Most of us have heard the term spinal tap, or have seen it on a tv medical drama show. It is known as a lumbar puncture, but what does this procedure involve and how is it utilized? What to know. This procedure is performed in the lower part of the back. It can be used for:
A spinal tap is performed by a doctor or nurse trained to do lumbar punctures. A specialized needle is inserted between the vertebrae to collect cerebrospinal fluid. Cerebrospinal fluid is a watery, colorless fluid that cushions the spinal cord and brain, protecting them from injury/damage. Questions may arise as to when an individual would need a spinal tap, how dangerous it is, and what to expect from this procedure? �
Spinal Tap Utilization
Spinal taps are often utilized in helping to diagnose infections of the central nervous system. One of the most common infections is meningitis. A sample of cerebrospinal fluid is taken, tested, and if infectious organisms are growing within, these are clue/s for determining and customizing a treatment plan and antibiotic therapy. The procedure also helps with:
Identifying central nervous system disorders, like multiple sclerosis, or epilepsy for example.
Diagnosing cancers that affect the brain or spinal cord
Administration of chemotherapy or anesthesia
Spinal taps are also used with imaging assistance.
For example, a contrast dye can be injected into the cerebrospinal fluid to get an anatomical view of the spinal cord and coverings. They are quite helpful when an individual cannot have an MRI done. �
Spinal cord coverings from a cross-section of a nerve
Spinal cord rear view
dorsal rootlets of the
the spinal nerve of
the posterior surface of the body of the vertebra
A spinal tap is done in a hospital or outpatient facility, depending on the reason for the tap. It is not an emergency procedure. Emergencies bring to mind situations and events that have to be done within seconds/minutes. A lumbar puncture does not entail that type of action.
Listen and follow the provider�s instructions regarding what to eat and drink.
An individual could be told to not eat or drink anything for a specific set of hours before.
Any prescription/s, over-the-counter meds, and drug allergies need to be disclosed to the medical team that will perform the procedure.
Individuals can wear their own clothes but preferably loose-fitting and comfortable should be the objective.
Once at the location a hospital gown is given to the patient for the procedure.
The day of the appointment, tell the doctor of any unusual symptoms.
Have a designated driver for the ride home, as sometimes a patient can feel weak and dizzy after the procedure.
A tap is a simple procedure that usually takes a half-hour or less to complete.
The patient sits bent forward or lying down on the side.
The knees should be pulled up as far as possible with the chin down into the chest curled into a ball.
This arcs the back and spaces out the vertebrae, so there is a wider area for the needle to enter.
The skin is cleaned with an antiseptic.
A sterile sheet or towel is placed over the patient that has an opening exposing the lower back.
Local anesthesia is injected to numb the area.
Unless the doctor instructs movement, remaining still is key as the advancement of the needle into the small area is a delicate procedure.
There is an initial what feels like a stinging sensation, but the patient does not feel the actual needle as it advances.
The needle gets inserted into the spinal space where the cerebrospinal fluid resides.
The cerebrospinal fluid pressure is measured.
Sometimes an ultrasound or specialized x-ray technique, known as fluoroscopy is used to locate the best place for the needle.
This is where the reason for the tap determines what action is taken. Either medicine is administered or a small amount of cerebrospinal fluid is taken.
The needle is retracted.
A bandage is applied.
Spinal tap pain is rare, but sometimes the needle can brush a nerve root when it is inserted. It could feel like an electric shock down the leg.
Once finished, the patient lies on their back for 30 to 60 minutes so the doctor can check for any abnormalities or affects. Being sent home depends on the reason for the tap. If there is unexplained fever, nausea, etc, a patient will not be sent home.
If it was an outpatient procedure the patient can leave and resume some simple activities after having a few hours of relaxation. Temporary pain meds are prescribed to address any discomfort. Results could come a day or a week later. They depend on the reason for the spinal tap.
Risks and Complications
It is considered a safe procedure with rare complications. The most common effect is a headache and usually comes on several hours, to a day or two later. These will not lead to any neurologic problems. Water or tea can help prevent and reduce the headache. Over-the-counter pain relievers can help too. However, if the headache continues after two days, call the doctor. A very small possibility of a more severe complication could happen including:
Brain herniation or movement of the brain tissue from the added pressure
Nerve or spinal cord damage
This is a very safe procedure with the medical team being highly trained and skilled professionals that are careful and gentle.
Auto Accident Doctors & Chiropractic Treatment
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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
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.
