Nonaccidental injury to the brain is frequently encountered in the emergency department, and more so where street crime is common. Injury to the brain can be self-inflicted or due to a fight, robbery, rape, or battering. Gunshot wounds are a not-infrequent cause of death in younger individuals and adults. Because death often follows such an injury, a forensic neuropathologist typically takes responsibility for the case. Neurologists seeing patients with neurologic injury should always have nonaccidental injury in mind and, particularly, should be primed toward the possibility of spousal abuse. In some instances, crime is obvious. In others, evidence is circumstantial and these cases eventually need jurisdiction. Neurologists who evaluate patients in the emergency department may be asked to render opinions in legal proceedings. Information on neurologic injury associated with assault is difficult to obtain elsewhere; thus, including it in this monograph provides some practical value. This chapter's major focus is on the conditions that have been best characterized, but it is necessarily tentative and caveated due to lack of data in this field.
General Forensic Considerations
A detailed history may not be readily available, and the law enforcement agency involved may provide additional details about the crime scene. When the type of insult is unclear, certain clues may point toward crime. Massive fracture of the skull with comparatively little injury to the brain may be due to an immobilized head striking a wall or floor and may suggest battering. Periorbital hematomas from the use of blunt instruments or fist impacts are common in spousal abuse. Left-sided facial injuries are more frequent than right-sided injuries, reflecting the simple logic that most assailants are right-handed.1,2 Facial fractures with dental fractures are also more common in assaults, and zygomatic complex fractures are more frequent than mandibular fractures.2,3,4 In general, the combination of head, neck, and facial injury is more likely in victims of domestic violence. Other criteria, such as delay between time of injury and arrival for treatment; reluctance of the patient's companion to leave the patient during the examination; trauma to the head, face, shoulders, breasts, and abdomen; and bilateral injuries, increase the possibility of abuse.5
Shaken Baby Syndrome
One stunning neurologic injury is shaken baby syndrome. Shaken baby syndrome has many synonyms (shaken impact syndrome or battered babies).6 Child abuse is a common cause of infant death but, as expected, a history suggesting neglect and foul play is commonly inconsistent or incomplete. One study on children admitted with subdural hematomas suggested that 59% had abusive injury.7 Shaken baby syndrome is typically observed in children less than 3 years of age, with a peak incidence in the first year.8,9,10 Epidemiologic studies might be complicated to interpret and less precise due to missed cases. However, a prospective epidemiologic study in pediatric units in Scotland found quite a high annual incidence of 24.6 per 100,000 children younger than 1 year. In the United States, it is common in urban regions and during autumn and winter months.11 Risk factors for shaken baby syndrome that have been identified include younger parents, low socioeconomic status, child disability, or being premature. Fathers, boyfriends, and female babysitters most often cause the injuries; less commonly, the mother of the child is the cause. Although the clinical features are well delineated, the syndrome is still clouded in controversy and overcharged in legal proceedings.12
Clinical Presentation is very dramatic, and progression to brain death is common. Brain death is a consequence of sustained increased intracranial pressure that is in close proximity to the injury. A prolonged episode of lucidity between injury and the onset of symptoms is highly uncommon. On examination, the infant is comatose, is commonly mildly to moderately anemic, and may display signs of severe disseminated intravascular coagulation. Pancreatic traumatic damage may be seen, with high amylase levels, and liver injury may also be present. Femur, humerus, and rib fractures and superficial bruises should be actively sought. A fairly common finding is bilateral retinal hemorrhage (±60%), which should be specifically sought.13 (A recent study found that more than 50% of nonophthalmologists did not visualize the retina.14) Presence of retinal hemorrhages together with retinal folds or detachments, which can be seen only by expert evaluation of an ophthalmologist, is much more suggestive of the diagnosis.15
Interpretation of Diagnostic Tests
The computed tomographic (CT) scan should include bone windows and may detect skull fractures that could be multiple and cross suture lines. The CT scan typically detects a subarachnoid hemorrhage and subdural hematomas but may also show diffuse brain edema indistinguishable from patterns seen in anoxic-ischemic injury. The brain is hypodense, with loss of white and gray matter differentiation but with sparing of the basal ganglia and posterior fossa structures.16 Intentional injury is more likely when the CT scan shows subdural hematoma over the convexity. In addition, subdural hematomas have a high proclivity, being located in the interhemispheric fissure. The age of the subdural hematoma may be difficult to estimate, and a magnetic resonance imaging (MRI) scan could be more useful in this determination.17 The presence of layers of subdural hematomas of different ages is very suggestive of nonaccidental head trauma. In some infants, fractures are absent and hygromas are found.18 Contrecoup lesions are perhaps more common and a reflection of acceleration/deceleration force.19
The CT scan may also include petechial or punctate hemorrhages along the gyral surfaces and the inferior surface of the frontal lobe and temporal and frontal poles (Fig. 20.1).
