CSF

CEREBROSPINAL FLUID

Wajdy J.Majid Assit.Prof. of clinical biochemistry College of Medicine University of Thi-Qar

In adults, the total volume of cerebrospinal fluid (CSF) is about 135 mL, produced at a rate of 500 mL/day. This is predominantly formed by plasma ultrafiltration through the capillary walls of the choroid plexuses in the brain’s lateral ventricles . CSF completely surrounding the brain and spinal cord; thus it supports and protects these structures against injury. Like lymph, CSF removes waste products of metabolism. Cerebrospinal fluid circulates very slowly, allowing contact with cells of the central nervous system (CNS). The uptake of glucose by these cells probably results in lower concentrations relative to plasma. Concentrations of analytes in the CSF should always be compared with those in plasma because alterations in the latter are reflected in the CSF even when CNS metabolism is normal. Flow is slowest, and therefore contact longest, in the lower lumbar region, where the subarachnoid space comes to an end; therefore, the composition of CSF from lumbar puncture is different from that of cisternal or ventricular puncture.

Examination of the cerebrospinal fluid Although biochemical investigation of the CSF is important, so is microbiological and cytological examination. Sample collection : Cerebrospinal fluid is usually collected by lumbar puncture. This procedure may be dangerous if the intracranial pressure is raised (potentially lethal brainstem herniation through the foramen magnum may occur), and the clinician should therefore check that there is no papilloedema before proceeding; sometimes brain imaging, for example computerized tomography (CT) scanning, may be indicated. Usually a total of about 5 mL of CSF should be collected as 1–2 mL aliquots into sterile containers and sent first for microbiological examinations; also specimen can then be used for biochemical analysis. If a CSF glucose concentration is indicated, 0.5 mL should be collected into a fluoride tube and promptly sent to the laboratory with a blood sample taken at the same time for random blood sugar.

Appearance Normal CSF is completely clear and colorless; slight turbidity is most easily detected by visual comparison with water . Spontaneous clotting Clotting occurs when there is excess fibrinogen in the specimen, usually associated with a very high protein concentration. This finding occurs with tuberculous meningitis or with tumors of the CNS. Colour A bright red colour may result from damage to a blood vessel during lumbar puncture (traumatic tap) or a recent hemorrhage into the subarachnoid space. Xanthochromia is defined as a yellow coloration of the CSF and results from altered haemoglobin , the color appearing several days after a subarachnoid hemorrhage and, depending on the extent of the bleeding, lasting for up to a week or more , or jaundice (which will be clinically obvious and may impart a yellow color to the CSF).

Infection : If there is an increased polymorphonuclear leucocyte count or a bacterial infection, the CSF glucose concentration may be very low because of increased metabolism of glucose. The CSF glucose concentration may be particularly low in pyogenic meningitis and tuberculous meningitis; but in viral meningitis, it is often normal. The estimation of CSF glucose does not reliably distinguish between different forms of infective meningitis because the result may be normal in any form. _Widespread malignant infiltration of the meninges : may also be associated with low CSF glucose concentrations.

Protein The CSF protein concentration in the lumbar spine is up to three times higher than that in the ventricles; the normal lumbar concentration is below 0.4 g/L . In newborn infants, because of the relatively high vascular permeability, the CSF protein concentration is about three times that of the adult. The CSF total protein concentration may be increased in the following situations : 1-In the presence of blood, due to haemoglobin and plasma proteins. 2-In the presence of pus, due to cell protein and to exudation from inflamed surfaces. 3- In non-purulent inflammation of cerebral tissue, when there may be a definite rise in total protein concentration despite the absence of detectable cells in the CSF. Cells may also be undetectable in some cases of bacterial meningitis, particularly in children, in immunocompromised patients, or if antibiotics have been given before lumbar puncture.

4- If there is blockage of the spinal canal Which, by impairing the flow of CSF distal to the block, allows longer for equilibrium with the circulation and so brings the composition of CSF slightly nearer to that of plasma (Froin’s syndrome). Increased pressure in the CSF may also increase protein. Such blockage may be caused by : – Spinal tumours,– Vertebral fractures,– Spinal tuberculosis.5- Where there is local synthesis of immunoglobulins By plasma cells within the CSF.

Other cerebrospinal fluid analytes C-reactive protein and lactate have also been used in certain circumstances to indicate bacterial infection. Procedure for examination of the cerebrospinal fluid Consider the following: Heavily blood stained (assuming a non-traumatic lumbar puncture) in three consecutive specimens: there has probably been a cerebral haemorrhage. Send for microbiological examination and for estimation for glucose and protein concentrations. Xanthochromic: in addition to the above tests, send the specimen for spectrophotometric examination.

Pleural Fluid -This is a plasma ultrafiltrate; there is usually less than 10 mL of this fluid in each pleural cavity. If the rate of removal is less than the rate of formation, pleural fluid will accumulate. -Decreased removal may be due to decreased pleural space pressure, for example bronchial obstruction, or impaired lymphatic drainage, for example neoplasm . Pleural fluid production is increased if there is decreased colloid osmotic pressure (for example hypoproteinaemia), increased capillary vessel permeability (for example infection) or hydrostatic pressure elevation (as in cardiac failure). Pleural effusion fluid can be divided into exudates and transudates .



Some causes of a pleural effusion :Exudates :Infective inflammatory, e.g. pneumonia or tuberculosis Non-infective inflammatory, e.g. pulmonary embolism, rheumatoid arthritis, Neoplasm, e.g. primary lung or secondaries Miscellaneous, e.g. trauma .Transudates :Congestive cardiac failure , Nephrotic syndrome , Cirrhosis and ascites , Hypothyroidism Pleural fluid is often ‘tapped’ with a needle (thoracentesis) and samples sent to the laboratory for analysis. A pleural fluid protein concentration of (greater than 3 g/dl) is suggestive of an exudate. Raised lactate dehydrogenase (LDH) activity in pleural fluid (more than 200 U/ L )is suggestive of exudates (malignancy, inflammatory process).

A pleural fluid is defined as an exudate if any one of the following three conditions is satisfied: - 1- pleural fluid LDH more than 0.6 the upper normal reference range for plasma, 2- pleural fluid to plasma protein ratio more than 0.5. 3- pleural fluid to plasma LDH ratio more than 0.6. Other biochemical tests (in addition to microbiological tests and cytology) on pleural fluid may include the following : Amylase activity may be raised in pleural effusions secondary to acute pancreatitis, although other causes include some malignant effusions and oesophageal rupture.

ASCITIC FLUID This is fluid in the peritoneal cavity. Sometimes fluid accumulation can be huge, occasionally exceeding 20 L, and may cause pressure symptoms such as abdominal distension and breathing difficulties. Ascitic fluid drainage (paracentesis) may be necessary to facilitate diagnosis and relieve symptoms . Like pleural fluid, ascites can be divided into exudates and transudates. Similar tests to those done for pleural fluid can be requested. However, it has been suggested that, rather than classifying into transudate or exudate, it may be more useful to classify the ascitic fluid upon the basis of the serum ascites albumin gradient (serum albumin concentration minus ascites albumin concentration). A high gradient of ( > 1.1 g/dl ) suggests portal hypertension, e.g. cirrhosis, constrictive pericarditis, kwashiorkor or cardiac failure, nephrotic syndrome . A gradient of ( < 1.1 g/dl ) is indicative of a non-portal hypertensive etiology, e.g. carcinoma, infection such as spontaneous bacterial peritonitis or pancreatitis .