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.
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
Pathology: da disease of the articular cartilage. Continuing mechanical stimulation follows by an initial increase in water and cartilage thickness. Gradual loss of proteoglycans and ground substance. Fissuring/splitting. Chondrocytes are damaged and release enzymes into the joint. Cystic progression and further cartilage loss. Subchondral bone is denuded and exposed to mechanical stresses. It becomes hypervascular forming osteophytes. Subchondral cysts and bone thickening/sclerosis develop.
Imaging plays a crucial role in Dx/grading and management
Clinically: pain on walking/rest, crepitus, swelling d/t synovitis, locking/catching d/t osseocartilaginous fragments and gradual functional loss. Knee OA typically presents as mono and oligoarthritis. DDx: morning pain/stiffness is >30-min DDx from inflammatory arthritis
Treatment: in mild to moderate cases-conservative care. Severe OA-total knee arthroplasty
May present as asymptomatic chondrocalcinosis, CPPD arthropathy resembling DJD with pan predominance of large subchondral cysts. Often found as isolated PFJ DJD
Pseudogout with an acute attack of knee pain resembling gouty arthritis
Radiography is the 1st step and often reveals the Dx
Arthrocentesis with polarized microscopy may be helpful to DDx between CPPD and Gouty arthritis
RA: an autoimmune systemic inflammatory disease that targets soft tissues of joints synovium, tendons/ligaments, bursae and extra-articular sites (e.g., eyes, lungs, cardiovascular system)
RA is the m/c inflammatory arthritis, 3% of women and 1% of men. Age: 30-50 F>M 3:1, but may develop at any age. True RA is uncommon in children and should not be confused with Juvenile Idiopathic Arthritis
RA most often affects small joints of the hands and feet as symmetrical arthritis (2nd 3rd MCP, 3rd PIPs, wrists & MTPs, sparing DIPs of fingers and toes)
Radiographically: RA presents with joint effusion leading to hyperemia and marginal erosions and periarticular osteoporosis. In the knee, the lateral compartment is affected more frequently leading to valgus deformity. Uniform aka concentric/symmetrical JSN affects all compartments and remains a key Dx clue
An absence of subchondral sclerosis and osteophytes. Popliteal cyst�(Baker’s cyst) may represent synovial pannus and inflammatory synovitis extending into the popliteal region that may rapture and extend into posterior leg compartment
N.B. Following initial RA joint destruction, it is not unusual to note superimposed 2nd OA
Radiography is the 1st step but early joint involvement may be undetectable by x-rays and can be helped by US and/or MRI.
Final Dx is based on Hx, clinical exam, labs, and radiology
Clinical pearls: patients with RA may present with a single knee being affected
Most patients are likely to have bilateral symmetrical hands/feet RA.
Cervical spine, particularly C1-2 is affected in 75-90% of cases throughout the course of the disease
N.B. Sudden exacerbation of joint pain in RA should not underestimate septic arthritis because patients with pre-existing RA are at higher risk of infectious arthritis. Joint aspiration may help with Dx.
RA (above left) vs. OA (above right)
RA: concentric (uniform) joint space loss, lack of osteophytes and juxta-articular osteopenia.
Clinical Pearls: patients with RA may present radiographically with subchondral sclerosis d/t superimposed DJD. The latter feature should not be interpreted as OA but instead considered as secondary OA
AP Knee Radiograph
Note marked uniform JSN, juxta-articular osteopenia and subchondral cystic changes
Clinical Pearls: subcortical cysts in RA will characteristically lack sclerotic rim noted in OA-associated subcortical cysts.
MRI is very sensitive and may aid during early Dx of RA.
T2 fat-sat or STIR and T1 + C gad contrast fat-suppressed sequences may be included
MRI Dx of RA: synovial inflammation/effusion, synovial hyperplasia, and pannus formation decreased cartilage thickness, subchondral cysts, and bone erosions
MRI is very sensitive to reveal juxt-articular bone marrow edema, a precursor to erosions
Intra-articular fibrinoid fragments known as “Rice bodies” are characteristic MR sign of RA
Note: T2 fat-sat sagittal MRI revealing large inflammatory joint effusion and pannus synovial proliferation (above arrowheads). No evidence of radiographic or MRI bone erosions present. Dx: RA
STIR MR Slices
Note: STIR MR slices in the axial (above bottom image) and coronal planes (above top image) demonstrate extensive synovitis/effusion (above arrowheads) and multiple erosions in the medial and lateral tibial plateau (above arrows)
Additionally, scattered patchy areas of bone marrow edema are noted (above asterisks) such marrow edema changes are indicative and predictive of future osseous erosions.
