CNS Infection: Meningitis, Encephalitis, Abscess and Others A CNS infection is an infection which involves the central nervous

system in some way. Meningitis is one of the most common and well known types, involving the meninges, the coverings of the brain and spinal cord. Other types of infections involve the brain or spinal cord directly. For example, a cerebral abscess is a bacterial brain infection and encephalitis is typically a viral infection of the brain. In general, an infection is a disease caused by the invasion of a disease-causing micro-organism or virus. The growth of the bacteria, virus or other invading organism in the human tissues causes damage and inflammation by a variety of mechanisms. Meningitis: Meningitis is one of the most common forms of infection affecting the nervous system. It is characterized by infection of the membranes covering the brain and spinal cord, centered in the cerebrospinal fluid that surrounds the nervous system.

Types of Meningitis o Spinal Meningitis o Bacterial Meningitis o Viral Meningitis o Fungal Meningitis Meningitis Symptoms Meningitis Treatment

Bacterial Meningitis

What Is It? Bacterial meningitis is a common form of meningitis, infection of the coverings of the brain and spinal cord, caused by various forms of bacteria. The bacteria grow primarily in the subarachnoid space in the cerebrospinal fluid, causing inflammation of the surrounding structures. Bacterial meningitis is one of the most severe forms of meningitis and is life-threatening if not treated promptly. It is a true medical emergency.

In adults, the most common causative organisms responsible for this disease include Neisseria meningitides and Streptococcus pneumoniaalthough several other bacteria can be implicated, including Haemophilus influenza, tuberculosis, gram negatives, Listeria monocytogenes and others.

Another common cause of meningitis are viruses. To learn more about viral causes, see the Viral Meningitis page.

What Types of Symptoms Are Typical? Meningitis symptoms generally include headache, high fever, stiff and/or painful neck, photophobia (avoidance of bright lights), nausea and vomiting and deteriorating level of consciousness.

How Is The Diagnosis Typically Made? If a patient presents with the signs and symptoms of meningitis they generally undergo an lumbar puncture (spinal tap) to obtain cerebrospinal fluid for analysis. This can help make the diagnosis of bacterial infection as well as help to guide treatment by isolating the causative organism so that antibiotic therapy can be tailored to the specific case.

What Are Some Common Treatments? Antibiotics directed toward the causative bacteria is the mainstay of treatment along with general supportive measures. The patients are generally hospitalized and antibiotics are given intravenously. The exact type and duration of treatment can vary from patient to patient depending on the severity of disease and the type of causative organism.

Alcoholic hepatitis is hepatitis (inflammation of the liver) due to excessive intake of alcohol. While distinct from cirrhosis, it is regarded as the earliest stage of alcoholic liver disease. Symptoms are jaundice, ascites (fluid accumulation in the abdominal cavity), fatigue and hepatic encephalopathy (brain dysfunction due to liver failure). Mild cases are self-limiting, but severe cases have a high risk of death. Severe cases may be treated with glucocorticoids.

Contents [hide]

1 Symptoms and signs 2 Diagnosis 3 Pathophysiology 4 Treatment and management

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4.1 Corticosteroids 4.2 Pentoxifylline

5 See also 6 References [edit]Symptoms and signs Alcoholic hepatitis is characterized by a variable constellation of symptoms, which may include feeling unwell, enlargement of the liver, development of fluid in the abdomen (ascites), and modest elevation of liver enzyme levels (as determined by liver function tests). Alcoholic hepatitis can vary from mild with only liver enzyme elevation to severe liver inflammation with development of jaundice, prolonged prothrombin time, and even liver failure. Severe cases are characterized by either obtundation (dulled consciousness) or the combination of elevated bilirubin levels and prolonged prothrombin time; the mortality rate in both severe categories is 50% within 30 days of onset. Alcoholic hepatitis is distinct from cirrhosis caused by long-term alcohol consumption. Alcoholic hepatitis can occur in patients with chronic alcoholic liver disease and alcoholic cirrhosis. Alcoholic hepatitis by itself does not lead to cirrhosis, but cirrhosis is more common in patients with long term alcohol consumption. Some alcoholics develop acute hepatitis as an inflammatory reaction to the cells affected by fatty change. This is not directly related to the dose of alcohol. Some people seem more prone to this reaction than others. This is called alcoholic steatonecrosis and the inflammation probably predisposes to liver fibrosis. [edit]Diagnosis The ratio of aspartate aminotransferase to alanine aminotransferase is usually 2 or more.[1] In most cases, the liver enzymes do not exceed 500. [edit]Pathophysiology Some signs and pathological changes in liver histology include:

