most likely in immunocompromised and children.
Milliary TB: pulmonary and system complication dissemination that can be fatal
Post-primary (secondary) or reactivation infection: Mostly in the Apices and posterior segments of the upper lobes )high PO2), 40%-cavitating lesions, patchy or confluent airspace disease, fibrocalcific. Latent features: nodal calcifications.
Dx: Acid-fast bacilli (AFB) smear and culture (sputum). HIV serology in all patients with TB and unknown HIV status
Rx: 4-drug regimen: isoniazid, rifampin, pyrazinamide, and either ethambutol or streptomycin.
Pulmonary Neoplasms (primary lung cancer vs. pulmonary metastasis)
Lung cancer: m/c cancer in men and 6th most frequent cancer in women. Strong association with carcinogens inhalation. Clinically: late discovery, depending on the location of the tumor. Pathology (types): Small cell (SCC) vs. Non-small cell carcinoma
Small cell: (20%) develops from neuroendocrine aka Kultchitsky cell, thus may secrete biologically active substances presenting with paraneoplastic syndrome. Typically located centrally (95%) at or near the mainstem/lobar bronchus. Most show poor prognosis and unresectable.
Non-small cell: Lung adenocarcinoma (40%) (M/C lung cancer), M/C in women and non-smokers. Others: Squamous cell (may present with cavitating lesion), Large cell and some others
Plain film (CXR): new or enlarged focal lesion, widened mediastinum suggestive of lymph node involvement, pleural effusion, atelectasis, and consolidation. SPN-may represents potential lung cancer especially if it contains irregular borders, feeding vessels, thick wall, in the upper lungs. Multiple lung nodules are likely to represent metastasis.
Best Modality: HRCT with contrast.
Other chest neoplasms: Lymphoma is v. common in the chest especially in mediastinal and internal mammary notes.
Overall M/C pulmonary neoplasms are a metastasis. Some tumors show a higher predilection for lung mets, e.g., Melanoma, but any cancer can metastasize to the lungs. Some mets referred as �Cannonball� metastasis
Rx: radiation, chemotherapy, resection
Pulmonary edema: a general term defines abnormal fluid accumulation outside vascular structures. Broadly divided into Cardiogenic (e.g., CHF, mitral regurgitation) and Non-cardiogenic with a multitude of causes (e.g., fluid overload, post-transfusion, neurological causes, ARDS, near drowning/asphyxiation, heroin overdose, and others)
Causes: increased in Hydrostatic pressure vs. decreased in oncotic pressure.
Imaging: CXR and CT: 2-types Interstitial and Alveolar flooding. Imaging presentation depends on stages
In CHF: Stage 1: redistribution of vascular flow (10- 18-mm Hg) noted as �cephalization� of the pulmonary vasculature. Stage 2: Interstitial edema (18-25-mm Hg) Interstitial edema: peribronchial cuffing, Kerley lines (lymphatics filled with fluid) A, B, C lines. Stage 3: Alveolar edema: airspace disease: patchy consolidations developing into diffuse airspace disease: Batwing edema, air bronchograms
Rx: 3 main goals: Initial O2 to keep O2 at 90% saturation
Next: (1) reduction of pulmonary venous return (preload reduction), (2) reduction of systemic vascular resistance (afterload reduction), and (3) inotropic support. Treat underlying causes (e.g., CHF)
Lung atelectasis: incomplete expansion of pulmonary parenchyma. The term “collapsed lung” is typically reserved for when the entire lung is collapsed
1) Resorptive (obstructive) atelectasis occurs as a result of complete obstruction of an airway (e.g. tumor, inhaled objects, etc.)
2) Passive (relaxation) atelectasis occurs when contact between the parietal and visceral pleura is disrupted (pleural effusion & pneumothorax)
3) Compressive atelectasis occurs as a result of any thoracic space-occupying lesion compressing the lung and forcing air out of the alveoli
4) Cicatricial atelectasis: occur as a result of scarring or fibrosis that reduces lung expansion as in granulomatous disease, necrotizing pneumonia, and radiation fibrosis
5) Adhesive lung atelectasis occurs from surfactant deficiency and alveolar collapse
6) Plate-like or discoid often developed after following general anesthesia
7) Imaging features: lung collapse, migration of lung fissures, deviation of the mediastinum, rising of the diaphragm, hyperinflation of adjacent unaffected lung
Mediastinum: pathology can be divided into those that result in a focal mass or those that result in diffuse disease involving the mediastinum. Additionally, air may track into the mediastinum in pneumomediastinum. Knowledge of mediastinal anatomy helps the Dx.
Pulmonary emphysema: loss of normal elastic tissue/elastic recoil of the lung with the destruction of capillaries and alveolar septum/interstitium.
Destruction of lung parenchyma due to chronic inflammation. Protease-mediated destruction of elastin. Air trapping/airspace enlargement, hyperinflation, pulmonary hypertension, and other changes. Clinical: progressive dyspnea, irreversible. By the time the forced expiratory volume in 1 second (FEV1 ) has fallen to 50% the patient is breathless upon minimal exertion and adapts to lifestyles.
COPD is the third leading cause of global death. Affects 1.4% of adults in the US. M:F = 1 : 0.9. Pts 45 years and older
Causes: Smoking and a-1-Antitrypsin deficiency (divided into centrilobular (smoking) and panacinar.
Imaging; signs of hyperinflation, air trapping, bullae, pulmonary hypertension.
SKULL FX: COMMON IN THE SETTINGS OF HEAD INJURIES. SKULL FX OFTEN POINT TO OTHER COMPLICATING FACTORS: INTRA-CRANIALHEMORRHAGING, CLOSED TRAUMATIC BRAIN INJURY AND OTHER SERIOUS COMPLICATIONS
SKULL X-RAYS ARE VIRTUALLY OBSOLETE IN EVALUATING HEAD INJURY. CT SCANNING W/O CONTRAST IS THE MOST IMPORTANT INITIAL STEP IN EVALUATION OF ACUTE HEAD TRAUMA. MRI HASA POOR ABILITY TO REVEAL SKULL FRACTURES, AND NOT TYPICALLY USED FOR AN INITIAL DX OF ACUTE HEAD TRAUMA.
SKULL FX ARE IDENTIFIED AS FXS OF SKULL VAULT, SKULL BASE AND FACIAL SKELETON EACH ASSOCIATED WITH SPECIFIC FEATURES AND HELP TO PREDICT COMPLICATIONS.
LINEAR SKULL FX: SKULL VAULT. M/C FX. CT SCANNING IS THE KEY TO EVALUATE ARTERIALEXTRADURAL HEMORRHAGING
X-RAY DDX: SUTURES VS. LINEAR SKULL FX. FX IS THINNER, �BLACKER� I.E. MORE LUCENT, CROSSESSUTURES,�AND VASCULAR GROOVES, LACKSSERRATIONS
RX: IF NO INTRACRANIAL BLEEDS THAT NO TREATMENT. NEUROSURGICAL CARE IF BLEEDSDETECTED BY CT SCANNING
DEPRESSED SKULL FX: 75% IN THE VAULT. CAN BE DEADLY. CONSIDERED AN OPEN FX. MOST CASES NEED NEUROSURGICALEXPLORATION ESPECIALLY IFFRAGMENTS DEPRESSED >1-CM.COMPLICATIONS: VASCULAR INJURY/HEMATOMAS, PNEUMOCEPHALUS, MENINGITIS, TBI, CSF LEAK, BRAIN HERNIATION ETC.
IMAGING: CT SCANNING W/O CONTRAST
BASILAR SKULL FX: CAN BE DEADLY. OFTEN ALONG OTHER MAJOR HEAD TRAUMA OF THE VAULT AND FACIALSKELETON, OFTEN WITH TBI AND MAJORINTRACRANIAL HEMORRHAGING. OFTEN OCCUR AS �HEADBAND� EFFECT OF IMPACT AND MECHANICAL TENSION THROUGH THE OCCIPUT AND TEMPORAL BONES THROUGH SPHENOID AND OTHER BASE OF SKULL BONES. CLINICALLY: RACCOON EYES, BATTEL SIGN, CSFRHINO/OTORRHEA.
NASAL BONES FX: 45% OF ALLFACEFXM/C IMPACT IS LATERAL(FIST BLOW ETC.) IF UNDISPLACEDNO TREATMENT, IF DISPLACED MAY COMPLICATE AIR FLOW AND RESPIRATORY PASSAGE, MAY BE ASSOCIATED WITH OTHER FACIAL/SKULL INJURY. X-RAYS 80%SENSITIVE, FOLLOWED BY CT INCOMPLEX INJURIES.
ORBITAL BLOW OUT FX: COMMONORBITAL INJURY D/T IMPACT ON THE GLOBE AND/OR ORBITAL BONE. FX OF ORBITAL FLOOR INTOMAXILLARY SINUS VS. MEDIAL WALL INTO ETHMOID SINUS. COMPLICATIONS: ENTRAPPEDINFERIOR RECTUS M, PROLAPSEORBITAL FAT,�AND SOFT TISSUES, HEMORRHAGING AND OPTIC NERVE DAMAGE. RX: CONCERNS OF GLOBE INJURY ARE IMPORTANT, GENERALLY TREATEDCONSERVATIVELY IF NO COMPLICATIONS PRESENT
TRIPOD FX: 2ND M/C FACIAL FX#AFTER NASAL (40% OF MIDFACEFX) 3-POINT FX-ZYGOMATICARCH, ORBITAL PROCESS OF ZYGOMATIC BONE & SIDE OF MAXILLARY SINUS WALL, MAXILLARY PROCESS OF ZYGOMATIC BONE.COMPLICATED BY NERVE INJURY, TEMPORALIS M DAMAGE ETC. CT SCANNING IS MORE INFORMATIVE THAT X-RAYS (WATER�S VIEW).
LEFORT FX: SERIOUS FX ALWAYS INVOLVES PTERYGOID PLATES, POTENTIALLY SEPARATINGMIDFACE AND ALVEOLAR PROCESS WITH TEETH FROM THE SKULL. CONCERNS: AIRWAYS, HEMOSTASIS, NERVE INJURIES. CT SCANNING IS REQUIRED. POTENTIAL RISK OF BASILAR SKULL FX
PING-PONG FX:�EXCLUSIVELY IN INFANTS. AN INCOMPLETE FX D/T FOCALDEPRESSION: FORCEPS DELIVERY, DIFFICULT LABOUR ETC. FOCALTRABECULAR MICROFRACTURIINGLEAVING DEPRESSION RESEMBLING APING-PONG. DX IS MAINLY CLINICALSEEN AS FOCAL DEFECT �DEPRESSION� IN THE SKULL. TYPICALLYNEUROLOGICALLY INTACT. CT MAY HELP IF BRAIN INJURY IS SUSPECTED. RX: OBSERVATIONAL VS. SURGICAL IN COMPLICATED INJURIES. SPONTANEOUSREMODELING HAS BEEN REPORTED
LEPTOMENINGEAL CYST (GROWING SKULL FX)- ARE AN ENLARGING SKULL FRACTURE THAT DEVELOPS ADJACENT TO POSTTRAUMATIC ENCEPHALOMALACIA
IT IS NOT A CYST, BUT AN EXTENSION OF THEENCEPHALOMALACIA THAT SEEN A FEW MONTHS POST-TRAUMA WITH PREVIOUS SKULL FX FOLLOWEDBY HERNIATION OF THE MENINGES AND ADJACENTBRAIN WITH PULSATIONS OF THE CSF. CT IS BEST ATDX THIS PATHOLOGY. INDICATES: GROWING FX AND ADJACENT ENCEPHALOMALACIA AS FOCALHYPOATTENUATING LESION.
DDX: INFILTRATING CELLS/METS/OTHER NEOPLASMSINTO SUTURES, EG, INFECTION ETC.
MANDIBULAR FXS: COMMON. POTENTIALLYCONSIDERED AN OPEN FX D/T INTRA-ORALEXTENSION. 40% FOCAL BREAK DESPITEMANDIBLE BEING A RING. DIRECT IMPACT(ASSAULT) M/C MECHANISM
PATHOLOGICAL FX D/T BONE NEOPLASMS, INFECTION ETC. IATROGENIC DURING ORAL SURGERY (TOOTH EXTRACTION)
IMAGING: MANDIBLE X-RAYS, PANOREX, CT SCANNING ESP. IN CASES OF ASSOCIATEDFACE/HEAD TRAUMA
COMPLICATIONS: AIRWAY OBSTRUCTION, HEMOSTASIS IS A MAJOR CONSIDERATION, DAMAGE TO MANDIBULAR N, OSTEOMYELITIS/CELLULITIS AND POTENTIAL SPREAD THROUGH FLOOR OF THE MOUTH (LUDWIGANGINA) AND NECK FASCIAL SOFT TISSUES INTOMEDIASTINUM. CANNOT BE NEGLECTED D/T HIGH MORTALITY RATES.
RX: CONSERVATIVE VS. OPERATIVE
Acute Intracranial Hemorrhage
EPI AKA EXTRADURAL: (EDH) TRAUMATIC RAPTURE OF MENINGEAL ARTERIES (MMA CLASSIC) WITH RAPIDLY FORMING HEMATOMA BETWEEN THE INNER SKULL AND OUTER DURA. CT SCANNING IS THE KEY TO DX: PRESENTS AS �LENTIFORM� I.E. BICONVEX COLLECTION OF ACUTE (HYPERDENSE) BLOOD THAT DOES NOT CROSSSUTURES AND HELPS WITH DDX OF A SUBDURAL HEMATOMA. CLINICALLY: HA, LUCID EPISODE INITIALLY AND DETERIORATING IN A FEW HOURS.COMPLICATIONS: BRAIN HERNIATION, CN PALSY. O/A GOOD PROGNOSIS IF QUICKLY EVACUATED.
SUBDURAL HEMATOMA (SDH): RAPTURE OF BRIDGINGVEINS BETWEEN INNER DURA AND THE ARACHNOID.SLOW BUT PROGRESSIVE BLEED. MAY PARTICULARLYAFFECT THE VERY YOUNG AND ELDERLY AND IN ALL AGES (MVA, FALLS ETC.) MAY DEVELOP IN �SHAKEN BABY SYNDROME�. DX MAY BE DELAYED AND WORSEN THE PROGNOSIS WITH HIGH FATALITIES. IN ELDERLY HEAD TRAUMA MAY BE MINOR OR NOT RECALLED. EARLYIMAGING WITH CT IS CRUCIAL. PRESENTS AS CRESCENTSHAPEDCOLLECTION THAT CAN CROSS SUTURES BUT STOPPED AT DURAL REFLECTIONS. DIFFERENTATTENUATION ON CT D/T DIFFERENT STAGES OF BLOODDECOMPOSITION: ACUTE, SUBACUTE,�AND CHRONIC.MAY FORM A CHRONIC COLLECTION-CYSTICHYGROMA. CLINICALLY: VARIABLE PRESENTATION, 45-60% PRESENT WITH SEVERELY DEPRESSED CNS STATUS, PUPILLARY INEQUALITY. OFTEN WITH INITIAL BRAIN CONTUSION, THEN A LUCID EPISODE BEFORE SEVERELYDETERIORATING. IN 30% CASES OF FATAL BRAIN INJURY PATIENTS HAD SDH. RX: URGENT NEUROSURGICAL.
SUBARACHNOID HEMORRHAGE (SAH): BLOOD IN THE SUB-ARACHNOID SPACE AS THE RESULT OF TRAUMATIC OR NON-TRAUMATIC ETIOLOGY: BERRY ANEURYSMS AROUND CIRCLE OF WILLIS.SAH 3% OF STROKES, 5% OF FETAL STROKES.CLINICALLY: PRESENTS AS A �THUNDERCLAP HEADACHE� DESCRIBED AS A �WORST HA INLIFE�. PT COLLAPSES MAY OR MAY NOT REGAIN CONSCIOUSNESS. PATHOGY: DIFFUSE BLOOD INSA SPACE 1)SUPRASELLAR CISTERN WITH DIFFUSE PERIPHERAL EXTENSION, 2)�PERIMESENCEPHALIC, 3) BASAL CISTERNS. BLOOD LEAKED INTO SA SPACE UNDERARTERIAL PRESSURE INDUCES GLOBAL INCREASE IN INTRACRANIAL PRESSURE, ACUTE GLOBAL ISCHEMIA WORSENED BY VASOSPASM AND OTHER CHANGES.