Eventually pathologic examination is an important adjunct in confirming the clinical diagnosis. However, the interpretation of injury is complex, and a meticulous autopsy is usually performed by experts in this field (Box 20.1).20 Important studies have recently been published.21,22
Prediction of Outcome
Many neonates and children progress to brain death and may become potential organ donors. Morbidity is substantial and ranges from 15% to 40%.23Morbidity in survivors includes spasticity, microcephaly, and seizure disorders.17
· Neonatal intensive care unit.
Hanging and Strangulation
Victims of hanging, a common method of suicide, will appear in the emergency department. Attempted strangulation of an intruder or strangulation in the setting of abuse may result in a similar injury. The pathophysiologic mechanisms may be entirely due to postanoxic brain injury.
Figure 20.1 On computed tomographic scans of shaken baby syndrome, both subarachnoid hemorrhage and subdural hematomas are seen (arrows). On chest X-ray, note multiple rib fractures (arrows).
Box 20.1. Injury in Shaken Baby Syndrome
The term shaken baby syndrome suggests that impact on a flat surface is necessary to create the injury. Some evidence suggests that shaking alone may not produce the angular acceleration to create shear injuries and subdural hematoma. Small axonal size predisposes a young brain to injury, but the shell of the skull base also allows the brain to rotate more readily.6 An “injury” should be distinguished from translational forces, such as falling down stairs. With skull fractures, skull bruises, or subgaleal hemorrhage, an impact can be assumed. Anoxic-ischemic injury seems to play a major role, which can be due to intentional suffocation as well. Other injuries include posterior rib fractures due to tight squeezing of the chest of the baby and should not be attributed to cardiopulmonary resuscitation (CPR) (none were found in 91 infants with CPR).19 An association between subdural and retinal bleeding has been found pathologically.21,22 Hemorrhage at die periphery (ora serrata) and posterior pole of the retina is more common.
There is a major difference between suicidal and judicial hangings. The fall from a lesser height may result in lesser prevalence of cervical spine injury (fracture or dislocation). Neck fracture occurs in fewer than 10% of hanging victims.24 Only a fall from a major height with a sudden stop may fracture the upper cervical vertebra and detach the pons from the medulla. Drug or alcohol ingestion was present in 70% of 44 cases reported from Australia.25
Many patients are found pulseless, apneic, and suspended free at the scene. Marks around the neck but also subconjunctival or facial petechial hemorrhages are quite common. If severe, these may be associated with tongue hemorrhages; one study suggested that gross tongue hemorrhages were more common in strangulation.26 Acute papilledema with hemorrhages may occur due to asphyxia. Myoclonus status epilepticus in comatose patients is observed frequently and reflects the seriousness of this injury (see Chapter 10). Brief generalized tonic-clonic seizures may occur as well. The responsible injury may be neck vein compression, carotid artery occlusion, or laryngeal injury leading to diffuse anoxic-ischemic impact.
Attempted strangulation is another condition that can produce neurologic injury, and many of the symptoms are initially nonneurologic. Patients who present to the emergency department may have petechiae of the skin of the upper eyelid and subconjunctival hemorrhages. Sore throat, hyper-ventilation, and uncontrollable shaking have been documented. Strangulation can cause a comatose state; then the abnormalities will involve lesions to areas that are susceptible to anoxia.
