However, the case studies ignore the discrimination of the incidence of the problem by race or socio economic classification. (Showers, 1992)
Generally, the brain and the blood vessels of the babies are considered to be highly vulnerable to the whiplash injuries as a result of their anatomic structures. Besides the head of the baby constitutes about 10% of the weight of the body which is only 2% among the adults. At infancy the muscles at neck are very weak in comparison to that of any other stages in the life. The weak neck muscles along with the weak head control fails to resist the force exerted by the whiplash. Moreover the tender cranial joints and open fontanelles of the babies are conducive to worsen the slitting and trimming effects of the forces exerted. As a result of this a slight whiplash movement stretches the brain and the blood vessels instantly. The linking veins of the brain are not strong enough to resist the slitting stresses and results in hemorrhages.
The unmyelinated brain of the baby contributes towards making it more tender and are conducive to slitting of the brain and the bridging blood vessels making the brain more vulnerable to the trimming influences. The ventricles and subarachnoid spaces of the babies are filled with comparatively more amounts of cerebrospinal fluid- CSF, that allows the brain to dislocate more quickly and more intensively at the time of violent shaking that progressively increases stretching and the following vessel trimmings. The common form of intracranial injury related to the SBS is the subdural hematoma and accepted as the most common cause of death among the shaking infants. The subdural bleeding is observed to have occurred as a result of the slitting of the bridging veins interlacing between the brains to the sagittal sinus. This may also give rise to subarachnoid hemorrhages that will cause the spinal fluid taps to be bloody. (Smith, 2003)
In some cases the executor clutches the baby so tightly that causes the return of the thorax and venous from blood vessels in the head to decline following an enhanced intracranial pressure and cerebral edema. Cerebral edema may constitute the only finding in diagnoses process sometimes coupled with subarachnoid hemorrhage. The subdural bleeding often is venous rather than arterial and as a result is slower. This may prolongs the appearance of the neurological distortion from 24 to 48 hours. As a result of the significant bleeding the subarachnoid hemorrhages being arterial are considered fatal.
One significant observation in respect of the SBS is intraocular bleeding. The retinal hemorrhages are considered to be a common symptom of the SBS that purports to diagnose for intracranial injury and are not associated with other visible external wounds. According to Kivlin the retinal hemorrhages are taken to be the most common ocular observation in SBS. These are found in about 50% to 100% of the children. An instantaneous enhancement in the intracranial pressure is remitted to the eyes through the optic nerve covering resulting in the enhanced intraocular pressure. The associated intracranial and retinal damages result in long-term and enduring visual deficiency in case of the 30% to 80% of the victimized infants. The retinal hemorrhages present with the children of below 4 years are required to be diagnosed in terms of SBS. The supplementary clinical observations are associated with traction abrasions of the periosteum of the long bones without fractures or staining. In about 25% of SBS incidents the Radiographs of the long bones disclose about the old and new fractures of the infants. (Smith, 2003)
Moreover, multiple metaphyseal fractures are evident in cases of proximal humerus, distal ulna and radius, distal femur, and proximal and distal tibia and fibula and sometimes are left unacknowledged. The presence of the neurogenic pulmonary edema-NPE in SBS cases are observed by Rubin, McMillan, Helfaer and Christian. Irregular symptoms occur in case of the patho-physiology of NPE. According to some analysts quick increase in intracranial pressure encourages a catecholamine surge which is considered critical for the promotion of pulmonary edema. Such theory of NPE blast injury emphasizes that an aggressive increase in the intracranial pressure next to the central nervous system abuse give rise to excessive catecholamine release and a significant increase in the peripheral vascular resistance. Such an enhancement is followed by a retransmission of blood from the normal circulation to the lower resistance vascular bed of the lungs. Combined with the vasoconstriction of the pulmonary bed the effects are observed on a momentary propagation in pulmonary capillary wedge pressure encouraging the...
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