DX: IMAGING: URGENT CT SCANNING W/O CONTRAST, CT ANGIOGRAPHY MAY HELP TO RULE OUT 99% OF SAH. LUMBAR PUNCTUREMAY HELP IN DELAYED PRESENTATION. AFTER INITIAL DX: MR ANGIOGRAPHY HELPS TO FIND THE CAUSE AND OTHER IMPORTANT FEATURES
IMAGING FEATURES: ACUTE BLOOD IS HYPERDENSE ON CT. FOUND IN DIFFERENTCYSTERNS: PERIMESENCEPHALIC, SUPRASELLA, BASAL, VENTRICLES,
RX: INTRAVENOUS ANTIHYPERTENSIVE MEDS, OSMOTIC AGENTS (MANNITOL) TO DECREASEICP. NEUROSURGICAL CLIPPING AND OTHER APPROACHES.
CNS Neoplasms: Benign vs. Malignant
BRAIN TUMORS REPRESENT 2% OF ALL CANCERS. ONE THIRD ARE MALIGNANT, OF WHICH METASTATIC BRAIN LESIONS ARE THE MOST COMMON
CLINICALLY PRESENT WITH LOCAL CNS ABNORMALITIES, INCREASED ICP, INTRACEREBRAL BLEEDING ETC. FAMILIALSYNDROMES: VON-HIPPEL-LANDAU, TUBEROUS SCLEROSIS, TURCOT SYNDROME, NF1 & NF2 INCREASE THE RISK. IN CHILDREN: M/C ASTROCYTOMAS, EPENDYMOMAS, PNETNEOPLASMS (E.G. MEDULLOBLASTOMA) ETC. DX: BASED ON WHO CLASSIFICATION.
IMAGING IS CRUCIAL: INITIAL SYMPTOMS MAY PRESENT AS SEIZURE, ICP SIGNS HA. EVALUATED BY CT AND MRI WITH IV GADOLINIUM.
IMAGING DETERMINES: INTRA-AXIAL VS. EXTRA-AXIALNEOPLASMS. METS FROM PRIMARY BRAIN NEOPLASMS MAYO CCUR VIA CSF AND LOCAL VESSELS INVASION
NOTE AXIAL CT SLICE OF MENINGIOMA WITH AVIDCONTRAST ENHANCEMENT.
AXIAL MRI ON FLAIR PULSE SEQUENCE REVEALED EXTENSIVE NEOPLASM AND MARKED CYTOTOXIC EDEMA OF THE BRAIN PARENCHYMA CHARACTERISTIC OF GRADE IV GLIOMA (GBM) WITH VERY POOR PROGNOSIS. ABOVE FAR RIGHT IMAGE: AXIAL MRI FLAIR: BRAIN METASTASIS FROM BREAST CANCER. MELANOMA IS COMMONLY METASTASIZESTO THE BRAIN (SEE PATH SPECIMEN) MRI CAN BE DIAGNOSTIC D/T HIGH SIGNAL ON T1 AND CONTRAST ENHANCEMENT.
RX: NEUROSURGICAL, RADIATION, CHEMOTHERAPY,�IMMUNOTHERAPY TECHNIQUES ARE EMERGING
Most healthcare providers use x-rays as a diagnostic tool to treat a variety of patient complaints, including chiropractors. They can help doctors identify the source of a problem or if there is something more going on. X-rays can also help chiropractors determine the best course of action for treatment. To understand more, let’s take a closer look at what they are and how they’re used in most chiropractic offices.
What are x-rays?
An x-ray is a very vigorous form of electromagnetic radiation that is similar to radio waves, ultraviolet radiation, microwaves, or visible light that is used to view the internal composition of a person or thing. A beam is focused on a specific part of a person�s body, such as the back, it produces a digital image of the skeletal structure.
The beam passes easily through skin and other soft tissues�but is unable to pass through bone and teeth. Soft tissue that is denser, such as organs, ligaments, and muscles, will be visible�but will be captured in shades of gray. Areas like the bowel or lungs appear on the film as black.
The use of chiropractic x-rays
Chiropractic x-rays provide vital information that can affect how the chiropractor chooses to treat a patient. In some cases, chiropractic care or spinal manipulation may not be an appropriate course of action at that time, and the patient may be started on a different, gentler therapy.
Other times, it can show the chiropractor how to best proceed in treating the patient. In short, patients can receive better, more well-rounded care which can better facilitate their healing and pain management.
Identify a condition or symptom, such as a spinal tumor or lesion�that would provide a medical reason that a specific course of care should not be done.
Obtain important biomechanical information that can aid in guiding treatment.
To stay apprised and maintain a record of a patient�s degenerative process.
Aid in identifying anomalies in the spine and joints that can affect treatment.
Allows patients to understand their condition and treatment plan better, allowing them to take ownership of the process and be more involved in their therapy and healing.
What does a chiropractor look for on an x-ray film?
When a chiropractor takes an x-ray of a patient, they are looking for things in several particular areas. The first thing they check is to make sure that there are no dislocations, fractures, cancer, infections, tumors, or other potentially dangerous conditions.
They then look for disk height and other signs of disk degeneration, bone density, bone spurs, joint spaces, and alignment. This allows them to identify conditions like scoliosis and other conditions that may require specific forms of treatment.
Many chiropractors prefer that the patient is in a weight-bearing position when taking spinal x-rays. This differs from the majority of medical facilities which have the patient lie down.
The advantage of weight-bearing x-rays as a diagnostic tool�is that it allows for measuring, i.e., leg length deficiency, scoliosis, and the narrowing of joint space. It can also show that certain bones, such as the tibia and fibula, are separating which can be an indication of a torn tendon or problem with the joint. A non-weight bearing x-ray cannot provide the same perspective,�and vital clues to a patient�s condition may be missed.
In all cases, Orthopedic hand surgical referral is required
Colles fx: m/c d/t FOOSH+pronation. m/c inOSP/elder women. Rare in men and if occurs need DEXA to avoid hip Fx etc. Young pts: high-energy trauma. Typically extra-articular.50%-cases show Ulna styloid (US) Fx.
Imaging: x-rad is sufficient, CT in complex Fx, MRI helps with ligament tears and TFC.
Rx: if extra-articular and <5-mm distal radius shortening and <5-degree dorsal angulation closed reduction+casting is sufficient. ORIF in complex cases.
�Image Dx: distal rad impaction/shortening,dorsal angulation of distal fragment, carefully examine if intra-articular extension, 50% US Fx
Smith Fx: Goyrand in French literature. Considered as reversed Colles, otherwise almost identical, I.e., 85% extra-articular, 50%US Fx, OSP/elderly women, young pts-high-energy trauma. Differences: mechanismFOOSHwith flexed wrist thus m. Less frequent.
Imaging steps: (see Colles Fx) C
Complications: similar to Colles Fx
Rad Dx: 85% extra-articular with volar(anterior) angulation of the distal fragment,radial shortening. Carefully examine cortical breach suspecting intra-articular extension that can be named as Smith type 2 or Reversed Barton Fx (next)
Rx: similar approach as in Colles.
Barton fx: FOOSH, impaction of distal radius similar to Colles but the Fx line extends from the dorsal radial aspect into radiocarpal joint resulting with dorsal slip/dislocation of the carpus.
Imaging: 1st sept x-radiography often with CTto examine intra-articular Fx extension and operative planning
Rad Dx: distal radius Fx extending from dorsal into the radiocarpal joint with a variable degree of displacement, the proximal slip of the carpus
If Fx line extends from the volar aspect into the wrist joint named Reversed Barton aka Smith type 2 (above bottom image)
Complications: similar to all distal radius Fx
Rx: operative with ORIF
Chauffeur’s/backfire Fx aka Hutchinson Fx: intra-articular Fx of Radial styloid. The name derives from the time when the car had to be started with a hand crank that could backfire inducing wrist dorsiflexion and radial deviation.
Imaging: x-radiography is sufficient. CT may be helpful if Fx not readily shown by x-rays.
Rx: operative with percutaneous lagscrewin all cases d/t intra-articularnature
Die-Punch Fx: impaction Fx by the Lunate bone into distal articularLunate fossa of the Radius. IntraarticularFx. Derives its name from a technique to shape (impress) a hole in industrial machining “die-punch.”FOOSH injury.
Imaging: 1st step x-rays, may be equivocal d/t subtle depression of the Lunate fossa then CT scanning is most informative.
Rad Dx: impacted lunate fossa region with intra-articular Fx extension. This can present as a comminuted Fxarticular Fx of the Distal Radius.
Rx: operative d/t intra-articular Fx
Construct arcs of Gilula when evaluating carpal injuries. An Important step required to avoid missing subtle changes in carpal alignment and cortical continuity
Scaphoid bone Fx: m/c Fx carpal bone. D/tFOOSH wrist extended radially deviated. Location of Fx is most important to prognosis: Waist-m/c location (70%). May have 70-100%chance of AVN. Proximal pole Fx: 20-30% with a high risk of non-union. Distal pole-10%shows better prognosis. Distal pole Fx is m/c in children. Key clinical sign; pain in the snuffbox.
Imaging: 1st step-x-radiography but 15-20%missed d/t occult Fx. Special views required. Thus MRI is the most sensitive and specific for early occult Fx. Bone scintigraphy has98/100% specificity & sensitivity esp. 2-3 days after the onset. Key rad. Dx: Fx line if evident, displacement and obscuration of scaphoid(navicular) fat pad, examine for scapholunate dissociation. If proximal bone appears sclerotic-AVN occurred. MRI: low on T1 & high on T2/STIR/FSPD d/t bone edema, a�low signalFx line can be noted.
Rx: Spica cast should be applied if clinically suspected even w/o x-ray findings. For waistFx-cast for 3-mo for prox pole 5-mo immobilization. ORIF or percutaneous pinning with a Herbert screw.
Scapholunate Ligaments Dissociation
SNAC wrist: scaphoid non-union advanced collapse. Often d/t non-union and dissociation of scapholunate ligaments (SLL)with progressive radiocarpal and intercarpalDJD. The Proximal scaphoid fragment is attached to Lunate with distal dissociating and rotating�signet ring� sign on x-rays.
SNAC wrist may often result in DISI
Rx: progressive DJD may lead to four-corner arthrodesis
Scapholunate advanced collapse (SLAC wrist): SLLdissociation with progressive intercarpal and radiocarpal DJD and volar or dorsal carpal displacement (DISI & VISI). Causes: trauma, CPPD, DJD, Kienboch disease (AVN of Lunate), Preiserdisease (AVN of Scaphoid).
SLL dissociation will lead to Dorsal or VolarIntercarlate aka Intercarpal Segmental Instability (DISIor VISI).
Rad Dx: Dx underlying cause. X-rays demonstrate dorsal or volar angulation of the Lunate with increased or decreased scapholunate angle on the lateral view. On frontal view: Terry Thomas sign or widening of scapholunate distance 3-4-mm as the upper limit of normal.
�MRI may help with ligament evaluation and pre-surgical planning
Rx: often operative with late DJD. Four-corner arthrodesis
Triquetrum Fx: 2nd m/c carpal bone Fx. M/C dorsal aspect is avulsed by the�tough Dorsal radiocarpal ligament. Cause: FOOSH.
Imaging: x-radiography wrist series is sufficient. Best revealed on the lateral view as an avulsed bone fragment adjacent to the dorsum of the Triquetrum. CT may help if radiographically equivocal.
Rx: conservative care
Complications: rare, may persist as pain on the dorsum of the wrist
Hook of the Hamate Fx: m/c occurs in batting sports (cricket, baseball, hockey, impact by a golf club, etc.) 2% of carpusFx.
Imaging: x-radiography may fail to detect an Fx unless “carpal tunnel view” is used. CT may help if x-rays unrewarding.
Clinically: pain, positive pull test, weak, painful grip. Deep ulnar n. Branch may be affected within the�Guyon canal.
Rx: usually non-operative, but chronic non-union may require excision.
DDx: bipartite hamate
�Lunate vs. Perilunate dislocation: Lunate is m/c dislocated carpal bone. Overall infrequent carpal injury. However, often missed!
Occurs with FOOSH and wrist extended and ulnar deviated. Imaging: 1st step x-rays. Ifunrewarding or require more complex injury evaluation CT scanning.
Key Rad DDx: DDx Lunate from perilunate dislocation. Lunate dislocation: lunate lost its contact with distal radius �spilled teacup� on the lateral. Perilunate dislocation: Lunate maintains its contact with distal radius despite the Capitatedorsally dislocated. Lunate dislocation is additionally helped to identify a �pie sign� d/t Lunate overlapping the Capitate
Rx: emergency reduction and operative repair of torn ligaments
Metacarpal & Phalangeal Injuries
Bennett Fx: intra-articular but noncomminuted impact-type Fx of the base of 1st MC bone of the thumb. X-radiography is sufficient.
Rad Dx: characteristic triangular fragment of bone on the ulnar aspect of the 1st MCbase, often with radial subluxation of the remaining radial aspect of the 1st MC
Complications: DJD, non-union, etc.
Rx: prone to instability/non-union requiring an operative care
Rolando Fx: aka comminuted Bennett with Y or T-configuration. More complex injury. It is unstable requiring operative care
Gamekeeper thumb: traditionally described as a chronic tear of the�ulnar (medial) collateral ligament at 1stMCP in English Gamekeepers’ who performed neck twisting/killing of small game. An acute injury may also be named as Skier’s thumb. This injury can be ligamentous w/o a fracture and an avulsion injury at the 1st proximal phalanx base.
Complication: Stener lesion or displacement of torn ligament over Adductor pollicis muscle that cannot heal w/o surgical repair. MRI Dx is required.
Avoid thumb stress views that can induce a Stenerlesion
Imaging: x-radiography followed by MRI to Dx Stenerlesion. MSK US can be used if MRI is unavailable.
�Stener lesion on MRI & MSUS: ulnar collateral stump is more superficial to Adductor pollicis aponeurosis and appears like a low signal mass-like stump forming so-called “yo-yo on the string sign” reported both on MRI and MSK US.
Rx: often operative
Boxer Fx: m/c MC Fx. An extra-articular usually non-comminuted or minimal comminuted Fx through m/c the 5th and sometimes the 4th MCneck-head junction (occasionally through the shaft) resulting in volar head angulation. Mechanism: direct impact as in clenched fist punching hard surface (e.g., facial bones/wall punching) hence 95% in young males.
Imaging: x-radiography hand series is sufficient
Rad Dx: Fx line transverse or oblique through MCneck with volar head angulation. Evaluate the degree of displacement, critical to report.
N.B. If the same mechanism fractures the 2ndand 3d MC in the same anatomic area, it may require operative care.
Phalangeal hand Fx: m/c skeleton Fx (10% of all Fx). Sports and industrial injuries dominate
Imaging: x-radiography with hand series or PA/lateral finger views will suffice
Rad Dx: if prox phalanx Fx, distal fragment is angled volarly with prox fragment dorsally. Distal phalanx may be angled dorsally. Key observation: nail bed injury, which considered an open Fx with a�risk of infection.
Rx: if <10-degree angulation-buddy-taping with motion rehab. CRPP vs. ORIF can be considered in complex cases-Orthopedic hand surgeon referral
Complication: loss of motion, necrosis, infection.May result with amputation
For additional common injuries: PIP is m/c dislocated joint. Mullet (Baseball) finger, Jersey finger and other injury refer to:
Felon: septic infection of the fingertip pulp typically with Staph.Aureus. Causes: needle prick(diabetics), paronychia, nail splinters, etc. m/c in index and thumb, presenting with pain, swelling, etc.
D/t specific pulp anatomy theinfection>swelling leads to pulp compartment syndrome-pressure and necrosis.
Rx: operative with incision distal to DIP, irrigation/debridement
Pediatric Wrist Injury
Incomplete Fx: Greenstick Fx, Torus (Buckle)Fx, Bowing (Plastic) deformity/Fx. D/t FOSHe.g. fell off the monkey bar. m/c affects <10-years-old.
Rx: usually non-operative (closed reduction and casting)
Distal Radioulnar Joint (DRUJ) Instability-common injury following trauma as in FOOSHwith wrist hyperextension and rotation and disruption of DRUJ ligaments and TFCcomplex. Avulsion of ulnar styloid with the�dorsal or volar displacement of distal ulnar should be noted.
Imaging steps: x-rays initially, MRI may identify ligaments and TFC damage, MSKUScan help with ligaments tearing.
Wrist DJD-typically is secondary to trauma, scapholunate dissociation, SLAC, SNAC wrist, CPPD, Keinboch or Preiser Disease and others.
May lead to major functional loss
Imaging: typically presents as radiocarpal JSL, subchondral sclerosis,osteophytosis, subcortical cysts, and loose bodies. Typically additional induces intercarpal degeneration and particularly Tri-scaphe joint.