Mallory's hyaline - a condition where pre-keratin filaments accumulate in hepatocytes. This sign is not limited to alcoholic liver disease, but is often characteristic.[2]

Ballooning degeneration - hepatocytes in the setting of alcoholic change often swell up with excess fat, water and protein; normally these proteins are exported into the bloodstream. Accompanied with ballooning, there is necrotic damage. The swelling is capable of blocking nearby biliary ducts, leading to diffuse cholestasis.[2]

Inflammation - neutrophilic invasion is triggered by the necrotic changes and presence of cellular debris within the lobules. Ordinarily the amount of debris is removed byKupffer cells, although in the setting of inflammation they become overloaded, allowing other white cells to spill into the parenchyma. These cells to hepatocytes with Mallory bodies.[2]

If chronic liver disease is also present:

Fibrosis

Cirrhosis - a progressive and permanent type of fibrotic degeneration of liver tissue. [edit]

Charles Gomersall and Sarah Ramsay Spectrum of conditions which includes:

Unstable angina Non-ST segment elevation MI (non-STEMI) ST elevation MI (STEMI)

The syndrome is characterized by a clinical syndrome of acute ischaemic chest pain with either rest pain or a crescendo pattern of pain on minimal exertion, associated with ECG changes of ischaemia (ST elevation or depression or T inversion). STEMI is then distinguished from other forms of acute coronary syndrome (ACS) by the presence of persistent ST elevation. Patients with often present in a similar manner. The distinction between non-STEMI and unstable angina is based on the presence or absence of a rise in cardiac enzymes or troponin. Pathophysiology

in majority of cases syndrome occurs when an atherosclerotic plaque ruptures, fissures or ulcerates and precipitates thrombus formation. This results in sudden total or near-total arterial occlusion. Alternativelythrombus may break off from a ruptured plaque and occlude a downstream vessel. systemic factors and inflammation also contribute to alterations in haemostatic and coagulation pathways and may play a part in the initiation of the intermittent thrombosis that is a characteristic of unstable angina. Inflammatory acute phase proteins, cytokines, chronic infections and catecholamine surges may enhance production of tissue factor, procoagulant activity or platelet hyperaggregability. in the case of Q wave infarct results in a spreading area of necrosis that reaches epicardium in 4-6 h full thickness infarct in rare cases may be due to coronary artery occlusion by emboli, congenital abnormalities, coronary spasm and a wide variety of systemic (particularly inflammatory) diseases initially infarcted muscle is softened leading to an increase in ventricular compliance but, as fibrosis takes place, compliance decreases poor correlation between angiographic severity of coronary stenosis and chance of acute occlusion Other causes of reduced myocardial blood flow include mechanical obstruction (e.g. air embolus), dynamic obstruction (e.g. vessel spasm), and inflammation or infection.

Diagnosis

Figure 1. Investigation and treatment algorithm. If initial troponin is measured <6 h from onset of pain test should be repeated 4 h later. STEMI Management NSTEMI & unstable angina Risk stratification Based on risk of ischaemic complications and risk of failure of medical therapy. Patients can be classified as being high, intermediate or low risk on the basis of a number of clinical features and the results of simple investigations (see table 1). The most important risk factors are:

Acute ST depression on the presenting ECG Elevated cardiac troponin Advanced age Pain at rest Haemodynamic instability

Treatment

aspirin 160-325 mg of non-enteric coated aspirin to chew and swallow as soon as the diagnostic impression of ACS formed (patients presenting within 24 h). Thereafter daily oral dose indefinitely clopidogrel low molecular weight heparin

o enoxaparin is preferred agent glycoprotein IIb/IIIa inhibitor o give IV to high risk patients o oral form contraindicated - associated with increased mortality angiography revascularization for high risk patients low and intermediate risk patients can be treated conservatively or invasively

Site of action of anti-platelet and anti-thrombotic agents Adjunctive treatment ACE inhibition

indicated in first 24 h for all patients who have had an episode of LV failure associated with MI, regardless of whether it persists or not or for patients with LV dysfunction or failure within 3-16 days after MI early initiation of treatment is important because much of the survival benefit is realised in the first 48 h

-blockade

IV blockade followed by oral early after infarction decreases mortality following STEMI (ISIS 1). (However patients not given thrombolysis). Give cardioselective blocker eg atenolol or metoprolol o as soon as possible and preferably within 2 hours of ACS o reactive airways disease and left ventricular dysfunction are not absolute contra-indications