Neurologic injury associated with spousal abuse is of major concern and may be underrecognized in the emergency department.27 Alcohol abuse, unemployment or intermittent unemployment, estranged husbands, or former boyfriends increase the risk.28 Head, neck, and facial injuries have been found as significant markers, but there is increasing evidence of the presence of arterial dissection associated with strangulation.29 The mechanism is thought to be compression of the carotid artery against the bony cervical vertebrae, resulting eventually in dissection of the media.30,31 Other suggestive injuries are defensive injuries of the forearm, bruises in various stages of healing, or any poorly explained injury.32 The time lapse between presentation may be months; thus, skin lesions may not be present.
Interpretation of Diagnostic Tests
The CT scan is rarely abnormal but may show the effects of severe anoxic-ischemic injury in the resuscitated patient.33 In these cases, massive edema with loss of white-gray matter differentiation and sulcal architecture is common (see Chapter 9). The cerebellum may be spared.34 Hypodensity in lentiform nuclei and thalami may be seen.35 One report noted bilateral lobar hematomas due to massive elevated cerebral venous pressure.
These could represent hemorrhagic infarcts with a mechanism comparable to cerebral venous sinus thrombosis.36
Magnetic Resonance Imaging
More or less specific findings have been reported on MRI, which has a much better sensitivity for lesions. Signal changes in the lentiform nuclei or the thalamus often are noted, but a rent lesion from sudden deceleration and flexion at the junction of the pons and medulla oblongata is more characteristic (Fig. 20.2). Severe anoxic injury is often combined with ischemic injury from cardiac arrest, even if brief; and, in permanently comatose patients, the cortex signal may be extremely hyperintense (Fig. 20.3).
Predictors of Outcome
The presence of a Glasgow coma score of 3, fixed dilated pupils, or cardiac arrest at the scene is associated with a grim outcome.37 Pulmonary edema is common. Delayed anoxic encephalopathy has been reported.39 It is very important to obtain a drug and alcohol screen in these patients, and their presence can markedly confound the assessment. Somatosensory evoked potentials (absent bilateral scalp potentials with preserved cervical cord potentials) may be considered for prognostication. Acute dystonia and an akinetic rigid syndrome have been reported, but these findings are nonspecific and a representation of anoxic injury to basal ganglia.40
· Medical intensive care unit for mechanical ventilation and support.
· A mandatory law for reporting domestic violence may exist.41
Gunshot Wounds to the Head
The impact to the brain when penetrated by a bullet is explosive and, due to its shock wave, enormously damaging. Not only do bullets penetrate the skull, brain, and vascular structures, but the great force and high pressure in the cavity of passage also damage the surrounding structures. Details of ballistics require special expertise and are not discussed here. However, some observations seem consistent. The entrance wound often leaves unburned residues in the skin (“tattooing”) and is typically smaller than the exit wound. The exit may be larger due to mushrooming of the bullet. Suicide wounds are often in the dominant temporal region or in the mouth, with an angulation matching the handedness. When multiple gunshot wounds are present, suicide is unlikely. However, penetration of the head without loss of impairment of consciousness due to the low energy of aged ammunition may result in multiple self-inflicted wounds.42 The brain stem and deeper structures of the brain are frequent sites of hemorrhage, and ectopic bone fragments are seen. Guns placed in the mouth may destroy the brain stem, or bullets may lodge under the skull base, damaging the carotid artery and cranial nerve XII.43 Gunshot wounds to the brain are complex injuries, with skull fracture, tracks of bone, and missile fragments. Often, an associated intracerebral hematoma determines the initial clinical condition. Cerebral contusions may be seen at the entry and exit sites.
Figure 20.2 Magnetic resonance imaging (left) shows rent in pontomesencephalic region typical of hanging. Hyperintensities of the lenticular nucleus are also noted in globus pallidus (right).
Figure 20.3 Anoxic injury leading to diffuse overwhelming cortical hyperintensities.
Evaluation of patients with gunshot wounds to the head involves assessment of the Glasgow coma score, but scores are very low. Patients not uncommonly present with fixed unreactive pupils, and extensor posturing. Early deterioration may be due to enlarging intracranial hematoma or acute subdural hematoma from a fall.