MRI may be helpful with early recognition of scapholunate dissociation, Lunate/Navicular AVN.
If isolated MCP OA noted considerCPPD & Hemochromatosis (Hook-like osteophytes)
Typically painless except 1st CMC OA
DIPs-Heberden nodes, PIPs-Bouchard nodes
Erosive OA (occasionally called�inflammatory OA�)
A Spectrum of OA but producing central proximal erosions at DIPs and PIPsresulting with very characteristic �gullwing� appearance. No systemic inflammation (no CRP, RF, Anti-CCP Ab)typically in middle-aged/elderly females, like Hand OA, often seen in families
Rheumatoid Arthritis (RA)-chronic systemic inflammatory disease of unknown etiology, targeting synovial joints, tendons with multiple systemic involvement (lung, CVS, Ocular, Skin, etc.) Pathology: Tcell>Macrophage/APC>mediatedautoimmune process resulting in pannus formation and gradual destruction of ST, cartilage, bone,�and other tissues. 3% FemalesVS.1% Males. Environmental triggers: infection, trauma, smoking,�and others in a genetically susceptible individual. 20-30%may be disabled after 10-years.
In adults: Radial head Fx is the m/c (33%) and accounts for 1.5-4% of all fractures. Etiology: FOOSH with forearm pronated. Associated injuries: elbow collateral ligaments tears. EssexLoprestiFx with interosseous membrane tearing and dislocation of the Distal Radio-Ulnar Joint(DRUJ)
Terrible triad: of the Radial head Fx, elbow dislocation and Coronoid process Fx (typically avulsed by the Brachialis M)
Imaging: 1st step is x-radiography with elbow series, CT scanning may help in complex cases, MRIif ligamentous injury.
In children: Supracondylar Fx of the distal humerus accounts for 90% of acute trauma. It is always d/t accidental trauma with FOOSH and elbow extended, rarely <5% with flexed elbow. MostSupracondylar Fx occur in children <10 y.o. Males>Females. Complications: malunion in cubitus varus aka Gunstock deformity, vascular injury and acute ischemic compartment syndrome with Volkmann contracture
Imaging: 1st step x-radiography can be sufficient. CT occasionally used in complex cases.
Radial head (RH) Fx: Mason classification helps to determine the degree of complexity and mode of treatment
Type 1- undisplaced is the m/c and stable contained by ligaments. On radiographs can be very subtle and evaluation of abnormal elbow fat pads is critical and often the only diagnostic clue
Type 2- displaced by 2-mm or > with rotational block
Type 3- comminuted >2-3 fragments and
Type4 is presented with RH fx, posterior elbow dislocation and sometimes Coronoid process fracture often d/t Brachialis M avulsion
Rx: Type 1 managed non-operatively by immobilization and movement rehab. Type 2- ORIF if rotational block. Type 3 and 4, ORIF and RH resection or RH arthroplasty
Note abnormally displaced anterior fat pad (orange arrow) and the emergence of the posterior fat pad (green arrow) that is usually deep in the olecranon fossa and not seen unless acute hemarthrosis or other effusiondevelopsFat pad signs are most reliable indicators of intra-articular elbow Fx
Mason type 1 RH Fx can be v. subtle and missed. Radiographic search should involve a�close evaluation of positive fat pad signs. Note anterior fat pad displacement aka Sail sign and the presence of the post fat pad d/t acute bleed
Monteggia fracture-dislocations: prox 1/3ulnar shaft Fx. with concomitant dislocation of PRUJ (radial head). FOOSH injury. Children4-12 y.o. Infrequent in adults.
X-rays readily reveal ulnar Fx, but radial head dislocation may be subtle and occasionally missed. This is a serious injury leading to elbow disability if Dx delayed 2-3 weeks or left untreated. X-rays are typically sufficient:Rx: casting vs. operative.
Supracondylar Fx: this is the M/C elbow Fx in children.
Especially, the un-displaced types 1(top right) is difficult to Dx. Abnormality of “fat pads” and anterior humeral line and radiocapitella line disturbance are often most reliable
Type 3 carries a particularly high risk for Volkmann contracture (vascular ischemic-necrosis of the anterior forearm muscle compartment
Elbow complaints in a young athlete
Epicondyle Fx: common pediatric injury, about 10%.Essentially an avulsion Fx and a MUCL tear. Medial epicondyle is m/c Fx. FOOSH is the m/c mechanism.M>F. If minimally displaced or undisplaced can be treated with casting esp. in non-dominant arm. If displaced as in this case, require ORIF.
Medial epicondyle avulsive Fx in a young baseball pitcher was coined a �little league elbow� in the 60sand now should be avoided to avoid confusion
OCD of the Capitellum is a common athletic injury induced by repeated compression/flexion. OCD must be DDx from Panner�s disease or osteochondritis typically presented in younger patients
Difficulty in diagnosis may stem�from multipleapophysis about the elbow (see CRITOE)
Imaging: 1st step: x-rays followed by MRI and MRarthrogramme if indicated.
CT may help with complex injury evaluation. MRI and MSKUS may help with a�ligament injury.
DJD of the elbow is uncommon and typically 2nd to trauma, occupation, CPPD, OCD of theCapitellum or other pathology. Clinically: pain, reduced ROM esp. in dominant arm, deterioration of ADL. Loss of terminal flexion and extension. 50% develop Ulnarcompressive neuropathy. Rx: conservative,arthroscopic debridement/osteophytes removal, capsular release. In older patients and not active patients Total Elbow Arthroplasty (TEA) can be used
Imaging: x-radiography is sufficient, CT helps with pre-operative planning
Inflammatory Arthritis: RA of the elbow is frequent (20-50%) and destructive d/t synovitis, pannus, bone/cartilage,�and ligamentous destruction/laxity. Clinically: begins after the onset of hands symptoms with, symmetrical swelling, pain, reduced ROM, flexion contracture. Presence of rheumatoid nodules can be noted along the olecranon and posterior forearm. Rx: DMARD, operative tendons repair.
Imaging: x-radiography with early non-specific effusion (fat pads),later: erosions, symmetric JSL, osteopenia. MSK US helps early Dx. MRI reveals synovitis; bone edema correlates with pre-erosive x-ray findings, synovial enhancement on FS T1+C.
Gouty Arthritis: may affect the elbow but less than in the lower extremity. Olecranon bursitis causing a �rising sun sign� on x-rays with or w/o bone erosions. Aspiration and polarised microscopy revealing needle-shaped negatively birefringent monosodium urate crystals. Rx: colchicine, other meds.
Septic Arthritis: consider in people with diabetes, IV drug users, concurrent RA, patients with active TB, gonococcal in young adults. Clinically presents as monoarthritis with or w/o constitutional signs. X-ray: poor detection in early stages. US may show effusion and high Doppler.MRI: effusion, osseous edema. Bone scintigraphy can help as well. Labs: CBC, ESR, CRP. Diagnostic arthrocentesis with gram staining and culture are crucial. Rx: Prompt IV antibiotics
Juvenile Idiopathic Arthritis (JIA) considered M/C chronic disease of childhood and preceded IBD infrequency. Dx is clinical and imaging: Criteria: Joint pain and swelling in a child 0-16-years for 6-weeks or longer. Many forms exist�M/C pauciarticular(oligoarticular) 40%, F>M, associated with ocular involvement (iridocyclitis) and potential blindness. Polyarticular and Systemic forms.
Elbow is frequently affected along with the knee, wrists,�and hands,�especially in polyarticular dz.
Labs: ESR/CRP RF-VE in most cases
Imaging: early x-ray features are non-specific. Later: osseous erosion, destruction of joint cartilage, overgrowth of articular epiphyses, early closure of physis. Delayed features: 2nd DJD, joint ankyloses.DDx: hemophilic arthropathy. Cervical radiographs are crucial.
Rx: DMARD, conservative care
Supracondylar process: 2% of the population. Described by Sir JohnStruthers in 1854. Fibrous band(Ligament of Struthers) may lead to compression of the Median N. DDx fromOsteochondroma that typically points away from the joint
Primary synovial chondrometaplasia�(Reichel Syndrome): abnormalmetaplasia of synovial cells shedding cartilage into joint potentially causing DJD, extrinsic bone erosion, synovitis, nerve compressions etc. Removedoperatively. Imaging: multiple osseocartilaginous loose bodies of relatively equal sizes in the joint cavityDDx with DJD and 2ndosteochondromatosis. MRI-low signal onT1 and T2 with potential joint effusion. Ina tight joint like the elbow may present with large joint distention.�
Panner�s Disease: osteochondrosis of theCapitellum typically in 5-10 y.o. young athlete DDX from OCD of Capitellum(discussed) that occurs in teenagers.Clinically: pain on activity. Recovery occurs in most cases by spontaneous healing. Imaging: x-rays reveal sclerosis and slight fragmentation of theCapitellum w/o loose body. MRI: low T1and high T2 signal in the entireCapitellum.
Soft Tissue & Bone Neoplasms about the Elbow
Lipoma: intramuscular, subcutaneous. Most common soft tissue neoplasms. Composed of fat but a substantial number may undergo fat necrosis-calcification-fibrosis. Typically remains benign. Occasionally difficult to DDx from a well-differentiated liposarcoma. Imaging: x radiography: radiolucent lesion well-circumscribed with or w/o calcification. US and MRI are important. On MRIT1high, T2 low SI.
Hemangioma: benign vascular lesion, often composed of multiple vascular channels. Capillary vs. cavernous. More common in children, but found in any age. May often form phleboliths (calcification). Imaging: x-rays reveal soft tissue mass containing phleboliths. MRI: T1-high or variable signal. T2-high signal in areas of slow flow. �bag of worms� sign. Biopsy best avoided. Rx: difficult: local excision vs. embolization vs. observation. High recurrence.
Peripheral Nerve sheath tumor (PNST): benign vs.malignant. Greater incidence in NF1 with a higher risk of malignant PNST. Benign PNST: Schwannoma vs.Neurofibroma. Spinal vs. peripheral nerves. Histology: Schwann cells interspersed with fibroblast and vessels.Clinically: pts in 20s and 30s, palpable mass with or w/o local pressure. Imaging: MRI: T1: split-fat sign, T2: target sign. T1+C enhancement
Soft Tissue Sarcomas: MFH, Synovial sarcoma,(discussed), Liposarcoma (more frequent in the retroperitoneum) Dx: MRI. Clinically: Dx is delayed d/t painless enlarging mass often ignored. Clinically palpable mass deserves MRI examination, US may be helpful. Biopsy confirms Dx.
Malignant bone Neoplasms: Children: OSA, Ewing�s sarcoma (discussed) Adults: Mets, Myeloma (discussed)
Proximal humeral Fx account for 4-6% of all Fxs. Osteoporotic (OSP) Fx in >60 y.o associated with minimal trauma with F: M 2:1 ratio. In young patients, acute high energy trauma predominates.
Complications: AVN humeral head, Axillary N paralysis.
Neer Classification: considers fractures along 4-anatomical lines with or w/o displacement >1-cm & 45-degree angulation
One part Neer Fx- no displacement or very minimal <1-cm/45-degree. Can affect 1-4 lines and M/C at greater tuberosity. 80% of proximal humeral Fx are one-part Neer.
Two-part Fx: 1-part is displaced >1-cm/45-degrees. m/c involves the surgical neck
Three-part Fx: 2-parts are displaced >1-cm/45-degrees.
Four-part Fx: all 4-parts can be displaced. Uncommon <1%
Imaging: 1st step-radiography, CT may be used in more complex cases. Orthopedic referral
Management: Neer one-part Fx is treated with Sling Immobilisation and progressive rehab
The vast majority of Fx in the elderly are treated non-operatively
Younger patients (40-65) may occasionally require hemiarthroplasty if 3 or 4-part Neer Fx present. Greater risk of AVN
Proximal Humerus Fractures
Note: Left image: Fx involving the anatomical neck and the greater tuberosity with minimal displacement <1-cm/45-degree thus Dx as one-part Fx. Right image: Small avulsion Fx of the greater tuberosity with significant displacement (>45-degrees & 1-cm) thus Dx as two-part Fx
Note: three-part Neer Fx (left) and four-part Neer Fx (right)> Management: operative in most cases in younger (40-65) patients
Refers to complete separation of the humerus from scapula glenoid. In 20-40s M: F 9:1 ratio, in60-80S M: F 3:1
Anatomy: Shoulder stability is sacrificed for mobility, and overall GHJD is the m/c among large joints in the body
Protective falls (e.g., FOOSH) and MVA are m/c causes. GHJ is most vulnerable in abduction, extension and external rotation. Anatomical factors: shallow glenoid, laxed ant-inferior capsule and GH ligaments. GHJD will induce severe tearing of major GHJ restraints. Associated osseous and labral injuries are common and may lead to chronic instability, DJD,�and functional changes
3-types: Anterior GHJD (95%)
Posterior GHJD (4%) especially associated with epileptic seizures, electrocution and can occur b/l
Inferior GHJD aka Laxatio Erecta (<1%) associated with severe trauma
Clinically: AGHJD presents with severe pain, the arm is externally rotated and adducted, severe limitation of movement. GHJD may persist as chronic dislocation.
Management: prompt reduction in ED under anesthesia or heavy sedation with Kocher technique top image (not used), External rotation method (middle) or Milch technique (can be used w/o anesthesia) and a few other methods. Delay in reduction correlates with greater risk of immediate and long-term�complications
Diagnostic Imaging Approach
Shoulder series x-radiography is sufficient. Additional Imaging with CT scanning and MRI may be helpful to Dx osseous, cartilage, labral/ligaments pathology
Anterior GHJD (95%). Subcoracoid position(top right) of the humerus is the m/c
Anterior GHJD may also occur as subglenoid(bottom left)and infrequently as subclavicular
Key to radiographic search is to evaluate associated Bankart and Hill-Sachs injuries
Occurs during anterior GHJD d/t impaction of the head into anterior-inferior glenoid. Variations exist (see next slide). BonyBankart can be seen on x-rays. So-called soft tissue Bankart requires MRI. Cartilage (soft)Bankart is the m/c.
Hill-Sachs aka Hatchet deformity (arrow postreduction)occurs during the same mechanism as Bankart, i.e., compression and impaction of posterolateral aspect of the head against the glenoid producing wedge-shape Fx. Hill-Sachs lesion may predispose to recurrent/chronic GHJD.
Bankart lesion may heal, but operative suture anchors are needed sometimes
CT arthrogram and MRI may be helpful
Types of Bankart Lesion
Note different types of Bankart lesion. Onlyosseous Bankart can be seen radiographically. Soft tissue Bankart requires MRI with and without intra-articular gadolinium(arthrogram).
Note: posterior GHJD with its characteristic signs:
Trough sign aka reverse Hill-Sachs. Occurs d/t anterolateral head impaction Fx
Rim sign: only occurs in the PGHJD d/t posterior position of the head and anterior glenoid-to humeral head distance 6-mm or greater
Light-bulb sign: d/t acute internal rotation of the humerus (head)
Inferior GHJD aka Laxatio Erecta
Severe hyperabduction and inferior displacement of the humerus. Greater chances of severe neurovascular injury and acromial Fx
The dislocated arm is hyperabducted and fixed with the elbow flexed and the arm above the head
ACJ Dislocation (ACJD)
ACJD: common injury, 9% of shoulder girdle injuries esp. in male athletes by a direct blow
Rockwood classification (left) evaluates tearing of AC and CC ligaments and regional muscles
Type1, 2, 3 among the m/c
Type 1: sprain of ACL w/o tearing
Type 2: tear of ACL and sprain of CCL
Type 3: tear of AC & CCL. The clavicle is elevated above the acromion. If <2-cm good results with conservative Rx.