Additional features: note thinning and destruction of joint cartilage
Bone neoplasms and tumor-like conditions affecting the knee can be benign or malignant. Age at Dx is crucial for DDx
In patients <40: Benign bone neoplasms: Osteochondroma, Enchondroma are relatively frequent
Fibrous cortical defect (FCD) & Non-ossifying fibroma (NOF) are particularly frequent in children
Giant cell tumor (GCT) is the m/c benign neoplasm of the knee in patients between 20-40 years of age
Malignant bone neoplasms in <40: m/c Osteosarcoma and 2nd m/c Ewing sarcoma
In patients >40: malignant neoplasms: m/c are secondaries d/t bone metastasis. Primary bone malignancy:�the m/c
Multiple Myeloma (MM). Less frequently:�a 2nd�peak of Osteosarcoma (post-radiation or Paget�s), Fibrosarcoma or Malignant�Fibrous�Histiocytoma�(MFH) of bone.
Clinically: knee pain, pathological fracture
Some tumor-like conditions like FCD/Non-ossifying fibroma are asymptomatic and may regress spontaneously. Occasionally NOF may present with pathologic fracture. N.B. any knee/bone pain in a child/adolescents should be�treated with clinical suspicion and adequately investigated.
Imaging: 1st step: radiography
MRI with T1+C is crucial for lesion characterization/regional extent, staging and pre-operative planning. CT may�help with pathologic Fxs detection. If malignant bone neoplasms considered, CXR/CT, PET-CT to investigate�metastatic spread and staging are important
Imaging Approach Bone Neoplasms
Approach to imaging Dx of bone neoplasms includes age, bone location (epiphysis vs. metaphysis vs. diaphysis), zone of transition surrounding the lesion, periosteal response, type of matrix, permeating or moth-eaten destruction vs. sclerotic, ground-glass, osteoid, cartilaginous matrix, soft tissue invasion, etc.
Key x-radiography features to DDx benign vs. malignant bone neoplasm:
Zone of transition: lesion is geographic with a narrow zone of transition vs. ill-defined wide zone of transition suggesting aggressive bone resorption
What type of bone destruction occurred: soap-bubbly appearance vs. osteolytic vs. osteosclerotic changes
Is there a round-glass matrix? Is there a well-defined rim of the sclerotic border with septations potentially suggesting slow growth and encapsulation like most benign processes.
Periosteal proliferation: solid vs. aggressive spiculated/sunburst/hair-on-end with local soft tissue invasion and Codman triangle (study next slide)
FCD & NOF
FCD & NOF or more appropriately Fibroxanthoma of the bone are benign bone processes that m/c seen in children. DDx based on the size with FCD presenting as <3-cm and NOF >3cm lesion composed of a fibrous heterogeneous matrix. FCD are asymptomatic and may regress in many cases. Some may progress to NOF. Location: identified in the knee region as an eccentric cortical based lesion.
FCD must be DDx from an avulsive irregularity d/t repeated stress along Linea aspera by extensors muscles
Management: leave-me-alone lesion. Occasionally NOF may progress and lead to pathologic fracture requiring orthopedic consult
Osteochondroma: m/c benign bone neoplasm. Knee is the m/c location. Contains all bone elements with a cartilaginous cap. Presented as pedunculated or sessile bone exostosis pointing away from the joint.
1% malignant degeneration to chondrosarcoma if solitary lesion and 10-15% in cases of HME
Other complications: fracture (top left image) pseudoaneurysm of the Popliteal artery, adventitious bursa formation
Hereditary Multiple Exostosis (HME)– autosomal dominant process. Presents with multiple osteochondromas (sessile-type dominates). May lead to limb deformities (Madelung deformity, coxa valga) reactive ST pressure, malignant degeneration
Dx: radiography, MRI helps to Dx malignant degeneration to chondrosarcoma by changes in size and activity of cartilaginous cap (>2-cm in adults may manifest malignant degeneration). MRI will also help with Dx of regional complications
HME & Knee Pain
37-y.o male with HME and knee pain. Axial T1, T2 and STIR MRI slices at the popliteal region. Large cartilaginous cap and possible compression of the popliteal artery by osteochondroma. MRA was performed to evaluate popliteal A. pseudoaneurysm (large arrow). Pathology specimen obtained from the cartilaginous cap showed increased cellularity suggestive of malignant degeneration. Operative care was planned
Giant Cell Tumor (GCT) aka Osteoclastoma
GCT- is a relatively common primary benign bone neoplasm. Age 25-40. M>F slightly.