Interpretation of Diagnostic Tests
CT scan images are shown in Figure 20.4. A bone window may identify small residue of metal or bone showing the track of the bullet or even lodging of a large fragment. Suicidal gunshots are often with guns placed against the temple or with the barrel inside the mouth, producing characteristic tracks. A CT scan is performed to detect parenchymal hematoma, subdural hematoma, or contrecoup lesions. The hematomas are along the tracks of the bullet in the ventricles or in the subdural space.
Figure 20.4 Examples of computed tomographic scans of patients with gunshot wounds. A: Gun placed on temple with bullet cutting through the brain horizontally and leaving a hemorrhage in its tracks. Examples of computed tomographic scans of patients with gunshot wounds. B: Shotgun with barrel in mouth, disposing most material in the occipital bone and lobe. C: Transventricular injury (track with intraventricular hematoma) with bone destruction (arrows) and intracranial air. Examples of computed tomographic scans of patients with gunshot wounds. D; Gunshot-induced intracranial hematoma with intra-ventricular hematoma. Air is visible in ventricles.
First Priority in Management
The management of gunshot wounds is similar to that of any other type of non-penetrating trauma.44 A large intracerebral hematoma with mass effect and imminent herniation should be removed. No further therapy can be offered to patients who, after initial resuscitation, have a Glasgow coma score of 3, no operable hematoma, and no major confounder such as drug ingestion.45 Reconstructive repair of the bone and dura should begin immediately.38 The wound is considered contaminated, and broad-spectrum antibiotics (vancomycin with cefotaxime) should be administered early. When injury to the cerebral vasculature is anticipated, angiography can be performed, but therapeutic options other than endovascular or surgical occlusion are limited. A major problem is the early development of disseminated intravascular coagulation. Its occurrence is related to the amount of brain tissue damage; thus, it is frequent in gunshot wounds. Its appearance on laboratory tests (e.g., increased D-dimer or fibrinogen split products) denotes a poor outcome. If there is evidence of a full track throughout the brain, there appears to be very little benefit of aggressive intracranial pressure management. A bolus of mannitol, 1–2 g/kg, can be administered to determine whether improvement is possible; but if none is present, salvage-ability is unlikely.
Predictors of Outcome
Important factors that determine outcome relate to the size of the parenchymal hematoma, the degree of destroyed parenchymal tissue, the development of cerebral edema, infection, and mass effect.46 The presence of contrecoup contusions could be an important additional determinant. Tension pneumocephalus may occur after penetrating injury to the frontal sinus or the anterior ethmoidal-cribriform plate area.47,48,49 Gradual enlargement may occur, with clinical deterioration that requires drainage and closure of the defect (Fig. 20.5).
Poor outcome is expected in comatose patients with extensor posturing at admission, abnormal pupils, CT scan demonstrating ventricular involvement, crossing of midsagittal or midventricular horizontal planes, intraparenchymal hemorrhage, and a high volume of contused or damaged brain.50,51 Evidence of increased intracranial pressure as noted by obliteration of the mesencephalic cisterns, presence of subarachnoid and interventricular hemorrhage, and intracranial hematoma are all associated with poor outcome, according to the National Institutes of Health Traumatic Coma Data Bank.52,53
Figure 20.5 Developing tension pneumocephalus after gunshot wound.
· Surgical debridement (removal of metal and bone fragments and necrotic tissue) and evacuation of growing hematomas.
· Triage to neurosurgical intensive care unit.
· With clinical suspicion of vascular injury, consider cerebral angiogram.
1. Gayford JJ: Wife-battering: a preliminary survey of 100 cases. BMJ 1:194, 1975.
2. Shepherd JP, Al-Kotany M, Subadan CJ, et al.: Assault and facial soft tissue injuries. Br J Plast Surg 40:614, 1987.
3. Perciaccante VJ, Ochs HA, Dodson TB: Head, neck, and facial injuries as markers of domestic violence in women. J Oral Maxillofac Surg 57:760, 1999.
4. Ochs HA, Neuenschwander MC, Dodson TB: Are head, neck and facial injuries markers of domestic violence? J Am Dent Assoc 127:757, 1996.
