Accidents and Injuries

• This is a brief review of some of the essential pediatric complaints encountered in clinical practice.
• Acute Trauma including acute head trauma
• Non-accidental Trauma in children (battered child)
• Musculoskeletal Complaints (Juvenile Idiopathic Arthritis, scoliosis,
• Common pediatric neoplasms (CNS & others)
• Infection
• Metabolic disease

Acute Pediatric trauma:

• FOOSH injuries (e.g. fell off the monkey-bar)
• Supracondylar Fx, elbow. Always d/t accidental trauma. <10-y.o.
• Extra-articular Fx
• 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 neurosurgeon

• 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.
• Reporting child abuse in Illinois:
• https://www2.illinois.gov/dcfs/safekids/reporting/pages/index.aspx

MSK Imaging Approach in Pediatrics

• 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.
• Complications may occur joint destruction, growth retardation/limb shortening, blindness, systemic complications, disability.

Most Common Pediatric Malignant Bone Neoplasms 

• 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.

References

•  www.radiopaedia.org
• https://reference.medscape.com

Head Trauma: Skull Fractures

• 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 TENSIONTHROUGH THE OCCIPUT AND TEMPORAL BONES THROUGH SPHENOID AND OTHER BASE OF SKULL BONES. CLINICALLY: RACCOON EYES, BATTEL SIGN, CSFRHINO/OTORRHEA.

Facial Fractures

• 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.
• CLINICALLY: PALPABLE CALVARIAL ENLARGEMENT, PAIN, NEUROLOGICAL SIGNS/SEIZURES. RX: NEUROSURGICAL CONSULT IS REQUIRED
• 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.
• ADULTS: M/C BENIGN NEOPLASM: MENINGIOMA. M/C PRIMARY: GLIOBLASTOMA MULTIFORME (GBM)METSESPECIALLY FROM LUNG, MELANOMA, AND BREAST.OTHERS: CNS LYMPHOMA
• 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

Inflammatory CNS Pathology 

CNS Infections

• BACTERIAL
• MYCOBACTERIAL
• FUNGAL
• VIRAL
• PARASITIC

Core Anatomy

• 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

• Radiographic examination (Chest X-ray CXR); excellent 1st step. Low cost, low radiation exposure, multiple clinical complaints evaluation
• CT scanning: chest CT, High-Resolution CT (HRCT)
• Chest pathology approach:
• Trauma
• Infection
• Neoplasms
• Pulmonary edema
• Pulmonary emphysema
• Atelectasis
• Pleural pathology
• Mediastinum

PA & Lateral CXR

• Additional views may be used:
• Lordotic view: helps to evaluate apical regions
• 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 indicated 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 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

Chest Trauma

• 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.
• Traumatic pneumothorax: lung laceration, blunt trauma, iatrogenic (chest tubes, etc.) acupuncture, etc.
• 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

Infection

• 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

Pulmonary TB 

• 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. Mainly if it contains irregular borders, feeding vessels, thick wall, in 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 totally 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 occur in diffuse disease involving the mediastinum. Additionally, air may track into the mediastinum in pneumomediastinum. Knowledge of mediastinal anatomy helps the Dx.
• Anterior mediastinal masses: thyroid, thymus, teratoma/germ cell tumors, lymphoma, lymphadenopathy, ascending aortic aneurysms
• Middle mediastinal masses: lymphadenopathy, vascular, bronchial lesions, etc.
• Posterior mediastinal masses: neurogenic tumours, aortic aneurysms, esophageal masses, spinal masses, aortic chain adenopathy

• 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.