GCT is the M/C benign sacral tumor. In 50% of cases, GCT occurs about the knee.
GCT is histologically benign, but lung Mets may develop esp. if in distal radius and hands, often termed Malignant GCT
<1% unresponsive/recurring GCTs may undergo malignant transformation to high-grade bone sarcoma
Pathology: histologically composed of osteoclasts-multinucleated giant cells with stromal cells derived from precursors monocyte-macrophage type. Produces cytokines and osteolytic enzymes. GCT may contain blood and associated with secondary Aneurysmal Bone Cyst (ABC)
Clinically: knee pain unresponsive to conservative care. Pathologic Fx may occur
Imaging: always begins with radiography followed by MRI and surgical biopsy that are crucial to Dx.
Rx: operative with curettage and cementing, a surgical appliance may be used if pathological fx present and cortical breach. In more severe cases other options available
Radiologic-pathologic Dx: osteolytic and soap-bubbly lesion typically involving metaphysis and into epiphysis (classic key feature) with subarticular extension. Zone of transition is generally narrow but occasionally in aggressive lesions wide zone of transition may be seen.
MRI: low T1, highT2/STIR, characteristic fluid-fluid levels noted that are present in GCT and ABC. Histology is crucial to Dx.
DDx: ABC, Brown cell tumor of HPT (osteoclastoma), Telangiectatic Osteosarcoma
Radiological rule: if the physeal growth plate is present Dx of GCT is taken off the list in favor of chondroblastoma and vice versa.
Primarily Soap-Bubbly Appearance of GCT
Coronal, Fat-Sat Sagittal & Axial MRI Slices of GCT
T1 coronal, T2 fat-sat sagittal and T2 axial MRI slices of GCT. Typically: low T1, highT2/STIR and fluid-fluid levels
Characteristic MRI Appearance of GCT
Fluid-fluid levels d/t different composition of blood degradation products
Important DDx: ABC
Malignant Neoplasms About the Knee
In children and very young adults, m/c primary malignant neoplasm is central aka intramedullary (osteogenic) osteosarcoma (OSA). Second peak of OS: >70 y.o d/t Paget�s (1%) and/or post radiation OSA.
The knee is the m/c location of OSA (distal femur, prox. Tibia)
A 2nd m/c malignant pediatric primary is Ewing sarcoma.
In adults >40 y.o. the m/c primary is Multiple Myeloma (MM) or Solitary Plasmacytoma
Overall m/c bone neoplasms in adults d/t bone Mets from lung, breast, prostate, renal cell, thyroid (discussed)
Dx: clinical and radiological with surgical biopsy
Imaging is crucial to Dx. 1st step x-radiography. MRI+ gad C is vital
CT scanning occasionally helps to evaluate pathological fracture
Central (Intramedullary) Osteosarcoma (OSA)
m/c age: 10-20. m/c location: knee, males>females. Increased risk in some
congenital syndromes and mutation of the retinoblastoma gene: Rothmund-Thompson AR syndrome.
Early Dx is important d/t 10-20% present with Lung Mets at Dx. Prognosis depends on stages. Early stages with local bone invasion and no
mets 76% of survival.
Rx: limb salvage procedures preferred with 8-12 weeks of chemo, amputation if encased neurovascular tissue, path Fx, etc.
Imaging: radiography and MRI.
Clinically: bone pain, Inc. Alkaline Phosphatase
Chest CT if lung Mets considered
Classic Rad Features of OSA
Osteoid forming a sclerotic mass with aggressive hair-on-end/speculated/sun-burst periosteal reaction, Codman’s triangle and soft tissue invasion. Order MRI for staging and extent. Chest CT is crucial for Lung Mets dx.
MRI is Crucial for Dx/Staging
Note sagittal T1 (left) and STIR (right) MR slices: large mass extending from distal femoral metaphysis to remaining shaft. A low signal on T1 and high on STIR d/t marrow invasion with edema, hemorrhaging and tumor invasion. Local ST invasion seen (white arrows). Periosteal lifting and Codman�s triangle (green arrow) are additional signs of aggressive neoplasm.