Imaging: x-radiography with b/l ACJ views with and w/o weights to compare both ACJs. In complex cases CT scanning esp. if Fx is considered
Management: Type 3 (>2-cm) & Types 4-6Operative
Type 3 ACJ Separation
Type 3 ACJ separation (top left)
More significant ACJD (bottom images) with clinical sign of acromion under the skin and resultant ORIF
Rotator Cuff Muscles (RCM) Pathology
RCM tendinopathy: collagenous degeneration of RCM particularly Supraspinatus M. tendon(SSMT) d/t overuse/degeneration-micro tearing with collagenous replacement. Impingement syndrome is a 2nd extrinsic cause. Presented clinically as pain and limited ROM
Imaging Dx: MSK US can be as accurate as MRI and better in some cases d/t dynamic evaluation v. cost effective
Key MRI clue is thickened inhomogeneous SSMTwith increased signal on all pulse sequences d/t fatty degeneration and inflammation (left images: T1 & T2 FS)
MSKUS findings: thickening of the SSMTsubstance with a change�in normal echogenicity.MSKUS is good to DDx with SSMT tears. US advantages are that it allows dynamic evaluation of painful structures
Partial tear of SSMT: partial (incomplete) tear ofSSMT may occur at the bursal and articular surface or interstitial, i.e., intra-substance/noncommunicating. Etiology: sub-acromial impingement, acute strain, and chronic microtrauma tendinosis
Clinically: pain on abd and flexion, impingement tests, Hawkins-Kennedy tests, etc. Pearls: partial tears can be more painful than complete tears
Imaging Dx: MSKUS is as good as MRI (N.B.some studies indicated MSKUS is more superior to MRI). Key MRI findings: gap/incomplete tear of SSMT filled with joint fluid +/- granulation tissue
MSKUS: decreased echogenicity of SSMT, thinning and partial tearing filled with fluid(anechoic areas arrows). Lost convexity of tendon bursal or articular interface.
Full Thickness SSMT (rot cuff) tear: degeneration/tearing of rot cuff. 2nd to impingement by Hooked acromion, overhead overuse or acute trauma. 7-25% of shoulder pain in the general population. Clinically: pain on impingement tests.
Imaging Dx: MSKUS is as good as MRI.Limitations: poor Dx of labral pathology. Key USDx: focal tendon interruption, an anechoic gap (fluid filled), hypoechoic tendon, tendon retraction, uncovered cartilage sign (bottom left, A: US B: MRI)
MRI: key Dx: insertional tear extending through entire SSMT crescent, retraction with fatty degeneration of SSMT and the muscle. If retraction is at 12 o�clock or greater (top images), it may not be anchored operatively
Rotator Cuff (RTC) Calcific Tendinitis: usually d/t calcium HADD crystals. Middle-aged women are most affected. Ranges from asymptomatic imaging finding to severe destructive arthropathy or Milwaukee shoulder(infrequent)
HADD has 3-pathological phases: formation resting-resorption.Mild-to-moderate pain esp. in resting phase.
Imaging: x-radiography: homogenous ovoid mineralization within RTCMT, m/c in SSMT. MRI: ovoid/globular decreased signal on all pulse sequences often with surrounding edema (bottom left)
Rx: self-resolution occurs. Advanced cases: operative aspiration etc.
Superior Labrum Anterior to Posterior (SLAP) Lesions/Tears
SLAP tears: FOOSH and throwing sports or chronic shoulder instability aka Multidirectional shoulder instability (in 20%). Type 1-9 exist but the M/C areType 1-4
In all 4-types superior labrum is affected with or w/oLHBMT anchor tear (see pictures). Clinically: pain, limitation of AROM with active compression tests, typically non-specific findings mimicking RTCpathology
Imaging is crucial: best imaging is MRI arthrography. Key signs: hyperintense linear fluid signal within superior labrum +/- extending along the LHBT on fat-suppressed fluid sensitive imaging and FS T1 arthrogram. Best observed on coronal slices.
Rx: small tears may heal, but unstable tears require operative care.
Key DDx: anatomical variants like Buford complex andSub-labral foramen
SLAP tear with a paralabral cyst (bottom right)
Normal variant DDx: sub labral foramen(bottom left) note: MR arthrography with contrast undercutting the labrum but w/o extending posteriorly to the LHBT
GHJ DJD: usually associated with a 2nd cause: trauma, instability, AVN, CPPD, etc. Presented with pain, crepitus and decreased ROM/function. Associated RTC disease may be present. Imaging; x-radiography is sufficient and provides grading/care planning.Major findings: joint narrowing, osteophytosis esp. at the inferior-medial head (orange arrow), subchondral sclerosis/cysts. Often noted superior head migration d/t RTC disease.
ACJ OA: common and typically primary with aging. Presents with ACJ loss and osteophytes. Osteophytes along the undersurface of the ACJ �keel osteophytes�(blue arrow) may lead to RTC muscle tear. Regional bursitis is other clinical feature of ACJ arthrosis.
Management: usually conservative depending on clinical signs/symptoms
Rheumatoid Arthritis GHJ: RA is a multisystem inflammatory disease affecting multiple joints lined by the synovium. GHJ RA is common (m/c large joints in RA knees/shoulders). Clinically: pain, limited ROM and instability, muscle weakness/wasting. Hands, feet,�and wrists are m/c affected. Imaging: x-radiography reveals periarticular erosions, uniform joint space loss, juxta-articular osteoporosis, subluxations,�and soft tissue swelling. MRI can help detect�commonly associated RTC tearing and instability. Early changes can be detected by MSKUS esp. with power Doppler use indicating hyperemia/inflammation.
Note: L shoulder x-ray revealing cartilage destruction and symmetrical joint loss, multiple erosions, and likely loss of RTCM support with superior head migration, ST effusion present.
Note: PDFS coronal and axial MRI slices of GHJ RA indicating marked inflammatory joint effusion, bone erosion/edema, synovial pannus formation and likely tear in RTC m. Management: Rheumatological referral and pharmacotherapy with DMARD. Operative care asRTCM repair. 10% of patients are disabled d/t RA
Neuropathic Osteoarthropathy aka Charcot’s shoulder: d/t neurovascular and neural periarticular damage. Multiple causes exist.M/c develops in diabetics in midfoot. Shoulder Charcot is m/c in Syringomyelia (25%), trauma paralysis, MS, etc. Dx: clinical(50% pain/swelling 50% painless destruction). Imaging is crucial. X-radiography is sufficient in well-established cases, but early Dx is challenging. MRI may help with early Dx and delayed complications. Rad Dx: Shoulder Charcot is m/c presented as atrophic type destructive arthropathy with humeral head appearing as if surgically amputated along with intra-articular debris, density, distention, dislocation, and other key features
Septic Shoulder: shoulder is the 3rd m/c followingknee>hips. Patients at risk: diabetics, RA pts, immunocompromised, I.V. drug users, indwelling catheters, etc. Routes: hematogenous (m/c), direct inoculation (iatrogenic, trauma etc.) adjacent spread(e.g. OM). Staph. Aureus (>50%) m/c.
Clinically: joint pain and dec. ROM, fever 60% only, toxemia, inc. ESR/CRP. Dx: imaging and joint aspiration/culture. RadDx: early x-rays often unremarkable except ST effusion/fat planes obscuration, joint widening. Later7-12 days patchy osteopenia, moth-eaten/permeating bone resorption, articular destruction, joint narrowing. May progress to severe joint destruction and ankyloses. Early Dx & I.V. antibiotics are crucial even before culture. Operative irrigation and joint drainage in some cases. Complications are possible esp. if Rx is delayed. MSKUS with needle aspiration may help. Note: (top image) non-traumatic joint widening with inferolateral head displacement d/t septic A dx: by needle aspiration Staph. Aures.
Ischemic Osteonecrosis of the humeral head may occur d/t trauma (Neer four-part Fx), Steroids, Lupus, Sickle cell, Alcoholism, Diabetes,�and many other conditions. Imaging is crucial: MRI detects earliest changes as intraosseous edema. X-ray features are late, presented as a collapse of subchondral bone with sclerosis �snow cap� sign, fragmentation, and progressive severe DJD
Management: orthopedic referral, core decompression in early cases, hemiarthroplasty in moderate and total arthroplasty in severe cases.
In adults >40, bone Mets d/t lung, breast, renal cell, thyroid CA & prostate are the m/c causes. Clinically: may mimic pain resemblingRTC/joint changes. Should be evaluated carefully. Key to Dx: Hx, PE and Imaging esp.in pts with known primary
Imaging: 1st step x-rays, MRI can help, Tc99bone scintigraphy helps to detect regional and distant disease. X-ray features: destructive lytic changes typically in prox humerus(red marrow) with or w/o path Fx. DDx: Mets, MM, lymphoma
Clinically: night pain, pain at rest, etc. Lab tests: unrewarding, in severe cases hypercalcemia may be noted.
Primary Malignant bone neoplasms (shoulder) Adults: M. Myeloma or Solitary plasmacytoma, Chondrosarcoma may transform from an enchondroma and some others. In children/teenagers: OSA vs. Ewing�s
Primary benign bone neoplasms (shoulder). Adults: Enchondroma (patients in their 20-30s)GCT. In children: Simple bone cyst (Unicameral Bone cyst), Osteochondroma, Aneurysmal Bone Cyst, Chondroblastoma (rare)
Imaging: 1st step x-radiography
MRI is essential to Dx. Especially in cases of primary malignant neoplasms Evaluate extent, soft tissue invasion, preoperative planning, staging, etc.
About 1.5 million people in the United States have rheumatoid arthritis. Rheumatoid arthritis, or RA, is a chronic, autoimmune disease characterized by pain and inflammation of the joints. With RA, the immune system, which protects our well-being by attacking foreign substances like bacteria and viruses, mistakenly attacks the joints. Rheumatoid arthritis most commonly affects the joints of the hands, feet, wrists, elbows, knees and ankles. Many healthcare professionals recommend early diagnosis and treatment of RA.
Rheumatoid arthritis is the most commonly diagnosed systemic inflammatory arthritis. Women, smokers, and those with a family history of the disease are most often affected. Criteria for diagnosis include having at least one joint with definite swelling that is not explained by another disease. The likelihood of a rheumatoid arthritis diagnosis increases with the number of small joints involved. In a patient with inflammatory arthritis, the presence of a rheumatoid factor or anti-citrullinated protein antibody, or elevated C-reactive protein level or erythrocyte sedimentation rate suggests a diagnosis of rheumatoid arthritis. Initial laboratory evaluation should also include complete blood count with dif- ferential and assessment of renal and hepatic function. Patients taking biologic agents should be tested for hepatitis B, hepatitis C, and tuberculosis. Earlier diagnosis of rheumatoid arthritis allows for earlier treatment with disease-modifying antirheumatic agents. Combinations of medications are often used to control the disease. Methotrexate is typically the first-line drug for rheumatoid arthritis. Biologic agents, such as tumor necrosis factor inhibitors, are generally considered second-line agents or can be added for dual therapy. The goals of treatment include minimiza- tion of joint pain and swelling, prevention of radiographic damage and visible deformity, and continuation of work and personal activities. Joint replacement is indicated for patients with severe joint damage whose symptoms are poorly controlled by medical management. (Am Fam Physician. 2011;84(11):1245-1252. Copyright � 2011 American Academy of Family Physicians.)
Rheumatoid arthritis (RA) is the most common inflammatory arthritis, with a lifetime prevalence of up to 1 percent worldwide.1 Onset can occur at any age, but peaks between 30 and 50 years.2 Disability is common and significant. In a large U.S. cohort, 35 percent of patients with RA had work disability after 10 years.3
Etiology and Pathophysiology
Like many autoimmune diseases, the etiology of RA is multifactorial. Genetic susceptibility is evident in familial clustering and monozygotic twin studies, with 50 percent of RA risk attributable to genetic factors.4 Genetic associations for RA include human leukocyte antigen-DR45 and -DRB1, and a variety of alleles called the shared epitope.6,7 Genome-wide association studies have identified additional genetic signatures that increase the risk of RA and other autoimmune diseases, including STAT4 gene and CD40 locus.5 Smoking is the major environmental trigger for RA, especially in those with a genetic predisposition.8 Although infections may unmask an autoimmune response, no particular pathogen has been proven to cause RA.9
RA is characterized by inflammatory pathways that lead to proliferation of synovial cells in joints. Subsequent pannus formation may lead to underlying cartilage destruction and bony erosions. Overproduction of pro-inflammatory cytokines, including tumor necrosis factor (TNF) and interleukin-6, drives the destructive process.10
Older age, a family history of the disease, and female sex are associated with increased risk of RA, although the sex differential is less prominent in older patients.1 Both current and prior cigarette smoking increases the risk of RA (relative risk [RR] = 1.4, up to 2.2 for more than 40-pack-year smokers).11
Pregnancy often causes RA remission, likely because of immunologic tolerance.12 Parity may have long-lasting impact; RA is less likely to be diagnosed in parous women than in nulliparous women (RR = 0.61).13,14 Breastfeeding decreases the risk of RA (RR = 0.5 in women who breastfeed for at least 24 months), whereas early menarche�(RR = 1.3 for those with menarche at 10 years of age or younger) and very irregular menstrual periods (RR = 1.5) increase risk.14 Use of oral contraceptive pills or vitamin E does not affect RA risk.15
Patients with RA typically present with pain and stiffness in multiple joints. The wrists, proximal interphalangeal joints, and metacarpophalangeal joints are most commonly involved. Morning stiffness lasting more than one hour suggests an inflammatory etiology. Boggy swelling due to synovitis may be visible (Figure 1), or subtle synovial thickening may be palpable on joint examination. Patients may also present with more indolent arthralgias before the onset of clinically apparent joint swelling. Systemic symptoms of fatigue, weight loss, and low-grade fever may occur with active disease.
In 2010, the American College of Rheumatology and European League Against Rheumatism collaborated to create new classification criteria for RA (Table 1).16 The new criteria are an effort to diagnose RA earlier in patients who may not meet the 1987 American College of Rheumatology classification criteria. The 2010 criteria do not include presence of rheumatoid nodules or radiographic erosive changes, both of which are less likely in early RA. Symmetric arthri- tis is also not required in the 2010 criteria, allowing for early asymmetric presentation.
In addition, Dutch researchers have developed and validated a clinical prediction rule for RA (Table 2).17,18 The purpose of this rule is to help identify patients with undifferentiated arthritis that is most likely to progress to RA, and to guide follow-up and referral.
Autoimmune diseases such as RA are often characterized by the presence of autoanti- bodies. Rheumatoid factor is not specific for RA and may be present in patients with other diseases, such as hepatitis C, and in healthy older persons. Anti-citrullinated protein antibody is more specific for RA and may play a role in disease pathogenesis.6 Approxi- mately 50 to 80 percent of persons with RA have rheumatoid factor, anti-citrullinated protein antibody, or both.10 Patients with RA may have a positive antinuclear antibody test result, and the test is of prognostic impor- tance in juvenile forms of this disease.19 C-reactive protein levels and erythrocyte sedimentation rate are often increased with active RA, and these acute phase reactants are part of the new RA classification criteria.16 C-reactive protein levels and erythrocyte sedimentation rate may also be used to follow disease activity and response to medication.
Baseline complete blood count with differential and assessment of renal and hepatic function are helpful because the results may influence treatment options (e.g., a patient with renal insufficiency or significant thrombocytopenia likely would not be prescribed a nonsteroidal anti-inflammatory drug [NSAID]). Mild anemia of chronic disease occurs in 33 to 60 percent of all patients with RA,20 although gastrointestinal blood loss should also be considered in patients taking corticosteroids or NSAIDs. Methotrexate is contraindicated in patients with hepatic disease, such as hepatitis C, and in patients with significant renal impairment.21 Biologic therapy, such as a TNF inhibitor, requires a negative tuberculin test or treatment for latent tuberculosis. Hepatitis B reactivation can also occur with TNF inhibitor use.22 Radiography of hands and feet should be performed to evaluate for characteristic periarticular erosive changes,�which may be indicative of a more aggressive RA subtype.10
Skin findings suggest systemic lupus erythematosus, systemic sclerosis, or psoriatic arthritis. Polymyalgia rheumatica should be considered in an older patient with symptoms primarily in the shoulder and hip, and the patient should be asked questions related to associated temporal arteritis.
Chest radiography is helpful to evaluate for sarcoidosis as an etiology of arthritis.�Patients with inflammatory back symptoms, a history of inflammatory bowel disease, or inflammatory eye disease may have spondyloarthropathy. Persons with less than six weeks of symptoms may have a viral process, such as parvovirus. Recurrent self-limited episodes of acute joint swelling suggest crystal arthropathy, and arthrocentesis should be performed to evaluate for monosodium urate monohydrate or calcium pyrophosphate dihydrate crystals. The presence of numerous myofascial trigger points and somatic symptoms may suggest fibromyalgia, which can coexist with RA. To help guide diagnosis and determine treatment strategy, patients with inflammatory arthritis should be promptly referred to a rheumatology subspecialist.16,17
Rheumatoid arthritis, or RA, is the most common type of arthritis. RA is an autoimmune disease, caused when the immune system, the human body’s defense system, attacks its own cells and tissues, particularly the joints. Rheumatoid arthritis is frequently identified by symptoms of pain and inflammation, often affecting the small joints of the hands, wrists and feet. According to many healthcare professionals, early diagnosis and treatment of RA is essential to prevent further joint damage and decrease painful symptoms. Dr. Alex Jimenez D.C., C.C.S.T. Insight
After RA has been diagnosed and an initial evaluation performed, treatment should begin. Recent guidelines have addressed the management of RA,21,22 but patient preference also plays an important role. There are special considerations for women of childbearing age because many medications have deleterious effects on pregnancy. Goals of therapy include minimizing joint pain and swelling, preventing deformity (such as ulnar deviation) and radiographic damage (such as erosions), maintaining quality of life (personal and work), and controlling extra-articular manifestations. Disease-modifying antirheumatic drugs (DMARDs) are the mainstay of RA therapy.
