create barcode c# .net Patients Who Have Been Comatose from the Time of Head Injury in Microsoft Office

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Patients Who Have Been Comatose from the Time of Head Injury
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Here the central problem, so ably set forth by Symonds, is the relationship between concussion and contusion Since consciousness is abolished at the moment of injury, one can hardly doubt the existence of concussion in such cases; but when hours and days pass without consciousness being regained, the second half of the usual de nition of concussion namely, that the paralysis of cerebral function be transitory is not satis ed Careful pathologic examination of such cases usually discloses evidence of increased intracranial pressure and of cerebral contusions, lacerations, subarachnoid hemorrhage, zones of infarction, and scattered intrace-
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rebral hemorrhages both at the point of injury (coup) and on the opposite side (contrecoup), in the corpus callosum, and between these points, along the line of force of the injury In some patients, the diffuse axonal type of injury is a prominent abnormality; most often, there are separate but strategically placed ischemic and hemorrhagic lesions in the upper midbrain and lower thalamic region, as already mentioned The tissue around the contusions is swollen, and in postmortem preparations the white matter in these regions appears pale in myelin stains Varying amounts of blood in the subdural space are usually present A major displacement of the thalamus and midbrain is frequently present, with compression of the opposite cerebral peduncle against the free margin of the tentorium as well as secondary midbrain hemorrhages and zones of necrosis; in some cases, there is frank transtentorial herniation It should be kept in mind that severe head injury is associated with an immediate arrest of respiration and sometimes with bradyarrhythmia and cardiac arrest The effects on the brain of these systemic changes may in themselves be suf ciently profound to cause coma Also, head injury often complicates alcohol and drug ingestion, so that the possibility of a toxic or metabolic encephalopathy as the cause (or a contributing cause) of stupor must always be considered Within this category of severe head injury and protracted coma, three clinical subgroups can be recognized: one in which cerebral and other bodily injuries are severe and may be incompatible with survival; a second in which improvement sets in within a few days or a week or two, followed by variable degrees of recovery but leaving the patient with residual neurologic signs; and a third and relatively small group in which the patients remain permanently comatose, stuporous, or profoundly reduced in their cerebral capacities, ie, in the so-called vegetative and minimally conscious states (see Chap 17) Of course there are many degrees of injury that fall between these three arbitrary subgroups In all of these patients, following the initial period of stabilization, the matters of interest are the clinical and radiologic assessments, with the purpose of uncovering a surgically remediable lesion namely a subdural or epidural hematoma or a treatable intraparenchymal hematoma In most cases, the discovery of such a mass lesion mandates surgical removal But unless it is the only lesion, the procedure often proves to be insuf cient and coma is likely to persist because of the associated cerebral damage The recognition and management of these hematomas are described further on The rst subgroup comprises patients who are so severely injured that their lives are obviously endangered When rst seen, such a patient may be in shock (possibly from rupture of a visceral organ or injury of the cervical cord), with hypotension, hypoxia, hypothermia, a fast thready pulse, and pale, moist skin If this state persists along with deep coma, widely dilated xed pupils, absent eye movements and corneal and pharyngeal re exes, accid limbs, stertorous and irregular respirations or respiratory failure, death usually follows in a short time Once respiration ceases and the electroencephalogram (EEG) becomes isoelectric, the clinical state corresponds to brain death, as described on page 306 However, the diagnosis of brain death should not be made immediately after injury, in order to allow time to exclude the effects of anoxia, drug or alcohol intoxication, and hypotension In some of these patients, the blood pressure and respirations stabilize; the degree of cerebral injury can then be evaluated over a period of hours by observing the depth of coma and the temperature, pulse, and blood pressure Deep coma with subnormal temperature and rising pulse rate are grave prognostic signs, as are a rapidly rising temperature and pulse rate with rapid, irregular respirations In some fatal cases, the tem-
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