Note an interesting feature that the epiphysis is spared d/t physeal plate serving temporarily as an additional barrier to the tumor spread.
Ewing sarcoma: age: 2-20, uncommon in black patients. 2nd m/c highly malignant bone neoplasm in children that typically arises from medullary cavity (Round cell tumors). Key symptom: bone pain that may mimic infection (ESR/CRP/WBC) Considered PNET Key Rad Dx: aggressive moth-eaten/permeative lucent lesions in the shaft of long bones with sizeable soft tissue invasion/typical onion skin periostitis. May produce saucerisation May affect flat bones. May appear as sclerotic in 33%. Early lung Mets (25-30%) bone-to-bone Mets Poor prognosis if delayed Dx. Imaging steps: 1st step x-rad, MRI is v. important followed by a biopsy. CXR/CT PET-CT Rx: combined rad-chemo, operative.
Note aggressive expansile osteolytic lesion in the distal femur metaphysis into epiphysis. No periosteal reaction present. Following further work up with abdominal and chest CT scanning, Dx of Renal cell carcinoma was established
Distal Mets into lower extremity are more common with lung, renal cell, thyroid and breast CA.
Renal cell and Thyroid will typically present with aggressive osteolytic expansile mass aka �blowout Mets.�
In general, imaging approach should consist of Radiographic knee series, followed by MRI if x-rays are unrewarding
Tc99 Bone scintigraphy is the modality of choice to evaluate metastatic bone disease
Soft Tissue Neoplasms About the Knee
Malignant fibrous histiocytoma (MFH) reclassified as Pleomorphic Undifferentiated Sarcoma (PUS) is the m/c S.T. sarcoma. MFH is aggressive biologically with poor prognosis M>F (1.2:1) 30-80 with a peak in a 6th decade. 25-40% of all adults sarcomas m/c extremities. Retroperitoneum next (worst prognosis d/t late Dx and large growth w/o symptoms) Clinically: painful, hard mass typically about the knee or thigh. Histology: poorly differentiated/undifferentiated malignant fibroblasts, myofibroblasts, and other mesenchymal cells Imaging: MRI is the modality of choice with T1, T2, T1+C. Typically appears as an aggressive heterogeneous mass intermediate to low signal on T1 and high signal on T2 with areas of necrosis and enhancement on T1+C. May appear misleadingly encapsulated w/o true capsule Management: operative with radiation and chemotherapy. Tumor depth is crucial for prognosis. 80% 5-year survival if <5cm deep in ST and 50% if >5-cm deep in ST.
Synovial sarcoma: common malignant ST neoplasm esp. in younger patients or older children/adolescents. M/C found in knee area Clinically: can present slowly as a palpable mass in the extremity often ignored d/t slow growth Imaging is the key: radiography may reveal ST. density/mass. Some synovial sarcomas may show calcification and mistaken for Myositis Ossificanse or heterotopic bone formation MRI with T1, T2 and T1+C are Dx modality of choice. Other modalities: US, CT are non-specific DDx: MFH Management: operative, chemo-radiation Prognosis: variable depending on size, invasion, metastasis
Types, location, and stability of tears are v. important during MRI Dx
Vertical/longitudinal tears especially occur in acute ACL tears. Some longitudinal tears found at the periphery or “red zone” may heal
Bucket handle tear: longitudinal tear in the inner edge that is deep and vertical extending through the long axis and may displace into a notch
Oblique/flap/parrot-beak are complex tears
Radial tear at 90-degree to plateau
Axial T2 WI fat-sat and coronal STIR slices of the posterior horn of the medial meniscus.
Note a radial tear of the posterior horn of the medial meniscus near the meniscal root. This is potentially an unstable lesion requiring operative care
The meniscus, in this case, is unable to provide a “hoop-stress mechanism.”
MRI Slices Coronal & Sagittal
Fat-sat coronal and sagittal proton density MRI slices revealing horizontal (cleavage) tear that is more typical in the aged meniscus
In some cases, when this tear does not contain a radial component, it may partially heal obviating the need for operative care
T2 w GRE Sagittal MRI Slice
Complex tear with a horizontal oblique and radial component.