Nitrates

no benefit demonstrated from routine use after STEMI safe and effective for the treatment of ischaemic chest pain during and after MI indicated for high risk non-STEMI and unstable angina patients GTN should NOT be used within 24 hours of use of sildenafil (Viagra)

Calcium antagonists

Statins

short acting dihydropyridines, particularly nifedipine, contraindicated no survival benefit from administration of longer acting agents or other calcium antagonists (eg diltiazem or verapamil)

reduced incidence of recurrent ischaemic events with early treatment after NSTEMI no data related to STEMI

Differential diagnosis

aortic dissection gastro-oesophageal disease including oesophageal rupture musculoskeletal disease mediastinitis

Early complications

arrhythmias cardiogenic shock

acute ventricular septal defect acute mitral regurgitation acute pulmonary oedema ventricular free wall rupture

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Prognosis

mortality approx 8% of patients who survive to reach hospital

RV infarction

has clinical significance out of proportion to amount of muscle damage relatively poor prognosis ? consider acute angioplasty volume load patient despite high RV filling pressures in order to increase cardiac output

Further reading

An osteoma (plural: "osteomata") is a new piece of bone usually growing on another piece of bone, typically the skull. It is abenign tumor. When the bone tumor grows on other bone it is known as "homoplastic osteoma"; when it grows on other tissue it is called "heteroplastic osteoma". Osteoma represents the most common benign neoplasm of the nose and paranasal sinuses. The cause of osteomata is uncertain, but commonly accepted theories propose embryologic, traumatic, or infectious causes. Osteomata are also found in Gardner's syndrome. Larger craniofacial osteomata may cause facial pain, headache, and infection due to obstructed nasofrontal ducts. Often, craniofacial osteoma presents itself through ocular signs and symptoms (such as proptosis).[1] Contents [hide]

1 Variants 2 See also 3 References 4 External links

inner table of skull the inner compact layer of the bones covering the brain. The brain is surrounded by cerebrospinal fluid (CSF), enclosed in meningeal covering, and protected inside the skull. Furthermore, the fascia and muscles of the scalp provide additional cushioning to the brain. Test results have shown that 10 times more force is required to fracture a cadaveric skull with overlaying scalp than the one without. [1] Although these layers play a

protective role, meningeal attachments to the interior of the skull may limit the movement of the brain, transmitting shearing forces on the brain. A transverse temporal bone fracture is shown in the image below.

Transverse temporal bone fracture (courtesy of Adam Flanders, MD, Thomas Jefferson University, Philadelphia, Pennsylvania) CSF plays a major role in coup and countercoup injuries to the brain. A blow to a stationary but moveable head causes acceleration, and the brain floating in CSF lags behind, sustaining an injury directly underneath the point of impact (coup injury). When a moving head hits the floor, sudden deceleration results in an injury to the brain on the opposite side (countercoup injury). Anatomy of fracture The causative forces and fracture pattern, type, extent, and position are important in assessing the sustained injury. The skull is thickened at the glabella, external occipital protuberance, mastoid processes, and external angular process and is joined by 3 arches on either side. The skull vault is composed of cancellous bone (diplo) sandwiched between 2 tablets, the lamina externa (1.5 mm), and the lamina interna (0.5 mm). The diplo does not form where the skull is covered with muscles, leaving the vault thin and prone to fracture. The skull is prone to fracture at certain anatomic sites that include the thin squamous temporal and parietal bones over the temples and the sphenoid sinus, the foramen magnum, the petrous temporal ridge, and the inner parts of the sphenoid wings at the skull base. The middle cranial fossa is the weakest, with thin bones and multiple foramina. Other places prone to fracture include the cribriform plate and the roof of orbits in the anterior cranial fossa and the areas between the mastoid and dural sinuses in the posterior cranial fossa. Skull fracture is described in Edwin Smith's papyrus, the oldest known surgical paper. [2] The papyrus describes a conservative and expectant approach to skull trauma, with better results compared with a more aggressive and less favorable approach described in Hippocratic medicine.[3] An extensive discussion of skull fractures and their management is available in the eleventh century manuscript, "Al-Qanun FilTibb" by Ibn-Sina (Avicenna). This book was a predecessor to the modern medicine literature. [4] The 15th century management of pediatric skull fractures is illustrated by a Turkish physician of the Ottoman Empire, Serefeddin Sabuncuolu (1385-1468) in his textbook "Cerrahiyyetu'l Haniyye" (Imperial Surgery). [5] Charles Bell first described occipital condylar fracture in 1817 based on an autopsy finding. [6] The same fracture was described for the first time as a radiograph finding in 1962 and by computed tomography (CT) in 1983.[7, 8] Fractures of the skull can be classified as linear or depressed. Linear fractures are either vault fractures or skull base fractures. Vault fractures and depressed fractures can be either closed or open (clean or dirty/contaminated). Skull fractures are classified in the image below.

