Wallach's Interpretation of Diagnostic Tests: Pathways to Arriving at a Clinical Diagnosis (104 page)
Authors: Mary A. Williamson Mt(ascp) Phd,L. Michael Snyder Md
Laboratory findings vary depending on the type of brain injury (e.g., contusion, laceration, subdural hemorrhage, extradural hemorrhage, subarachnoid hemorrhage). There may also be laboratory findings due to complications of the brain injury (e.g., pneumonia, meningitis).
Basilar skull fracture
results in the disruption of the barriers between the sinonasal cavity and the anterior and middle cranial fossae and subsequent leak of CSF into the nasal cavity or ear (see eBook Figure 4-23). This communication with the CNS can lead to infectious complications, resulting in morbidity and mortality.
1
Laboratory Evaluation for CSF Rhinorrhea
Beta-2-transferrin
is produced by neuraminidase activity within the CNS; it is found in the CSF, perilymph, and aqueous humor. Immunofixation electrophoresis with anti-transferrin-precipitating antibody is performed to differentiate CSF desialated transferrin from nasal secretions. The assay has a high sensitivity and specificity. This is currently the recommended laboratory test for identifying the presence of CSF in sinonasal fluid.
2,3
Testing for the glucose content in rhinorrhea with the use of glucose oxidase paper is not recommended for the following reasons: reducing substances in lacrimal gland secretions and nasal mucus may cause false-positive results and meningitis may lower the glucose level in the CSF leading to a false-negative result. The test is not specific for the side or site of leak.
Beta-trace protein,
also known as prostaglandin D synthase, has been used to diagnose CSF rhinorrhea in multiple studies, with a sensitivity of 92% and specificity of 100%. It is synthesized primarily in arachnoid cells, oligodendrocytes, and the choroid plexus, but it is also present in the testes, heart, and serum, and it is nonspecific for CSF. Prostaglandin D synthase may also be altered in renal failure, MS, cerebral infarction, and certain CNS tumors. This test is not specific for the side or site of leak and can be difficult to collect if the leak is intermittent.
4
References
1. Lindstrom DR, Toohill RJ, Loehrl TA, et al. Management of cerebrospinal fluid rhinorrhea: the Medical College of Wisconsin experience.
Laryngoscope.
2004;114(6):969–974.
2. Porter MJ, Brookes GB, Zeman AZ, et al. Use of protein electrophoresis in the diagnosis of cerebrospinal fluid rhinorrhoea.
J Laryngol Otol.
1992;106(6):504–506.
3. Ryall RG, Peacock MK, Simpson DA. Usefulness of beta 2-transferrin assay in the detection of cerebrospinal fluid leaks following head injury.
J Neurosurg.
1992;77(5):737–739.
4. Pretto Flores L, De Almeida CS, Casulari LA. Positive predictive values of selected clinical signs associated with skull base fractures.
J Neurosurg Sci.
2000;44:77.
ACUTE EPIDURAL HEMORRHAGE
Epidural hemorrhage (bleeding between the dura and skull) is a rare but serious complication of head injury. It is most commonly due to an injury of the arteries predominantly the middle meningeal artery. It is found in up to 4% of patients surviving injury and up to 15% of autopsy series (see eBook Figure 4-24).
1,2
Patients usually present with a lucid interval following the head injury. Expansion of the hematoma eventually causes pressure on the brain with shift of the tissues. Symptoms include abnormalities of cranial nerve III function or weakness of the extremities on the contralateral side. Severe bleeds may progress to transtentorial or uncal herniation and death.
Epidural hemorrhage may also be due to nontraumatic etiologies including: infection, coagulopathy, vascular and congenital malformations, and tumors. Rarely, it may occur during hemodialysis, pregnancy, and cardiac surgery.
3,4
It may also occur in the epidural space of the spinal cord following spinal procedures.
5
Lumbar puncture is contraindicated in cases where epidural hemorrhage is suspected, due to the risk of herniation. Diagnosis is primarily based on neuroimaging with unenhanced CT. Differentiation of epidural versus subdural hematoma can be made on imaging as epidural hematoma will not cross suture lines and has a lensshaped appearance.
CSF is usually under increased pressure; it is colorless unless there is associated cerebral contusion, laceration, or subarachnoid hemorrhage in which case it will be xanthochromic or bloody.
References
1. Bullock MR, Chesnut R, Ghajar J, et al. Surgical management of acute epidural hematomas.
Neurosurgery.
2006;58:S7.
2. Mayer S, Rowland L. Head injury. In: Rowland L, ed.
Merritt’s neurology
. Philadelphia, PA: Lippincott Williams & Wilkins; 2000:401.
3. Szkup P, Stoneham G. Case report: spontaneous spinal epidural haematoma during pregnancy: case report and review of the literature.
Br J Radiol.
2004;77:881.
4. Takahashi K, Koiwa F, Tayama H, et al. A case of acute spontaneous epidural haematoma in a chronic renal failure patient undergoing haemodialysis: successful outcome with surgical management.
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1999;14:2499.
5. Sokolowski MJ, Garvey TA, Perl J II, et al. Prospective study of postoperative lumbar epidural hematoma: incidence and risk factors.
Spine.
2008;33:108.
SUBDURAL HEMATOMA
ACUTE
Acute subdural hematoma
is most commonly due to the shearing effect on the bridging veins between the brain and the dural sinus during trauma. Occasionally, it may also be due to arterial injury or low CSF pressure. It is a complicating factor in up to 20% of severe traumatic brain injuries (see eBook Figure 4-25).
1
Most patients develop coma following injury, but some have a transient “lucid interval” after the acute injury, followed by a progressive neurologic decline to coma.
2
Lumbar puncture is contraindicated due to the risk of herniation. The diagnosis is readily made on CT of the brain with subdural hematomas appearing as crescentshaped lesions as opposed to the lens-shaped lesion of the epidural hematoma.