DMARDs can be biologic or nonbiologic (Table 3).23 Biologic agents include monoclonal antibodies and recombinant receptors to block cytokines that promote the inflammatory cascade responsible for RA symptoms. Methotrexate is recommended as the first- line treatment in patients with active RA, unless contraindicated or not tolerated.21 Leflunomide (Arava) may be used as an alternative to methotrexate, although gastrointestinal adverse effects are more common. Sulfasalazine (Azulfidine) or hydroxychloroquine (Plaquenil) pro-inflammatory as monotherapy in patients with low disease�activity or without poor prognostic features (e.g., seronegative, non-erosive RA).21,22
Combination therapy with two or more DMARDs is more effective than monotherapy; however, adverse effects may also be greater.24 If RA is not well controlled with a nonbiologic DMARD, a biologic DMARD should be initiated.21,22 TNF inhibitors are the first-line biologic therapy and are the most studied of these agents. If TNF inhibitors are ineffective, additional biologic therapies can be considered. Simultaneous use of more than one biologic therapy (e.g., adalimumab [Humira] with abatacept [Orencia]) is not�recommended because of an unacceptable rate of adverse effects.21
NSAIDs and Corticosteroids
Drug therapy for RA may involve NSAIDs and oral, intramuscular, or intra-articular corticosteroids for controlling pain and inflammation. Ideally, NSAIDs and corticosteroids are used only for short-term management. DMARDs are the preferred therapy.21,22
Dietary interventions, including vegetarian and Mediterranean diets, have been�studied in the treatment of RA without convincing evidence of benefit.25,26 Despite some favorable outcomes, there is a lack of evidence for the effectiveness of acupuncture in placebo-controlled trials of patients with RA.27,28 In addition, thermotherapy and therapeutic ultrasound for RA have not been studied adequately.29,30 A Cochrane review of herbal treatments for RA concluded that gamma-linolenic acid (from evening primrose or black currant seed oil) and Tripterygium wilfordii (thunder god vine) have potential benefits.31 It is important to inform patients that serious adverse effects have been reported with use of herbal therapy.31
Exercise and Physical Therapy
Results of randomized controlled trials sup- port physical exercise to improve quality of life and muscle strength in patients with RA.32,33 Exercise training programs have not been shown to have deleterious effects on RA disease activity, pain scores, or radiographic joint damage.34 Tai chi has been shown to improve ankle range of motion in persons with RA, although randomized trials are limited.35 Randomized controlled trials of Iyengar yoga in young adults with RA are underway.36
Duration of Treatment
Remission is obtainable in 10 to 50 percent of patients with RA, depending on how remission is defined and the intensity of therapy.10 Remission is more likely in males, nonsmokers, persons younger than 40 years, and in those with late-onset disease (patients older than 65 years), with shorter duration of disease, with milder disease activity, without elevated acute phase reactants, and without positive rheumatoid factor or anti-citrullinated protein antibody findings.37
After the disease is controlled, medication dosages may be cautiously decreased to the minimum amount necessary. Patients will require frequent monitoring to ensure stable symptoms, and prompt increase in medication is recommended with disease flare-ups.22
Joint replacement is indicated when there is severe joint damage and unsatisfactory control of symptoms with medical management. Long-term outcomes are support, with only 4 to 13 percent of large joint replacements requiring revision within 10 years.38 The hip and knee are the most commonly replaced joints.
Although RA is considered a disease of the joints, it is also a systemic disease capable of involving multiple organ systems. Extra-articular manifestations of RA are included in Table 4.1,2,10
Patients with RA have a twofold increased risk of lymphoma, which is thought to be caused by the underlying inflammatory�process, and not a consequence of medical treatment.39 Patients with RA are also at an increased risk of coronary artery disease, and physicians should work with patients to modify risk factors, such as smoking, high blood pressure, and high cholesterol.40,41 Class III or IV congestive heart failure (CHF) is a contraindication for using TNF inhibitors, which can worsen CHF outcomes.21 In patients with RA and malignancy, caution is needed with continued use of DMARDs, especially TNF inhibitors. Biologic DMARDs, methotrexate, and leflunomide should not be initiated in patients with active herpes zoster, significant fungal infection, or bacterial infection requiring antibiotics.21 Complications of RA and its treatments are listed in Table 5.1,2,10
Patients with RA live three to 12 years less than the general population.40 Increased mortality in these patients is mainly due to accelerated cardiovascular disease, especially in those with high disease activity and chronic inflammation. The relatively new biologic therapies may reverse progression of atherosclerosis and extend life in those with RA.41
Data Sources: A PubMed search was completed in Clinical Queries using the key terms rheumatoid arthritis, extra-articular manifestations, and disease-modifying antirheumatic agents. The search included meta-analyses, randomized controlled trials, clinical trials, and reviews. Also searched were the Agency for Healthcare Research and Quality evidence reports, Clinical Evidence, the Cochrane database, Essential Evidence, and UpToDate. Search date: September 20, 2010.
Author disclosure: No relevant financial affiliations to disclose.
In conclusion, rheumatoid arthritis is a chronic, autoimmune disease which causes painful symptoms, such as pain and discomfort, inflammation and swelling of the joints, among others. The joint damage characterized as RA is symmetrical, meaning it generally affects both sides of the body. Early�diagnosis is essential for treatment of RA. The scope of our information is limited to chiropractic and spinal health issues. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at�915-850-0900�.
Curated by Dr. Alex Jimenez
Additional Topic Discussion: Relieving Knee Pain without Surgery
Knee pain is a well-known symptom which can occur due to a variety of knee injuries and/or conditions, including�sports injuries. The knee is one of the most complex joints in the human body as it is made-up of the intersection of four bones, four ligaments, various tendons, two menisci, and cartilage. According to the American Academy of Family Physicians, the most common causes of knee pain include patellar subluxation, patellar tendinitis or jumper’s knee, and Osgood-Schlatter disease. Although knee pain is most likely to occur in people over 60 years old, knee pain can also occur in children and adolescents. Knee pain can be treated at home following the RICE methods, however, severe knee injuries may require immediate medical attention, including chiropractic care.
1. Etiology and pathogenesis of rheumatoid arthritis. In: Firestein GS, Kelley WN, eds. Kelley�s Textbook of Rheu- matology. 8th ed. Philadelphia, Pa.: Saunders/Elsevier; 2009:1035-1086. 2. Bathon J, Tehlirian C. Rheumatoid arthritis clinical and laboratory manifestations. In: Klippel JH, Stone JH, Crofford LJ, et al., eds. Primer on the Rheumatic Dis- eases. 13th ed. New York, NY: Springer; 2008:114-121. 3. Allaire S, Wolfe F, Niu J, et al. Current risk factors for work disability associated with rheumatoid arthritis. Arthritis Rheum. 2009;61(3):321-328. 4. MacGregor AJ, Snieder H, Rigby AS, et al. Characteriz- ing the quantitative genetic contribution to rheumatoid arthritis using data from twins. Arthritis Rheum. 2000; 43(1):30-37. 5. Orozco G, Barton A. Update on the genetic risk fac- tors for rheumatoid arthritis. Expert Rev Clin Immunol. 2010;6(1):61-75. 6. Balsa A, Cabezo?n A, Orozco G, et al. Influence of HLA DRB1 alleles in the susceptibility of rheumatoid arthritis and the regulation of antibodies against citrullinated proteins and rheumatoid factor. Arthritis Res Ther. 2010;12(2):R62. 7. McClure A, Lunt M, Eyre S, et al. Investigating the via- bility of genetic screening/testing for RA susceptibility using combinations of five confirmed risk loci. Rheuma- tology (Oxford). 2009;48(11):1369-1374. 8. Bang SY, Lee KH, Cho SK, et al. Smoking increases rheu- matoid arthritis susceptibility in individuals carrying the HLA-DRB1 shared epitope, regardless of rheumatoid factor or anti-cyclic citrullinated peptide antibody sta- tus. Arthritis Rheum. 2010;62(2):369-377. 9. Wilder RL, Crofford LJ. Do infectious agents cause rheu- matoid arthritis? Clin Orthop Relat Res. 1991;(265): 36-41. 10. Scott DL, Wolfe F, Huizinga TW. Rheumatoid arthritis. Lancet. 2010;376(9746):1094-1108. 11. Costenbader KH, Feskanich D, Mandl LA, et al. Smoking intensity, duration, and cessation, and the risk of rheu- matoid arthritis in women. Am J Med. 2006;119(6): 503.e1-e9. 12. Kaaja RJ, Greer IA. Manifestations of chronic disease during pregnancy. JAMA. 2005;294(21):2751-2757. 13. Guthrie KA, Dugowson CE, Voigt LF, et al. Does preg- nancy provide vaccine-like protection against rheuma- toid arthritis? Arthritis Rheum. 2010;62(7):1842-1848. 14. Karlson EW, Mandl LA, Hankinson SE, et al. Do breast- feeding and other reproductive factors influence future risk of rheumatoid arthritis? Results from the Nurses� Health Study. Arthritis Rheum. 2004;50(11):3458-3467. 15. Karlson EW, Shadick NA, Cook NR, et al. Vitamin E in the primary prevention of rheumatoid arthritis: the Women�s Health Study. Arthritis Rheum. 2008;59(11): 1589-1595. 16. Aletaha D, Neogi T, Silman AJ, et al. 2010 rheumatoid arthritis classification criteria: an American College of Rheumatology/European League Against Rheumatism collaborative initiative [published correction appears in Ann Rheum Dis. 2010;69(10):1892]. Ann Rheum Dis. 2010;69(9):1580-1588. 17. van der Helm-van Mil AH, le Cessie S, van Dongen H, et al. A prediction rule for disease outcome in patients with recent-onset undifferentiated arthritis. Arthritis Rheum. 2007;56(2):433-440. 18. Mochan E, Ebell MH. Predicting rheumatoid arthritis risk in adults with undifferentiated arthritis. Am Fam Physi- cian. 2008;77(10):1451-1453. 19. Ravelli A, Felici E, Magni-Manzoni S, et al. Patients with antinuclear antibody-positive juvenile idiopathic arthri- tis constitute a homogeneous subgroup irrespective of the course of joint disease. Arthritis Rheum. 2005; 52(3):826-832. 20. Wilson A, Yu HT, Goodnough LT, et al. Prevalence and outcomes of anemia in rheumatoid arthritis. Am J Med. 2004;116(suppl 7A):50S-57S. 21. Saag KG, Teng GG, Patkar NM, et al. American College of Rheumatology 2008 recommendations for the use of nonbiologic and biologic disease-modifying antirheu- matic drugs in rheumatoid arthritis. Arthritis Rheum. 2008;59(6):762-784. 22. Deighton C, O�Mahony R, Tosh J, et al.; Guideline Devel- opment Group. Management of rheumatoid arthritis: summary of NICE guidance. BMJ. 2009;338:b702. 23. AHRQ. Choosing medications for rheumatoid arthritis. April 9, 2008. http://www.effectivehealthcare.ahrq.gov/ ehc/products/14/85/RheumArthritisClinicianGuide.pdf. Accessed June 23, 2011. 24. Choy EH, Smith C, Dore? CJ, et al. A meta-analysis of the efficacy and toxicity of combining disease-modify- ing anti-rheumatic drugs in rheumatoid arthritis based on patient withdrawal. Rheumatology (Oxford). 2005; 4 4 (11) :1414 -1421. 25. Smedslund G, Byfuglien MG, Olsen SU, et al. Effective- ness and safety of dietary interventions for rheumatoid arthritis. J Am Diet Assoc. 2010;110(5):727-735. 26. Hagen KB, Byfuglien MG, Falzon L, et al. Dietary inter- ventions for rheumatoid arthritis. Cochrane Database Syst Rev. 2009;21(1):CD006400. 27. Wang C, de Pablo P, Chen X, et al. Acupuncture for pain relief in patients with rheumatoid arthritis: a systematic review. Arthritis Rheum. 2008;59(9):1249-1256. 28. Kelly RB. Acupuncture for pain. Am Fam Physician. 2009;80(5):481-484. 29. Robinson V, Brosseau L, Casimiro L, et al. Thermother- apy for treating rheumatoid arthritis. Cochrane Data- base Syst Rev. 2002;2(2):CD002826. 30. Casimiro L, Brosseau L, Robinson V, et al. Therapeutic ultrasound for the treatment of rheumatoid arthritis. Cochrane Database Syst Rev. 2002;3(3):CD003787. 31. Cameron M, Gagnier JJ, Chrubasik S. Herbal therapy for treating rheumatoid arthritis. Cochrane Database Syst Rev. 2011;(2):CD002948. 32. Brodin N, Eurenius E, Jensen I, et al. Coaching patients with early rheumatoid arthritis to healthy physical activ- ity. Arthritis Rheum. 2008;59(3):325-331. 33. Baillet A, Payraud E, Niderprim VA, et al. A dynamic exercise programme to improve patients� disability in rheumatoid arthritis: a prospective randomized con- trolled trial. Rheumatology (Oxford). 2009;48(4): 410-415. 34. Hurkmans E, van der Giesen FJ, Vliet Vlieland TP, et al. Dynamic Exercise programs (aerobic capacity and/or mus- cle strength training) in patients with rheumatoid arthri- tis. Cochrane Database Syst Rev. 2009;(4):CD006853. 35. Han A, Robinson V, Judd M, et al. Tai chi for treat- ing rheumatoid arthritis. Cochrane Database Syst Rev. 2004;(3):CD004849. 36. Evans S, Cousins L, Tsao JC, et al. A randomized con- trolled trial examining Iyengar yoga for young adults with rheumatoid arthritis. Trials. 2011;12:19. 37. Katchamart W, Johnson S, Lin HJ, et al. Predictors for remis- sion in rheumatoid arthritis patients: a systematic review. Arthritis Care Res (Hoboken). 2010;62(8):1128-1143. 38. Wolfe F, Zwillich SH. The long-term outcomes of rheu- matoid arthritis: a 23-year prospective, longitudinal study of total joint replacement and its predictors in 1,600 patients with rheumatoid arthritis. Arthritis Rheum. 1998;41(6):1072-1082. 39. Baecklund E, Iliadou A, Askling J, et al. Association of chronic inflammation, not its treatment, with increased lymphoma risk in rheumatoid arthritis. Arthritis Rheum. 2006;54(3):692-701. 40. Friedewald VE, Ganz P, Kremer JM, et al. AJC editor�s consensus: rheumatoid arthritis and atherosclerotic cardiovascular disease. Am J Cardiol. 2010;106(3): 442-447. 41. Atzeni F, Turiel M, Caporali R, et al. The effect of phar- macological therapy on the cardiovascular system of patients with systemic rheumatic diseases. Autoimmun Rev. 2010;9(12):835-839.
M/C dislocation of the foot at tarsal-metatarsal articulation (Lisfranc joint). Direct impact or landing and plantar or dorsal flexing the foot. Lisfranc ligament holding 2nd MT base and 1st Cu is torn. Manifests with or w/o fracture-avulsion.
Imaging: 1st step: foot radiography in most cases sufficient to Dx. MSK US may help: show disrupted Cu1-Cu2. Ligament and widened space > 2.5mm. MRI may help but not essential. Weight-bearing view aids Dx.
2-types: homolateral (1st MTP joint in contact) and divergent (2-5 MT displaced laterally and 1st MT medially)
Management: operative fixation is crucial
N.B. Atraumatic Lisfranc dislocation is a frequent complication of a diabetic Charcot foot
Osteochondral Injury of the Talus (OCD)
Common. Non-traumatic found in superior-medial talar dome. Traumatic may affect supero-lateral dome.
Clinically: pain/effusion/locking. Imaging is crucial.
1st step: radiography may reveal focal radiolucent concavity/halo, fragment.
MRI helpful esp. if OCD is cartilaginous and to demonstrate bone edema.