Classification of skull fractures

Linear skull fracture Linear fracture results from low-energy blunt trauma over a wide surface area of the skull. It runs through the entire thickness of the bone and, by itself, is of little significance except when it runs through a vascular channel, venous sinus groove, or a suture. In these situations, it may cause epidural hematoma, venous sinus thrombosis and occlusion, and sutural diastasis, respectively. Differences between sutures and fractures are summarized in Table 1. Table 1. Differences Between Skull Fractures and Sutures (Open Table in a new window) Fractures Sutures

Greater than 3 mm in width Widest at the center and narrow at the ends Runs through both the outer and the inner lamina of bone, hence appears darker Usually over temporoparietal area Usually runs in a straight line Angular turns Basilar skull fracture

Less than 2 mm in width Same width throughout Lighter on x-rays compared with fracture lines At specific anatomic sites Does not run in a straight line Curvaceous

In essence, a basilar fracture is a linear fracture at the base of the skull. It is usually associated with a dural tear and is found at specific points on the skull base. Temporal fracture Temporal bone fracture is encountered in 75% of all skull base fractures. The 3 subtypes of temporal fractures are longitudinal, transverse, and mixed.[9] A transverse temporal bone fracture and a longitudinal temporal bone fracture are shown below.

Transverse temporal bone fracture (courtesy of Adam Flanders, MD, Thomas Jefferson University,

Philadelphia, Pen nsylvania) Longitudinal temporal bone fracture (courtesy of Adam Flanders, MD, Thomas Jefferson University, Philadelphia, Pennsylvania) Longitudinal fracture occurs in the temporoparietal region and involves the squamous portion of the temporal bone, the superior wall of the external auditory canal, and the tegmen tympani. These fractures may run either anterior or posterior to the cochlea and labyrinthine capsule, ending in the middle cranial fossa near the foramen spinosum or in the mastoid air cells, respectively. Longitudinal fracture is the most common of the 3 subtypes (70-90%). Transverse fractures begin at the foramen magnum and extend through the cochlea and labyrinth, ending in the middle cranial fossa (5-30%).

Mixed fractures have elements of both longitudinal and transverse fractures. Yet another classification system of temporal bone fractures has been proposed. This system divides temporal bone fractures into petrous and nonpetrous fractures; the latter includes fractures that involve mastoid air cells. These fractures do not present with cranial nerve deficits.[10] Occipital condylar fracture Occipital condylar fracture results from a high-energy blunt trauma with axial compression, lateral bending, or rotational injury to the alar ligament. These fractures are subdivided into 3 types based on the morphology and mechanism of injury. [11] An alternative classification divides these fractures into displaced and stable, ie, with and without ligamentous injury. [12] Type I fracture is secondary to axial compression resulting in comminution of the occipital condyle. This is a stable injury. Type II fracture results from a direct blow, and, despite being a more extensive basioccipital fracture, type II fracture is classified as stable because of the preserved alar ligament and tectorial membrane. Type III fracture is an avulsion injury as a result of forced rotation and lateral bending. This is potentially an unstable fracture. Clivus fractures Fractures of the clivus are described as a result of high-energy impact sustained in motor vehicle accidents. Longitudinal, transverse, and oblique types have been described in the literature. A longitudinal fracture carries the worst prognosis, especially when it involves the vertebrobasilar system. Cranial nerves VI and VII deficits are usually coined with this fracture type. [13] Depressed skull fracture Depressed skull fractures, as shown in the image below, result from a high-energy direct blow to a small surface area of the skull with a blunt object such as a baseball bat. Comminution of fragments starts from the point of maximum impact and spreads centrifugally. Most of the depressed fractures are over the frontoparietal region because the bone is thin and the specific location is prone to an assailant's attack. A free piece of bone should be depressed greater than the adjacent inner table of the skull to be of clinical significance and requiring elevation.

Depressed skull fracture (courtesy of Adam Flanders, MD, Thomas Jefferson University, Philadelphia, Pennsylvania) A depressed fracture may be open or closed. Open fractures, by definition, have either a skin laceration over the fracture or the fracture runs through the paranasal sinuses and the middle ear structures, resulting in communication between the external environment and the cranial cavity. Open fractures may be clean or contaminated/dirty. Previous Next