This type of tear is very unstable and in most cases may need operative care
Bucket Handle Tear
Bucket handle tear are m/c in the medial meniscus esp. with acute ACL and MCL tear
MRI signs; double PCL sign on sagittal slices
Absent “bow-tie” sign and others
Most cases require operative care
DDx From Meniscal Degeneration
Occasionally meniscal tears need to be DDx from meniscal degeneration which may also appear bright (high signal) on fluid-sensitive MRI
The simplest rule is that if there is a true meniscal tear aka Grade 3 lesion, it always reaches/extends to the tibial plateau surface
The Role of MSK Ultrasound (US) in Knee Examination
MSK US of the knee permits high resolution and dynamic imaging of primarily superficial anatomy (tendons, bursae, capsular ligaments)
MSK US cannot adequately evaluate cruciate ligaments and the menisci in their entirety
Thus MR imaging remains modality of choice
Potential Pathologies Successfully Evaluated by MSK US
Patellar tendionosis/patellar tendon rupture
Quadriceps tendon tear
Pes Anserine bursitis
Popliteal cyst (Baker cyst)
Inflammation/joint effusion with synovial thickening and hyperemia can be imaged with US (e.g., RA) especially with the addition of color power Doppler
Patient Presented With Atraumatic Knee Pain & Swelling
Radiography revealed sizeable soft tissue density within the superficial pre-patella region along with mild-to-moderate OA
MSK US demonstrated large septated heterogeneous fluid collection with mild positive Doppler activity on the periphery indicating inflammation d/t Dx of Superficial pre-patella bursitis
Long Axis US Images
Note normal lateral meniscus and fibers of LCL (above bottom image) compared to
Horizontal degenerative cleavage tear along with protrusion of lateral meniscus and LCL bulging (above top image)
Major limitation: unable to visualize the entire meniscus and the ACL/PCL
MRI referral is suggested
Rupture of Distal Tendon of Quadriceps
Note rupture of distal tendon of the Quadriceps muscle presented as fiber separation and fluid (hypo to anechoic) fluid collection within the substance of the tendon
Advantages of MSK US over MRI to evaluate superficial structures:
Disadvantages: limited depth of structures, inability to evaluated bone and cartilage, etc.
Osteochondral Knee Injuries (OI)
osteochondral knee injuries can occur in children 10-15 y.o presented as Osteochondritis Dissecance (OCD) and in mature skeleton m/c following hyperextension and rotation trauma, particularly in ACL tear.
OCD-typically develops from repeated forces in immature bone and affects m/c postero-lateral portion of the medial femoral condyle.
OI in mature bone occurs m/c during ACL tears mainly affecting so-called terminal sulcus of the lateral femoral condyle at the junction of the weight-bearing portion opposed to tibial plateau and the part articulating with the patella
Osteochondral injuries may potentially damage the articular cartilage causing secondary OA. Thus need to be evaluated surgically
Imaging plays an important role and should begin with radiography often followed by MR imaging and orthopedic referral.
95% associated with some trauma. Other etiology: ischemic bone necrosis especially in adults
Other common location for osteochondral injuries: elbow (capitellum), talus
1st step: radiography may detect osteochondral fragment potentially attached or detached
Location: a posterior-lateral aspect of the medial femoral condyle. Tunnel (intercondylar notch) view is crucial
MRI: modality of choice >90% specificity and sensitivity. Crucial for further management. T1-low signal demarcating line with T2 high signal demarcating line that signifies detachment and unlikely healing. Refer to orthopedic surgeon
Management: stable lesion esp. in younger children>off weight-bearing-heals in 50-75%
Unstable lesion and older child or impending physeal closure>operative fixation.
Result from valgus or varus stress with or w/o axial loading
Associated with periarticular soft tissues injury
High-stress injury m/c due to jumps falls and axial loading, often with the splitting of the tibial plateau. Men>women. Patients are in their 30s
Low impact or no trauma in patients with osteoporosis d/t insufficiency fractures
Impaction injury is more common with depression of tibial plateau. Women>men. Patients are in their 70s
Lateral Tibial Plateau Fractures More Common
Functional anatomy plays a significant role
60% of weight bearing is by the medial plateau
The medial plateau is more concave
Lateral plateau is slightly higher and more convex. Valgus stress impacts lateral plateau.
Tibial plateau fractures considered intra-articular and prone to delayed healing, non-union, meniscal injury (m/c lateral) ACL tear, secondary OA. Other complications: compartment syndrome, vascular injury.
Management: operative in many cases especially if >3-mm step-off at the plateau
If medial plateau or bicondylar Fxs present, ORIF will be required.