Jones Fx: extra-articular Fx of proximal metaphysis of the 5th MT. Prone to non-union. Often fixed operatively.
Pseudo-Jones: intra-articular avulsion of 5th MT styloid/base by eccentric contraction of Peroneus Brevis M. Managed conservatively: boot-cast immobilization. Both Jones & Pseudo-Jones Dx by foot series radiography.
Stress Fx. Calcaneus, 2nd, 3rd, 5th MTs. Repeated loading (running) or “March foot” 2nd/3rd MT. Clinically: pain on activity, reduced by rest. Dx: x-rays often unrewarding earlier. MRI or MSK US may help. Managed: Conservatively. Complications; progress into complete Fx
Turf toe: common athletic hyperextension of 1st MTP-sesamoid/plantar plate complex is tearing. 1st MTP unstable/loose. Managed operatively.
Arthritis of the Foot & Ankle
DJD of the ankle: uncommon a primary OA. Typically develops as 2nd to trauma/AVN, RA, CPPD, Hemophilic arthropathy, Juvenile Idiopathic Arthritis, etc. manifests as DJD: osteophytes, JSL, subchondral cysts all seen on x-rays
Inflammatory Arthritis: RA may develop in the ankle or any synovial joint. Will typically presents with symmetrical Hands/feet RA initially (2nd, 3rd MCP, wrists, MTPs in feet) usually with erosion, uniform JSL, juxta-articular osteopenia, and delayed subluxations.
HLA-B27 spondyloarthropathies: commonly affect lower extremity: heel, ankle esp in Reactive (Reiter). Erosive-productive bone proliferation is a crucial Dx.
Gouty Arthritis: common in the lower extremity. Ankle, mid-foot foot esp 1st MTPs. Initial onset: acute gouty arthritis with ST effusion and no erosions/tophi. Chronic tophaceous gout: peri-articular, intra-osseous punched-out erosions with over-hanging edges, no initial JSL/osteopenia, ST. Tophi may be seen.
Miscellaneous arthropathy: PVNS. Not common. Affects 3-4th decades of life. The result of synovial proliferation with Macrophages and multi-nucleated Giant Cells filled with hemosiderin and fatty accumulation may lead to inflammation, cartilage damage, extrinsic bone erosions. Dx: x-rays are insensity, MRI modality of choice. Synovial biopsy. Management: operative, can be difficult.
(Charcot’s joint) Common and on the rise d/t epidemic in type 2 DM. May present with pain initially (50% of cases) and painless destructive arthropathy as a late manifestation. Early Dx: delayed. Imaging is crucial: x-rays: initially unrewarding, some SF effusion is seen. MRI helps with early Dx and extremity off-loading. Late Dx: irreversible dislocations, collapse, disability. Note: Lisfrance dislocation in Charcot joint
M/C mid-foot (TM joint) in 40% of cases, ankle 15%. Progression: Rocker-bottom foot, ulcerations, infections, increased morbidity, and mortality.
Early Dx: by MRI is crucial. Suspect it in patients with type 2 DM especially if early non-traumatic foot/ankle pain reported.
Arthritis is characterized as the inflammation of one or multiple joints. The most common symptoms of arthritis include pain and discomfort, swelling, inflammation, and stiffness, among others. Arthritis may affect�any joint in the human body, however, it commonly develops in the knee. � Knee arthritis can make everyday�physical activities difficult. The most prevalent types of arthritis are osteoarthritis and rheumatoid arthritis, although there are well over 100 distinct forms of arthritis, affecting children and adults alike. While there is no cure for arthritis, many treatment approaches can help treat the symptoms of knee arthritis.
Anatomy of the Knee
� The knee is the largest and strongest joint in the human body. It is made up of the lower end of the thigh bone,�or femur, the top end of the shin bone, or tibia, and the kneecap, or patella. The ends of the three bones are covered with articular cartilage, a smooth, slippery structure which protects and cushions the bones when bending and straightening the knee.
� Two wedge-shaped parts of cartilage, known as the meniscus, function as shock absorbers between the bones of the knee to help cushion the joint and provide stability. The knee joint is also surrounded by a thin lining known as the synovial membrane. This membrane releases a fluid which lubricates the cartilage and also helps reduce friction in the knee. The significant kinds of arthritis that affect the knee�include osteoarthritis, rheumatoid arthritis, and post-traumatic arthritis.
� Osteoarthritis is the most common type of arthritis which affects the knee joint. This form of arthritis is a degenerative, wear-and-tear health issue which occurs most commonly in people 50 years of age and older, however, it may also develop in younger people.
� In osteoarthritis, the cartilage in the knee joint gradually wears away. As the cartilage wears away, the distance between the bones decreases. This can result in bone rubbing and it can�create painful bone spurs. Osteoarthritis generally develops slowly but the pain may worsen over time.
� Rheumatoid arthritis is a chronic health issue which affects multiple joints throughout the body, especially the knee joint. RA is also symmetrical, meaning it often affects the same joint on each side of the human body.
� In rheumatoid arthritis, the synovial membrane that covers the knee joint becomes inflamed and swollen, causing knee pain, discomfort, and stiffness. RA is an autoimmune disease, which means that the immune system attacks its own soft tissues. The immune system attacks healthy tissue,�including tendons, ligaments and cartilage, as well as softens the bone.
� Posttraumatic arthritis is a form of arthritis that develops after damage or injury to the knee. By way of instance, the knee joint may be harmed by a broken bone, or fracture, and result in post-traumatic arthritis years after the initial injury. Meniscal tears and ligament injuries can cause additional wear-and-tear on the knee joint, which over time can lead to arthritis and other problems.
Symptoms of Knee Arthritis
� The most common symptoms of knee arthritis include pain and discomfort, inflammation, swelling, and stiffness. Although sudden onset is probable, the painful symptoms generally�develop gradually over time. Additional symptoms of knee arthritis can be recognized as follows:
The joint may become stiff and swollen, making it difficult to bend and straighten the knee.
Swelling and inflammation may be worse in the morning, or when sitting or resting.
Vigorous activity might cause the pain to flare up.
Loose fragments of cartilage and other soft tissue may interfere with the smooth motion of the joints, causing the knee to lock or stick through motion. It could also creak, click, snap or make a grinding sound, known as crepitus.
Pain can cause a sense of fatigue or buckling from the knee.
Many individuals with arthritis may also describe increased joint pain with rainy weather and climate changes.
Diagnosis for Knee Arthritis
� During the patient’s appointment for diagnosis of knee arthritis, the healthcare professional will talk about the symptoms and medical history, as well as conduct a physical examination. The doctor may also order imaging diagnostic tests, such as X-rays, MRI or blood tests for further diagnosis. During the physical examination, the doctor will search for:
Joint inflammation, swelling, warmth, or redness
Tenderness around the knee joint
Assortment of passive and active movement
Instability of the knee joint
Crepitus, the grating sensation inside the joint, with motion
Pain when weight is placed on the knee
Issues with gait, or manner of walking
Any signs of damage or injury to the muscles, tendons, and ligaments surrounding the knee joint
Involvement of additional joints (an indicator of rheumatoid arthritis)
Imaging Diagnostic Tests
X-rays. These imaging diagnostic tests produce images of compact structures, such as bones. They can help distinguish among various forms of arthritis. X-rays for knee arthritis may demonstrate a portion of the joint distance, changes in the bone as well as the formation of bone spurs, known as osteophytes.
Additional tests. Sometimes, magnetic resonance imaging, or MRI, scans, computed tomography, or CT,�scans, or bone scans are required to ascertain the condition of the bone and soft tissues of the knee.
� Your doctor may also recommend blood tests to determine which type of arthritis you have. With some kinds of arthritis, such as rheumatoid arthritis, blood tests can help with the proper identification of the disease.
Although the knee joint is one of the strongest and largest joints in the human body, it is often prone to suffering damage or injury, resulting in a variety of conditions. In addition, however, other health issues, such as arthritis, can affect the knee joint. In network for most insurances of El Paso, TX, chiropractic care can help ease painful symptoms associated with knee arthritis, among other health issues. Dr. Alex Jimenez D.C., C.C.S.T. Insight
Treatment for Knee Arthritis
� Non-surgical treatment approaches are often recommended before considering surgical treatment for knee arthritis. Healthcare professionals may recommend a variety of treatment options, including chiropractic care, physical therapy, and lifestyle modifications, among others.
� Lifestyle modifications. Some lifestyle modifications can help protect the knee joint and impede the progress of arthritis. Minimizing physical activities which aggravate the condition, will put less strain on the knee. Losing weight may also help lessen stress and pressure on the knee joint, resulting in less painful symptoms and increased function.
� Chiropractic care and physical therapy.�Chiropractic care utilizes full body chiropractic adjustments to carefully restore any spinal misalignments, or subluxations, which may�be causing symptoms, including arthritis. The doctor may also recommend physical therapy to create an individualized exercise and physical activity program for each patient’s needs.�Specific exercises will help increase range of motion and endurance, as well as help strengthen the muscles in the lower extremities.
� Assistive devices. Using assistive devices, such as a cane, shock-absorbing shoes or inserts, or a brace or knee sleeve, can decrease painful symptoms. A brace helps with function and stability, and may be particularly useful if the arthritis is based on one side of the knee. There are two types of braces that are often used for knee arthritis: A “unloader” brace shifts weight from the affected section of the knee, while a “support” brace helps support the entire knee load.
� Drugs and/or medications. Several types of medications are useful in treating arthritis of the knee. Since individuals respond differently to medications, your doctor will work closely with you to determine the medications and dosages which are safe and effective for you.
� The healthcare professional may recommend surgical treatment if the patient’s knee arthritis causes severe disability and only if the problem isn’t relieved with non-surgical treatment. Like all surgeries, there are a few risks and complications with surgical treatment for knee arthritis. The�doctor will discuss the possible problems with the patient.
� Arthroscopy. During arthroscopy, physicians use instruments and small incisions to diagnose and treat knee joint problems. Arthroscopic surgery isn’t frequently used in the treatment of arthritis of the knee. In cases where osteoarthritis is accompanied with a degenerative meniscal tear, arthroscopic surgery may be wise to treat the torn meniscus.
� Cartilage grafting. Normal cartilage tissue may be taken from a tissue bank or through a different part of the knee to fill out a hole in the articular cartilage. This process is typically considered only for younger patients.
� Synovectomy. The lining damaged by rheumatoid arthritis is eliminated to reduce swelling and pain.
� Osteotomy. In a knee osteotomy, either the tibia (shinbone) or femur (thighbone) is cut then reshaped to relieve stress and pressure on the knee joint. Knee�osteotomy is utilized when early-stage osteoarthritis has damaged one facet of the knee joint. By changing the weight distribution, this can relieve and enhance the function of the knee.
� Total or partial knee replacement (arthroplasty).�The�doctor will remove the damaged bone and cartilage, then place new plastic or metal surfaces to restore the function of the knee�and its surrounding structures.
� Following any type of surgery for knee�arthritis will involve a period of recovery. Recovery time and rehabilitation will depend on the type of surgery performed. It’s essential to talk with your healthcare professional to determine the best treatment option for your�knee arthritis. The scope of our information is limited to chiropractic and spinal health issues. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at�915-850-0900�.
� Curated by Dr. Alex Jimenez �
Additional Topic Discussion: Relieving Knee Pain without Surgery
� Knee pain is a well-known symptom which can occur due to a variety of knee injuries and/or conditions, including�sports injuries. The knee is one of the most complex joints in the human body as it is made-up of the intersection of four bones, four ligaments, various tendons, two menisci, and cartilage. According to the American Academy of Family Physicians, the most common causes of knee pain include patellar subluxation, patellar tendinitis or jumper’s knee, and Osgood-Schlatter disease. Although knee pain is most likely to occur in people over 60 years old, knee pain can also occur in children and adolescents. Knee pain can be treated at home following the RICE methods, however, severe knee injuries may require immediate medical attention, including chiropractic care.
The knee is one of the most complex joints in the human body, consisting of the thigh bone, or femur, the shin bone, or tibia, and the kneecap, or patella, among other soft tissues. Tendons connect the bones to the muscles while ligaments connect the bones of the knee joint. Two wedge-shaped pieces of cartilage, known as the meniscus, provide stability to the knee joint. The purpose of the article below is to demonstrate as well as discuss the anatomy of the knee joint and its surrounding soft tissues.
Context: Information regarding the structure, composition, and function of the knee menisci has been scattered across multiple sources and fields. This review contains a concise, detailed description of the knee menisci�including anatomy, etymology, phylogeny, ultrastructure and biochemistry, vascular anatomy and neuroanatomy, biomechanical function, maturation and aging, and imaging modalities.
Evidence Acquisition: A literature search was performed by a review of PubMed and OVID articles published from 1858 to 2011.
Results: This study highlights the structural, compositional, and functional characteristics of the menisci, which may be relevant to clinical presentations, diagnosis, and surgical repairs.
Conclusions: An understanding of the normal anatomy and biomechanics of the menisci is a necessary prerequisite to understanding the pathogenesis of disorders involving the knee.
Keywords:knee, meniscus, anatomy, function
Once described as a functionless embryonic remnant,162 the menisci are now known to be vital for the normal function and long-term health of the knee joint.� The menisci increase stability for femorotibial articulation, distribute axial load, absorb shock, and provide lubrication and nutrition to the knee joint.4,91,152,153
Injuries to the menisci are recognized as a cause of significant musculoskeletal morbidity. The unique and complex structure of menisci makes treatment and repair challenging for the patient, surgeon, and physical therapist. Furthermore, long-term damage may lead to degenerative joint changes such as osteophyte formation, articular cartilage degeneration, joint space narrowing, and symptomatic osteoarthritis.36,45,92 Preservation of the menisci depends on maintaining their distinctive composition and organization.
Anatomy of Menisci
The word meniscus comes from the Greek word m?niskos, meaning �crescent,� diminutive of m?n?, meaning �moon.�
Meniscal Phylogeny and Comparative Anatomy
Hominids exhibit similar anatomic and functional characteristics, including a bicondylar distal femur, intra-articular cruciate ligaments, menisci, and asymmetrical collateral.40,66 These similar morphologic characteristics reflect a shared genetic lineage that can be traced back more than 300 million years.40,66,119
In the primate lineage leading to humans, hominids evolved to bipedal stance approximately 3 to 4 million years ago, and by 1.3 million years ago, the modern patellofemoral joint was established (with a longer lateral patellar facet and matching lateral femoral trochlea).164 Tardieu investigated the transition from occasional bipedalism to permanent bipedalism and observed that primates contain a medial and lateral fibrocartilaginous meniscus, with the medial meniscus being morphologically similar in all primates (crescent shaped with 2 tibial insertions).163 By contrast, the lateral meniscus was observed to be more variable in shape. Unique in Homo sapiens is the presence of 2 tibial insertions�1 anterior and 1 posterior�indicating a habitual practice of full extension movements of the knee joint during the stance and swing phases of bipedal walking.20,134,142,163,168
Embryology and Development
The characteristic shape of the lateral and medial menisci is attained between the 8th and 10th week of gestation.53,60 They arise from a condensation of the intermediate layer of mesenchymal tissue to form attachments to the surrounding joint capsule.31,87,110 The developing menisci are highly cellular and vascular, with the blood supply entering from the periphery and extending through the entire width of the menisci.31 As the fetus continues to develop, there is a gradual decrease in the cellularity of the menisci with a concomitant increase in the collagen content in a circumferential arrangement.30,31 Joint motion and the postnatal stress of weightbearing are important factors in determining the orientation of collagen fibers. By adulthood, only the peripheral 10% to 30% have a blood supply.12,31
Despite these histologic changes, the proportion of tibial plateau covered by the corresponding meniscus is relatively constant throughout fetal development, with the medial and lateral menisci covering approximately 60% and 80% of the surface areas, respectively.31
Gross examination of the knee menisci reveals a smooth, lubricated tissue (Figure 1). They are crescent-shaped wedges of fibrocartilage located on the medial and lateral aspects of the knee joint (Figure 2A). The peripheral, vascular border (also known as the red zone) of each meniscus is thick, convex, and attached to the joint capsule. The innermost border (also known as the white zone) tapers to a thin free edge. The superior surfaces of menisci are concave, enabling effective articulation with their respective convex femoral condyles. The inferior surfaces are flat to accommodate the tibial plateau (Figure 1).28,175
Medial meniscus. The semicircular medial meniscus measures approximately 35 mm in diameter (anterior to posterior) and is significantly broader posteriorly than it is anteriorly.175 The anterior horn is attached to the tibia plateau near the intercondylar fossa anterior to the anterior cruciate ligament (ACL). There is significant variability in the attachment location of the anterior horn of the medial meniscus. The posterior horn is attached to the posterior intercondylar fossa of the tibia between the lateral meniscus and the posterior cruciate ligament (PCL; Figures 1 and and2B).2B). Johnson et al reexamined the tibial insertion sites of the menisci and their topographic relationships to surrounding anatomic landmarks of the knee.82 They found that the anterior and posterior horn insertion sites of the medial meniscus were larger than those of the lateral meniscus. The area of the anterior horn insertion site of the medial meniscus was the largest overall, measuring 61.4 mm2, whereas the posterior horn of the lateral meniscus was the smallest, at 28.5 mm2.82
The tibial portion of the capsular attachment is the coronary ligament. At its midpoint, the medial meniscus is more firmly attached to the femur through a condensation in the joint capsule known as the deep medial collateral ligament.175 The transverse, or �intermeniscal,� ligament is a fibrous band of tissue that connects the anterior horn of the medial meniscus to the anterior horn of the lateral meniscus (Figures 1 and and2A2A).
