Burst fracture

A burst fracture is a type of compression fracture which results in distruption of the posterior vertebral body cortex with retropulsion into the spinal canal. When in the thoraco lumbar level it tends to occur between T9 and L5 levels ³.  Burst fractures may be stable or unstable.

Pathology

Mechanism

It is a result of a compressive high energy injury (axial loading), much like the Jefferson fracture.  Typically it occurs following a fall, landing on the feet, from a significant height.

The intervertebral disc is driven into the vertebral body below.

All patients require a CT to assess the injury and evaluate the extent of retropulsed fragments which may enter the spinal canal.

Radiographic features

General features include

• 'burst' vertebral body on axial CT.
• loss of posterior vertebral height on lateral views.
• retropulsed fragments in the spinal canal.
• interpedicular widening

Cardiogenic and Non-cardiogenic
Pulmonary Edema

General Considerations Increase in the fluid in the lung Generally, divided into cardiogenic and non-cardiogenic categories. Congestive heart failure is the leading diagnosis in hospitalized patients older than 65 Pathophysiology Fluid first accumulates in and around the capillaries in the interlobular septa (typically at a wedge pressure of about 15 mm Hg) Further accumulation occurs in the interstitial tissues of the lungs Finally, with increasing fluid, the alveoli fill with edema fluid (typically wedge pressure is 25 mm Hg or more) Causes Cardiogenic pulmonary edema. Heart failure Coronary artery disease with left ventricular failure. Cardiac arrhythmias Fluid overload -- for example, kidney failure. Cardiomyopathy Obstructing valvular lesions -- for example, mitral stenosis  Myocarditis and infectious endocarditis Non-cardiogenic pulmonary edema -- due to changes in capillary permeability Smoke inhalation. Head trauma Overwhelming sepsis. Hypovolemia shock Re-expansion  By drainage of a large pleural effusion with thoracentesis Of the lung collapsed by a large pneumothorax High altitude pulmonary edema Disseminated intravascular coagulopathy (DIC) Near-drowning Overwhelming aspiration  Heroin overdose Adult (acute) respiratory distress (deficiency) syndrome (ARDS)  Clinical syndrome consisting of Pulmonary edema associated with severe respiratory distress Cyanosis refractory to oxygen administration Decreased lung compliance Lower pulmonary capillary wedge pressure (PCW < 18mm Hg) than cardiogenic pulmonary edema Most patients who survive have normal-appearing lungs Some patients develop pulmonary fibrosis Clinical Findings Shortness of breath Hemoptysis Orthopnea Dyspnea on exertion Cough, wheezing Anxiety and restlessness Cyanosis Imaging Findings Radiographic findings can lag behind physiologic changes The key findings of cardiogenic pulmonary edema Kerley B lines (septal lines) Seen at the lung bases, usually no more than 1 mm thick and 1 cm long, perpendicular to the pleural surface Pleural effusions Usually bilateral, frequently the right side being larger than the left If unilateral, more often on the right Fluid in the fissures Thickening of the major or minor fissure Peribronchial cuffing Visualization of small doughnut-shaped rings representing fluid in thickened bronchial walls Collectively, the above four findings comprise pulmonary interstitial edema The heart may or may not be enlarged When the fluid  enters the alveoli themselves, the airspace disease is typically diffuse, and there are no air bronchograms Non-cardiogenic pulmonary edema Bilateral, peripheral air space disease with air bronchograms or central bat-wing pattern Kerley B lines and pleural effusions are uncommon Typically occurs 48 hours or more after the initial insult Stabilizes at around five days and may take weeks to completely clear On CT Gravity-dependent consolidation or ground glass opacification Air bronchograms are common Differential Diagnosis Diffuse pneumonia Massive aspiration  Pulmonary hemorrhage  Treatment Cardiogenic pulmonary edema and non-cardiogenic pulmonary edema, with the exception of ARDS, can resolve within hours to several days Cardiogenic pulmonary edema is usually treated with a combination of Oxygen Diuretics Lasix, etc. Nitrates Nitroglycerin, etc. Natriuretic peptides Nesiritide, etc. Morphine Inotropic agents Dopamine, dobutamine, digoxin, etc. Angiotensin converting enzyme (ACE) inhibitors Beta-blockers Carvedilol, etc. For non-cardiogenic pulmonary edema, the predisposing condition should be treated Treatment is supportive Ventilator management. Antibiotic therapy, when necessary Corticosteroids