Imaging Plays A Crucial Role
Begins with x-radiography. X-radiography may not reveal the complexity and extent of this injury.
CT scanning w/o contrast will further delineate fracture complexity and pre-operative planning
MR imaging may be considered to evaluate for internal derangement: meniscal, ACL injuries.
Shatzke classification may help to evaluate the complexity of this injury
Key Diagnostic Sign
AP and lateral horizontal beam (cross table) left knee radiograph. Note subtle depression of the lateral plateau manifested by the lateral plateau appearing at the same level or lower as the medial. A critical diagnostic sign is the presence of fat-blood-interphase or FBI sign on cross-table lateral (above arrow) indicating intra-articular knee fracture
Lipohemarthorosis aka FBI Sign
Can be detected by radiography, CT or MR imaging
FBI sign is a reliable secondary radiographic sign of intra-articular knee fractures, regardless of how small they are
Mechanism: fracture results with acute hemarthrosis
Hemarthrosis will also occur w/o Fx. However, Fx will result with a fatty marrow being released into the joint cavity. Fat is a less dense medium (lighter) and will appear on the top of the hemorrhage if the patient is held in the supine position for 5-10-minutes before the cross-table radiograph is taken
FBI sign confirms the intra-articular Fx.
ACL/PCL, meniscal tears will not result in FBI sign
Lateral Tibial Plateau Fx
Lateral tibial plateau Fx that was managed operatively
Most common complication: premature secondary OA
More complex injuries may result in more extensive operative care
Knee Internal Derangement
Acute or chronic injuries of meniscal fibrocartilages and ligamentous restraints
Tears of the ACL and posterior horn of the medial meniscus are the most common
Acute ACL tears, however, often result with a lateral meniscus tear
Acute ACL tear may occur as a combined injury of the ACL, MCL, and medial meniscus
Functional anatomy: ACL prevents anterior displacement of the tibia and secondary varus stress
MCL functions together with ACL in resisting external rotation of the tibia especially when the foot is planted (closed chain position)
MCL is firmly attached to the medial meniscus, explaining the classic triad of ACL, MCL and medial meniscal tear (O’Donahue terrible triad)
Cruciate ligaments (ACL/PCL) are intra-articular but extra-synovial. Less likely to be torn in closed pack position (full extension). When all articular facets of tibia and femur are in full contact, the ACL/PCL are at least tension and stable
When the knee is flexed 20-30-degrees or more ACL is taut and remains unstable
ACL is a significant mechanoreceptor that feeds the info to CNS about the joint position. Thus the majority of previous ACL tears will lead to some degree of knee instability
Functional Anatomy of ACL
Diagnosis of ACL Tear
Diagnosis of ACL tear requires MR imaging
Concerns exist of not only ligamentous injuries but injuries to the articular cartilage and menisci.
Most vendors will perform at least: one T1 WI in coronal or sagittal planes. Sagittal and coronal Proton-density slices to evaluate cartilaginous structures. Fast spin-echo sagittal, axial and coronal T2 fat-saturated or sagittal and coronal STIR images are crucial to demonstrate edema within the substance of knee ligaments
ACL is aligned along the Blumensaat line or oblique line corresponding the intercondylar roof of Femoral condyles. Lack of such alignment by the ACL is significant for ACL tear
Imaging Dx of Internal Derangement
MRI shows 78-100% sensitivity and 78-100% specificity
Primary signs of ACL tear: non-visualization of ACL (above green arrow), loss of its axis along the Blumensaat line (above triangle heads), wavy appearance and substance tear (above white arrow) or edema and cloud-like indistinctness (above yellow arrow)
Reliable Secondary Signs of ACL Tear
May be observed on the radiographs and MRI
Segond avulsion fracture (80% specificity for ACL tear) (next slide)
Deep femoral notch sign indicating osteochondral fracture (above bottom images) and
Pivot -shift bone marrow edema in the posterolateral tibial condyle d/t external rotation and often valgus impact by the lateral femoral condyles (above top image)
Segond Fracture (Avulsion by ITB)
Segond fracture at Gerdy’s tubercle. A vital sign of the ACL tear seen on both radiographs and MRI
Management of ACL Tears
In acute cases, usually operative using cadaveric or autograft (patella ligament or hamstring) ACL reconstruction
Complications: graft tear, instability and premature DJD, joint stiffness d/t lack of postoperative rehab or gaft shortening. More rare, infection, a formation of intraosseous synovial cysts, etc.
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