Lateral meniscus. The lateral meniscus is almost circular, with an approximately uniform width from anterior to posterior (Figures 1 and and2A).2A). It occupies a larger portion (~80%) of the articular surface than the medial meniscus (~60%) and is more mobile.10,31,165 Both horns of the lateral meniscus are attached to the tibia. The insertion of the anterior horn of the lateral meniscus lies anterior to the intercondylar eminence and adjacent to the broad attachment site of the ACL (Figure 2B).9,83 The posterior horn of the lateral meniscus inserts posterior to the lateral tibial spine and just anterior to the insertion of the posterior horn of the medial meniscus (Figure 2B).83 The lateral meniscus is loosely attached to the capsular ligament; however, these fibers do not attach to the lateral collateral ligament. The posterior horn of the lateral meniscus attaches to the inner aspect of the medial femoral condyle via the anterior and posterior meniscofemoral ligaments of Humphrey and Wrisberg, respectively, which originate near the origin of the PCL (Figures 1 and and22).75
Meniscofemoral ligaments. The literature reports significant inconsistencies in the presence and size of meniscofemoral ligaments of the lateral meniscus. There may be none, 1, 2, or 4.? When present, these accessory ligaments transverse from the posterior horn of the lateral meniscus to the lateral aspect of the medial femoral condyle. They insert immediately adjacent to the femoral attachment of the PCL (Figures 1 and and22).
In a series of studies, Harner et al measured the cross-sectional area of the ligaments and found that the meniscofemoral ligament averaged 20% of the size of the PCL (range, 7%-35%).69,70 However, the size of the insertional area alone without knowledge of the insertional angle or collagen density does not indicate their relative strength.115 The function of these ligaments remains unknown; they may pull the posterior horn of the lateral meniscus in an anterior direction to increase the congruity of the meniscotibial fossa and the lateral femoral condyle.75
Ultrastructure and Biochemistry
The meniscus is a dense extracellular matrix (ECM) composed primarily of water (72%) and collagen (22%), interposed with cells.9,55,56,77 Proteoglycans, noncollagenous proteins, and glycoproteins account for the remaining dry weight.� Meniscal cells synthesize and maintain the ECM, which determines the material properties of the tissue.
The cells of the menisci are referred to as fibrochondrocytes because they appear to be a mixture of fibroblasts and chondrocytes.111,177 The cells in the more superficial layer of the menisci are fusiform or spindle shaped (more fibroblastic), whereas the cells located deeper in the meniscus are ovoid or polygonal (more chondrocytic).55,56,178 Cell morphology does not differ between the peripheral and central locations in the menisci.56
Both cell types contain abundant endoplasmic reticulum and Golgi complex. Mitochondria are only occasionally visualized, suggesting that the major pathway for energy production of fibrochondrocytes in their avascular milieu is probably anaerobic glycolysis.112
In normal, healthy menisci, tissue fluid represents 65% to 70% of the total weight. Most of the water is retained within the tissue in the solvent domains of proteoglycans. The water content of meniscal tissue is higher in the posterior areas than in the central or anterior areas; tissue samples from surface and deeper layers had similar contents.135
Large hydraulic pressures are required to overcome the drag of frictional resistance of forcing fluid flow through meniscal tissue. Thus, interactions between water and the matrix macromolecular framework significantly influence the viscoelastic properties of the tissue.
Collagens are primarily responsible for the tensile strength of menisci; they contribute up to 75% of the dry weight of the ECM.77 The ECM is composed primarily of type I collagen (90% dry weight) with variable amounts of types II, III, V, and VI.43,44,80,112,181 The predominance of type I collagen distinguishes the fibrocartilage of menisci from articular (hyaline) cartilage. The collagens are heavily cross-linked by hydroxylpyridinium aldehydes.44
The collagen fiber arrangement is ideal for transferring a vertical compressive load into circumferential �hoop� stresses (Figure 3).57 Type I collagen fibers are oriented circumferentially in the deeper layers of the meniscus, parallel to the peripheral border. These fibers blend the ligamentous connections of the meniscal horns to the tibial articular surface (Figure 3).10,27,49,156 In the most superficial region of the menisci, the type I fibers are oriented in a more radial direction. Radially oriented �tie� fibers are also present in the deep zone and are interspersed or woven between the circumferential fibers to provide structural integrity (Figure 3).# There is lipid debris and calcified bodies in the ECM of human menisci.54 The calcified bodies contain long, slender crystals of phosphorous, calcium, and magnesium on electron-probe roentgenographic analysis.54 The function of these crystals in not completely understood, but it is believed that they may play a role in acute joint inflammation and destructive arthropathies.
Noncollagenous matrix proteins, such as fibronectin, contribute 8% to 13% of the organic dry weight. Fibronectin is involved in many cellular processes, including tissue repair, embryogenesis, blood clotting, and cell migration/adhesion. Elastin forms less than 0.6% of the meniscus dry weight; its ultrastructural localization is not clear. It likely interacts directly with collagen to provide resiliency to the tissue.**
Located within a fine meshwork of collagen fibrils, proteoglycans are large, negatively charged hydrophilic molecules, contributing 1% to 2% of dry weight.58 They are formed by a core protein with 1 or more covalently attached glycosaminoglycan chains (Figure 4).122 The size of these molecules is further increased by specific interaction with hyaluronic acid.67,72 The amount of proteoglycans in the meniscus is one-eighth that of articular cartilage,2,3 and there may be considerable variation depending on the site of the sample and the age of the patient.49
By virtue of their specialized structure, high fixed-charge density, and charge-charge repulsion forces, proteoglycans in the ECM are responsible for hydration and provide the tissue with a high capacity to resist compressive loads.� The glycosaminoglycan profile of the normal adult human meniscus consists of chondroitin-6-sulfate (40%), chondroitin-4-sulfate (10% to 20%), dermatan sulfate (20% to 30%), and keratin sulfate (15%; Figure 4).65,77,99,159 The highest glycosaminoglycan concentrations are found in the meniscal horns and the inner half of the menisci in the primary weightbearing areas.58,77
Aggrecan is the major proteoglycan found in the human menisci and is largely responsible for their viscoelastic compressive properties (Figure 5). Smaller proteoglycans, such as decorin, biglycan, and fibromodulin, are found in smaller amounts.124,151 Hexosamine contributes 1% to the dry weight of ECM.57,74 The precise functions of each of these small proteoglycans on the meniscus have yet to be fully elucidated.
Meniscal cartilage contains a range of matrix glycoproteins, the identities and functions of which have yet to be determined. Electrophoresis and subsequent staining of the polyacrylamide gels reveals bands with molecular weights varying from a few kilodaltons to more than 200 kDa.112 These matrix molecules include the link proteins that stabilize proteoglycan�hyaluronic acid aggregates and a 116-kDa protein of unknown function.46 This protein resides in the matrix in the form of disulfide-bonded complex of high molecular weight.46 Immunolocalization studies suggest that it is predominantly located around the collagen bundles in the interterritorial matrix.47
The adhesive glycoproteins constitute a subgroup of the matrix glycoproteins. These macromolecules are partly responsible for binding with other matrix molecules and/or cells. Such intermolecular adhesion molecules are therefore important components in the supramolecular organization of the extracellular molecules of the meniscus.150 Three molecules have been identified within the meniscus: type VI collagen, fibronectin, and thrombospondin.112,118,181
The meniscus is a relatively avascular structure with a limited peripheral blood supply. The medial, lateral, and middle geniculate arteries (which branch off the popliteal artery) provide the major vascularization to the inferior and superior aspects of each meniscus (Figure 5).9,12,33-35,148 The middle geniculate artery is a small posterior branch that perforates the oblique popliteal ligament at the posteromedial corner of the tibiofemoral joint. A premeniscal capillary network arising from the branches of these arteries originates within the synovial and capsular tissues of the knee along the periphery of the menisci. The peripheral 10% to 30% of the medial meniscus border and 10% to 25% of the lateral meniscus are relatively well vascularized, which has important implications for meniscus healing (Figure 6).12,33,68 Endoligamentous vessels from the anterior and posterior horns travel a short distance into the substance of the menisci and form terminal loops, providing a direct route for nourishment.33 The remaining portion of each meniscus (65% to 75%) receives nourishment from synovial fluid via diffusion or mechanical pumping (ie, joint motion).116,120
Bird and Sweet examined the menisci of animals and humans using scanning electron and light microscopy.23,24 They observed canal-like structures opening deep into the surface of the menisci. These canals may play a role in the transport of fluid within the meniscus and may carry nutrients from the synovial fluid and blood vessels to the avascular sections of the meniscus.23,24 However, further study is needed to elucidate the exact mechanism by which mechanical motion supplies nutrition to the avascular portion of the menisci.
The knee joint is innervated by the posterior articular branch of the posterior tibial nerve and the terminal branches of the obturator and femoral nerves. The lateral portion of the capsule is innervated by the recurrent peroneal branch of the common peroneal nerve. These nerve fibers penetrate the capsule and follow the vascular supply to the peripheral portion of the menisci and the anterior and posterior horns, where most of the nerve fibers are concentrated.52,90 The outer third of the body of the meniscus is more densely innervated than the middle third.183,184 During extremes of flexion and extension of the knee, the meniscal horns are stressed, and the afferent input is likely greatest at these extreme positions.183,184
The mechanoreceptors within the menisci function as transducers, converting the physical stimulus of tension and compression into a specific electrical nerve impulse. Studies of human menisci have identified 3 morphologically distinct mechanoreceptors: Ruffini endings, Pacinian corpuscles, and Golgi tendon organs.�� Type I (Ruffini) mechanoreceptors are low threshold and slowly adapting to the changes in joint deformation and pressure. Type II (Pacinian) mechanoreceptors are low threshold and fast adapting to tension changes.�� Type III (Golgi) are high-threshold mechanoreceptors, which signal when the knee joint approaches the terminal range of motion and are associated with neuromuscular inhibition. These neural elements were found in greater concentration in the meniscal horns, particularly the posterior horn.
The asymmetrical components of the knee act in concert as a type of biological transmission that accepts, transfers, and dissipates loads along the femur, tibia, patella, and femur.41 Ligaments act as an adaptive linkage, with the menisci representing mobile bearings. Several studies have reported that various intra-articular components of the knee are sensate, capable of generating neurosensory signals that reach spinal, cerebellar, and higher central nervous system levels.?? It is believed that these neurosensory signals result in conscious perception and are important for normal knee joint function and maintenance of tissue homeostasis.42
The meniscus is cartilage which provides structural and functional integrity to the knee. The menisci are two pads of fibrocartilaginous tissue which spread out friction in the knee joint when it undergoes tension and torsion between the shin bone, or tibia, and the thigh bone, or femur. The understanding of the anatomy and biomechanics of the knee joint is essential towards the understanding of knee injuries and/or conditions. Dr. Alex Jimenez D.C., C.C.S.T. Insight
The biomechanical function of the meniscus is a reflection of the gross and ultrastructural anatomy and of its relationship to the surrounding intra-articular and extra-articular structures. The menisci serve many important biomechanical functions. They contribute to load transmission,�� shock absorption,10,49,94,96,170 stability,51,100,101,109,155 nutrition,23,24,84,141 joint lubrication,102-104,141 and proprioception.5,15,81,88,115,147 They also serve to decrease contact stresses and increase contact area and congruity of the knee.91,172
In a study on ligamentous function, Brantigan and Voshell reported the medial meniscus to move an average 2 mm, while the lateral meniscus was markedly more mobile with approximately 10 mm of anterior-posterior displacement during flexion.25 Similarly, DePalma reported that the medial meniscus undergoes 3 mm of anterior-posterior displacement, while the lateral meniscus moves 9 mm during flexion.37 In a study using 5 cadaveric knees, Thompson et al reported the mean medial excursion to be 5.1 mm (average of anterior and posterior horns) and the mean lateral excursion, 11.2 mm, along the tibial articular surface (Figure 7).165 The findings from these studies confirm a significant difference in segmental motion between the medial and lateral menisci. The anterior and posterior horn lateral meniscus ratio is smaller and indicates that the meniscus moves more as a single unit.165 Alternatively, the medial meniscus (as a whole) moves less than the lateral meniscus, displaying a greater anterior to posterior horn differential excursion. Thompson et al found that the area of least meniscal motion is the posterior medial corner, where the meniscus is constrained by its attachment to the tibial plateau by the meniscotibial portion of the posterior oblique ligament, which has been reported to be more prone to injury.143,165 A reduction in the motion of the posterior horn of the medial meniscus is a potential mechanism for meniscal tears, with a resultant �trapping� of the fibrocartilage between the femoral condyle and the tibial plateau during full flexion. The greater differential between anterior and posterior horn excursion may place the medial meniscus at a greater risk of injury.165
The differential of anterior horn to posterior horn motion allows the menisci to assume a decreasing radius with flexion, which correlates to the decreased radius of curvature of the posterior femoral condyles.165 This change of radius allows the meniscus to maintain contact with the articulating surface of both the femur and the tibia throughout flexion.
The function of the menisci has been clinically inferred by the degenerative changes that accompany its removal. Fairbank described the increased incidence and predictable degenerative changes of the articular surfaces in completely meniscectomized knees.45 Since this early work, numerous studies have confirmed these findings and have further established the important role of the meniscus as a protective, load-bearing structure.
Weightbearing produces axial forces across the knee, which compress the menisci, resulting in �hoop� (circumferential) stresses.170 Hoop stresses are generated as axial forces and converted to tensile stresses along the circumferential collagen fibers of the meniscus (Figure 8). Firm attachments by the anterior and posterior insertional ligaments prevent the meniscus from extruding peripherally during load bearing.94 Studies by Seedhom and Hargreaves reported that 70% of the load in the lateral compartment and 50% of the load in the medial compartment is transmitted through the menisci.153 The menisci transmit 50% of compressive load through the posterior horns in extension, with 85% transmission at 90� flexion.172 Radin et al demonstrated that these loads are well distributed when the menisci are intact.137 However, removal of the medial meniscus results in a 50% to 70% reduction in femoral condyle contact area and a 100% increase in contact stress.4,50,91 Total lateral meniscectomy results in a 40% to 50% decrease in contact area and increases contact stress in the lateral component to 200% to 300% of normal.18,50,76,91 This significantly increases the load per unit area and may contribute to accelerated articular cartilage damage and degeneration.45,85
The menisci play a vital role in attenuating the intermittent shock waves generated by impulse loading of the knee with normal gait.94,96,153 Voloshin and Wosk showed that the normal knee has a shock-absorbing capacity about 20% higher than knees that have undergone meniscectomy.170 As the inability of a joint system to absorb shock has been implicated in the development of osteoarthritis, the meniscus would appear to play an important role in maintaining the health of the knee joint.138
The geometric structure of the menisci provides an important role in maintaining joint congruity and stability.## The superior surface of each meniscus is concave, enabling effective articulation between the convex femoral condyles and flat tibial plateau. When the meniscus is intact, axial loading of the knee has a multidirectional stabilizing function, limiting excess motion in all directions.9
Markolf and colleagues have addressed the effect of meniscectomy on anterior-posterior and rotational knee laxity. Medial meniscectomy in the ACL-intact knee has little effect on anterior-posterior motion, but in the ACL-deficient knee, it results in an increase in anterior-posterior tibial translation of up to 58% at 90o of flexion.109 Shoemaker and Markolf demonstrated that the posterior horn of the medial meniscus is the most important structure resisting an anterior tibial force in the ACL-deficient knee.155 Allen et al showed that the resultant force in the medial meniscus of the ACL-deficient knee increased by 52% in full extension and by 197% at 60� of flexion under a 134-N anterior tibial load.7 The large changes in kinematics due to medial meniscectomy in the ACL-deficient knee confirm the important role of the medial meniscus in knee stability. Recently, Musahl et al reported that the lateral meniscus plays a role in anterior tibial translation during the pivot-shift maneuver.123
Joint Nutrition and Lubrication
The menisci may also play a role in the nutrition and lubrication of the knee joint. The mechanics of this lubrication remains unknown; the menisci may compress synovial fluid into the articular cartilage, which reduces frictional forces during weightbearing.13
There is a system of microcanals within the meniscus located close to the blood vessels, which communicates with the synovial cavity; these may provide fluid transport for nutrition and joint lubrication.23,24
The perception of joint motion and position (proprioception) is mediated by mechanoreceptors that transduce mechanical deformation into electric neural signals. Mechanoreceptors have been identified in the anterior and posterior horns of the menisci.*** Quick-adapting mechanoreceptors, such as Pacinian corpuscles, are thought to mediate the sensation of joint motion, and slow-adapting receptors, such as Ruffini endings and Golgi tendon organs, are believed to mediate the sensation of joint position.140 The identification of these neural elements (located mostly in the middle and outer third of the meniscus) indicates that the menisci are capable of detecting proprioceptive information in the knee joint, thus playing an important afferent role in the sensory feedback mechanism of the knee.61,88,90,158,169
Maturation and Aging of The Meniscus
The microanatomy of the meniscus is complex and certainly demonstrates senescent changes. With advancing age, the meniscus becomes stiffer, loses elasticity, and becomes yellow.78,95 Microscopically, there is a gradual loss of cellular elements with empty spaces and an increase in fibrous tissue in comparison with elastic tissue.74 These cystic areas can initiate a tear, and with a torsional force by the femoral condyle, the superficial layers of the meniscus may shear off from the deep layer at the interface of the cystic degenerative change, producing a horizontal cleavage tear. Shear between these layers may cause pain. The torn meniscus may directly injure the overlying articular cartilage.74,95
Ghosh and Taylor found that collagen concentration increased from birth to 30 years and remained constant until 80 years of age, after which a decline occurred.58 The noncollagenous matrix proteins showed the most profound changes, decreasing from 21.9% � 1.0% (dry weight) in neonates to 8.1% � 0.8% between the ages of 30 to 70 years.80 After 70 years of age, the noncollagenous matrix protein levels increased to 11.6% � 1.3%. Peters and Smillie observed an increase in hexosamine and uronic acid with age.131
McNicol and Roughley studied the variation of meniscal proteoglycans in aging113; small differences in extractability and hydrodynamic size were observed. The proportions of keratin sulfate relative to chondroitin-6-sulfate increased with aging.146
Petersen and Tillmann immunohistochemically investigated human menisci (ranging from 22 weeks of gestation to 80 years), observing the differentiation of blood vessels and lymphatics in 20 human cadavers. At the time of birth, nearly the entire meniscus was vascularized. In the second year of life, an avascular area developed in the inner circumference. In the second decade, blood vessels were present in the peripheral third. After 50 years of age, only the peripheral quarter of the meniscal base was vascularized. The dense connective tissue of the insertion was vascularized but not the fibrocartilage of the insertion. Blood vessels were accompanied by lymphatics in all areas.���
Arnoczky suggested that body weight and knee joint motion may eliminate blood vessels in the inner and middle aspects of the menisci.9 Nutrition of meniscal tissue occurs via perfusion from blood vessels and via diffusion from synovial fluid. A requirement for nutrition via diffusion is the intermittent loading and release on the articular surfaces, stressed by body weight and muscle forces.130 The mechanism is comparable with the nutrition of articular cartilage.22
Magnetic Resonance Imaging of The Meniscus
Magnetic resonance imaging (MRI) is a noninvasive diagnostic tool used in the evaluation, diagnosis, and monitoring of the menisci. MRI is widely accepted as the optimal imaging modality because of superior soft tissue contrast.
On cross-sectional MRI, the normal meniscus appears as a uniform low-signal (dark) triangular structure (Figure 9). A meniscal tear is identified by the presence of an increased intrameniscal signal that extends to the surface of this structure.
Several studies have evaluated the clinical utility of MRI for meniscal tears. In general, MRI is highly sensitive and specific for tears of the meniscus. The sensitivity of MRI in detecting meniscal tears ranges from 70% to 98%, and the specificity, from 74% to 98%.48,62,105,107,117 The MRI of 1014 patients before an arthroscopic examination had an accuracy of 89% for pathology of the medial meniscus and 88% for the lateral meniscus.48 A meta-analysis of 2000 patients with an MRI and arthroscopic examination found 88% sensitivity and 94% accuracy for meniscal tears.105,107
There have been discrepancies between MRI diagnoses and the pathology identified during arthroscopic examination.��� Justice and Quinn reported discrepancies in the diagnosis of 66 of the 561 patients (12%).86 In a study of 92 patients, discrepancies between the MRI and arthroscopic diagnoses were noted in 22 of the 349 (6%) cases.106 Miller conducted a single-blind prospective study comparing clinical examinations and MRI in 57 knee examinations.117 He found no significant difference in sensitivity between the clinical examination and MRI (80.7% and 73.7%, respectively). Shepard et al assessed the accuracy of MRI in detecting clinically significant lesions of the anterior horn of the meniscus in 947 consecutive knee MRI154 and found a 74% false-positive rate. Increased signal intensity in the anterior horn does not necessarily indicate a clinically significant lesion.154
The menisci of the knee joint are crescent-shaped wedges of fibrocartilage that provide increased stability to the femorotibial articulation, distribute axial load, absorb shock, and provide lubrication to the knee joint. Injuries to the menisci are recognized as a cause of significant musculoskeletal morbidity. Preservation of the menisci is highly dependent on maintaining its distinctive composition and organization.
In conclusion, the knee is the largest and most complex�joint in the human body. However, because the knee can commonly become damaged as a result of an injury and/or condition, it’s essential to understand the anatomy of the knee joint in order for patients to receive proper treatment.� The scope of our information is limited to chiropractic and spinal health issues. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at�915-850-0900�.
Curated by Dr. Alex Jimenez
Additional Topic Discussion: Relieving Knee Pain without Surgery
Knee pain is a well-known symptom which can occur due to a variety of knee injuries and/or conditions, including�sports injuries. The knee is one of the most complex joints in the human body as it is made-up of the intersection of four bones, four ligaments, various tendons, two menisci, and cartilage. According to the American Academy of Family Physicians, the most common causes of knee pain include patellar subluxation, patellar tendinitis or jumper’s knee, and Osgood-Schlatter disease. Although knee pain is most likely to occur in people over 60 years old, knee pain can also occur in children and adolescents. Knee pain can be treated at home following the RICE methods, however, severe knee injuries may require immediate medical attention, including chiropractic care.
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Reveal infrasyndesmotic Fx of fibular malleolus (Weber A)
Conservative care in the form of short-leg walking cast/boot can be used. Good recovery. If no evidence of osteochondral injury, relatively low chances of post-traumatic OA
No further imaging required. MRI may help to reveal bone contusion and osteochondral injury
Weber B at Level of Syndesmosis
Can be stable or unstable. On occasions, the decision is made during operative exploration.
CT scanning may help with further evaluation
Management: depends on stability. Additional stabilization required if syndesmosis is ruptured
AP, medial oblique and lateral views reveal Weber C – suprasyndesmotic injury with abnormal joint widening d/t disruption of the tib-fib syndesmosis. Very unstable injury.
Occasionally, when Weber C Fx positioned 6-cm from the tip of the lateral malleolus, it may be termed as Pott’s ankle Fx (name after Percival Pott’s who has proposed the original classification of ankle fractures based on their stability and degree of rotation). The term is somewhat outdated.
Management: operative with additional stabilization of the syndesmosis
Often spiral fracture of the proximal fibula combined with an unstable ankle injury
No immediate ankle fracture is noted radiographically, thus can be missed on ankle views and require tibia and fibula views
Rad features: widening of the ankle d/t syndesmosis tear and sometimes deltoid ligament disruption. Interosseous membrane is torn with proximal fibular Fx caused by pronation with external-rotation force
Bimalleolar & Trimalleolar Fx
Above top images Bimalleolar Fx v. unstable, the result of pronation and abduction/external rotation. Rx: ORIF.
Trimalleolar Fx: 3-parts ankle Fx. Medial and lateral malleolus and avulsion of the posterior aspect of tibial plafond. More unstable. Rx: operative
Pediatric Fx affecting older child when the medial side of the physis is closed or about to close with lateral side till open. Avulsion by the anterior tibi-fibular ligament. Complications: 2nd dry/premature OA. Rx: can be conservative if stable by boot cast immobilization.
Pediatric Growth Plate Injuries
Salter-Harris classification helps to diagnose and prognosticate physeal injuries.
Helpful mnemonic: SALTR
S: type 1-slip through the growth plate
A: type 2-above, Fx extends into the metaphysis
L: type 3-lower, intra-articular Fx extends through the epiphysis
T: type4, “through” Fx extends through all: physis, metaphysis, and epiphysis.
R: type 5, “ruined.” Crush injury to physis leading to complete death of the growth plate
Type 1 and 5: present with no fracture
Type 2: has the best prognosis and considered the most common.
Management: referral to a pediatric orthopedic surgeon
Complications: early physis closure, limb shortening, premature OA and others.
Most frequent tarsal Fx. 17% open Fx
Mechanisms: axial loading (intra-articular Fx into sub-talar and calcaneal-cuboid joints in 75% cases). Avulsion by Achilles tendon (m/c in osteoporotic bone). Stress (fatigue) Fx.
Intra-articular Fx carries a poor prognosis. Typically comminuted. Rx: operative.
B/I calcaneal intra-articular fx with associated vertebra compression Fx with associated vertebral compression Fx (T10-L2) often termed Casanova aka Don Juan (Lover’s) fx.
Imaging: x-radiography with added “heel view” 1st step. CT scanning is best for Dx and pre-op planning.
M/C fractured tarsal bone is the Talus. M/C region: talar neck (30-50%). Mechanism: Axial loading in dorsiflexion. Complications: Ischemic osteonecrosis (AVN) of the talus. Premature (2nd OA). Imaging: 1st step: radiographs, CT can be helpful with further delineation
Hawkins classification helps with Dx, prognosis & treatment. “Hawkins sign’ on plain film/CT scan may help with AVN Dx. (above blue arrows indicate good prognosis d/t radiolucent line indicating no AVN because the bone is vascularized and hence resorbed)
Rx: Type 1: conservative with short leg cast or boot (risk of AVN-0-15%), Type 2-4-ORIF (risk of AVN 50%-100%)
Septic arthritis – d/t bacterial or fungal contamination of the joint. SA may cause rapid joint destruction and requires prompt Dx and antibiotic administration
Joints affected: large joints with rich blood supply (knee 50%>hips>shoulders).
Routs of Infection:
1) Hematogenous is m/c
2) Spread from an adjacent site
3) Direct implantation (e.g., trauma, iatrogenically)
Patients at risk: children, diabetics, immunocompromised, pre-existing joint damage/inflammation, e.g., RA, etc.
I.V. drug users are particularly at risk and also may contaminate atypical joints “the S joints” SIJ, SCJ, Symphysis pubis, ACJ, etc.
Clinically: may vary and depends on host immune response and bacterial virulence. May present with rapid onset or exacerbation of pre-existing joint pain, swelling, limitation of ROM. General signs of malaise, fever, fatigue and elevated ESR, CRP, Leucocytosis may be present.
N.B. Diabetics and immunocompromised may present with fewer manifestations and lack of fever d/t declining immune response
Dx: clinical, radiological and laboratory. Arthrocentesis may be necessary for culture, cell count and purulent synovial examination
Management: I.V. antibiotics
Imaging Dx: begins with radiography but in the early stage most likely will be unremarkable. MRI can be sensitive and help with early identification of joint effusion, bone edema, etc. US may be helpful in the superficial joints and children. US helps with needle guidance. Bone scintigraphy may be used occaisonally if MRI is contraindicated
Routes of Joint Contamination
1. Hematogenous (M/C)
2. Spread from the adjacent site
3. Direct inoculation
M/C organism-Staph aureus
N.B Gonococcal infection may be a top differential in some cases
IV drug users: Pseudomonas, candida
Sickle cell: Salmonella
Animal (cats/dogs) bites: Pasteurella
Occasionally fungal contamination may occur
Initially non-specific ST/joint effusion, obscuration/distortion of fat planes. Because it takes 30% of compact and 50-75% trabecular bone to be destroyed before seen on x-rays, radiography is insensitive to some of the early changes. MR imaging is the preferred modality
If MRI is not available or contraindicated. Bone scintigraphy with Tc-99 MDT can help
In children, US preferred to avoid ionizing radiation. In children, US can be more sensitive than in adults due to lack of bone maturation
Early findings are unrewarding. Early features may include joint widening d/t effusion. Soft tissue swelling and obscuration/displacement of fat planes
1-2 weeks: periarticular and adjacent osseous changes are manifesting as patchy demineralization, moth-eaten, permeating bone destruction, loss, and indistinctness of the epiphyseal “white cortical line” with an increase in soft tissue swelling. MRI may be helpful with early Dx.
Late features: complete joint destruction and ankyloses
N.B. Septic arthritis may progress rapidly within days and requires early I.V. antibiotic to prevent major joint destruction
T1 & T2 Knee MRI
T1 (above left) and T2 fat-sat sagittal knee MRI slices reveal loss of normal marrow signal on T1 and increase on T2 due to septic edema. Bone sequestrum d/t osteomyelitis progressing into septic arthritis is noted. Marked joint effusion with adjacent soft tissue edema is seen. Dx: OSM and septic arthritis
Imaging may help the Dx of the septic joint. However, the final Dx is based on Hx, physical examination, blood tests and most importantly synovial aspiration (arthrocentesis)
Synovial fluid should be sent for Gram staining, culture, glucose testing, leukocyte count, and differential determination
ESR/CRP may be elevated
Synovial fluid: WBC can be 50,000-60,000/ul, with 80% neutrophils with depleted glucose levels Gram stain: in 75% gram-positive cocci. Gram staining is less sensitive in gonococcal infection with only 25% of cultures +
In 9% of cases, blood cultures are the only source of pathogen identification and should be obtained before antibiotic treatment
Gout: MSU deposition in and around joints and soft tissues. Elevated levels of serum uric acid (UA) (>7mg/dL) caused by overproduction or under-excretion of uric acid
Once UA reached/exceeded 7mg/dL, it will deposit in the peripheral tissues. Primary gout: disturbed metabolism of nucleic acids and purines break down. Secondary gout: increased cell turnover: Psoriasis, leukemia, multiple myeloma, hemolysis, chemotherapy, etc.
Gout presents with 5-characteristic stages:
1)asymptomatic hyperuricemia (years/decades)
acute attacks of gouty arthritis (waxes and wanes and lasts for several years)
Interval phase between attacks
Chronic tophaceous gout
Depends� on stages
Acute attacks: acute joint pain “first and the worst” even painful to light touch
DDx: septic joint (both may co-exist) bursitis etc.
Gouty arthritis typically presents as monoarthropathy
Chronic tophaceous stage: deposits in joints, ear pinna, ocular structures, and other regions. Nephrolithiasis etc. Men>women. Obesity, diet, and age >50-60.
Radiography: early attacks are unremarkable and may present as non-specific joint effusion
Chronic tophaceous gout radiography: punched out peri-articular, para-articular and intraosseous erosions with overhanging edges. A characteristic rim of sclerosis and internal calcification, soft tissue tophi. Target sites: lower extremity m/c
Rx: allopurinol, colchicine (esp. preventing acute episodes and maintenance)
Synovial aspiration with polarized microscopy reveal negatively birefringent needle-shaped MSU crystals with large inflammatory PMN presence. DDx: positively birefringent rhomboid-shaped CPPD crystals (above bottom right) seen in Pseudogout and CPPD
Density and joint effusion punched out osseous erosion with overhanging margins, overall preservation of bone density, internal calcifications Dx: chronic tophaceous gout
MRI Gout Features
Erosions with overhanging margins, a low signal on T1 and high on T2 and fat-suppressed images. Peripheral contrast enhancement of tophaceous deposits d/t granulation tissue
Dx: final Dx; synovial aspiration and polarized microscopy
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