5. Flitcraft A: Physicians and domestic violence: challenges for prevention. Health Aff (Millwood) 12:154, 1993.
6. American Academy of Pediatrics: Committee on Child Abuse and Neglect. Shaken baby syndrome: rotational cranial injuries–technical report. Pediatrics 108:206, 2001.
7. Feldman KW, Bethel R, Shugerman RP: The cause of infant and toddler subdural hemorrhage: a prospective study. Pediatrics 108:636, 2001.
8. David TJ: Shaken baby (shaken impact) syndrome: non-accidental head injury in infancy. J R Soc Med 92:556,1999.
9. Duhaime AC, Christian CW, Rorke LB, et al.: Nonacci-dental head injury in infants–the “shaken-baby syndrome.” N Engl J Med 338:1822, 1998.
10. Duhaime AC, Gennarelli TA, Thibault LE, et al.: The shaken baby syndrome. J Neurosurg 66:409, 1987.
11. Barlow KM, Minns RA: Annual incidence of shaken impact syndrome in young children. Lancet 356:1571, 2000.
12. Uscinski R: Shaken baby syndrome: fundamental questions. Br J Neurosurg 16:217, 2002.
13. Conway EE Jr: Nonaccidental head injury in infants: “the shaken baby syndrome revisited.” Pediatr Ann 27:677, 1998.
14. Morad Y, Kim YM, Mian M, et al. Nonophthalmologist accuracy in diagnosing retinal hemorrhages in the shaken baby syndrome. J Pediatr 142:431, 2003.
15. Kivlin JD, Simons KB, Lazoritz S, et al.: Shaken baby syndrome. Ophthalmology 107:1246, 2000.
16. Petitti N, Williams DW III: CT and MR imaging of nonaccidental pediatric head trauma. Acad Radiol 5:215, 1998.
17. Caffey J: The whiplash shaken infant syndrome: manual shaking by the extremities with whiplash-induced intracranial and intraocular bleedings, linked with residual permanent brain damage and mental retardation. Pediatrics 54:396, 1974.
18. Wells RG, Vetter C, Laud P: Intracranial hemorrhage in children younger than 3 years. Arch Pediatr Adolesc Med 156:252, 2002.
19. Spevak MR, Kleinman PK, Belanger PL, et al.: Cardio-pulmonary resuscitation and rib fractures in infants. A postmortem radiologic-pathologic study.JAMA 272:617, 1994.
20. Case ME, Graham MA, Handy TC, et al.: Position paper on fatal abusive head injuries in infants and young children. Am J Forensic Med Pathol 22:112, 2001.
21. Geddes JF, Hackshaw AK, Vowles GH, et al.: Neuropathology of inflicted head injury in children. I. Patterns of brain damage. Brain 124:1290, 2001.
22. Geddes JF, Vowles GH, Hackshaw AK, et al.: Neuropathology of inflicted head injury in children. II. Microscopic brain injury in infants. Brain 124:1299, 2001.
23. King WJ, MacKay M, Sirnick A: Shaken baby syndrome in Canada: clinical characteristics and outcome of hospital cases. CMAJ 168:155, 2003.
24. Feigin G: Frequency of neck organ fractures in hanging. Am J Forensic Med Pathol 20:128, 1999.
25. McClane GE, Strack GB, Hawley D: A review of 300 attempted strangulation cases: part II. Clinical evaluation of the surviving victim. J Emerg Med 21:311, 2001.
26. Bockholdt B, Maxeiner H: Hemorrhages of the tongue in the postmortem diagnostics of strangulation. Forensic Sci Int 126:214, 2002.
27. Corrigan JD, Wolfe M, Mysiw WJ, et al. Early identification of mild traumatic brain injury in female victims of domestic violence. Am J Obstet Gynecol (Suppl) 188:S71, 2003.
28. Kyriacou DN, Anglin D, Taliaferro E, et al.: Risk factors for injury to women from domestic violence. N Engl J Med 341:1892, 1999.
29. Nadareishvili Z, Norris JW: Stroke from traumatic arterial dissection. Lancet 354:159, 1999.
30. Purvin V: Unilateral headache and ptosis in a 30-year-old woman. Surv Ophthalmol 42:163, 1997.
31. Malek AM, Higashida RT, Halbach W, et al.: Patient presentation, angiographic features, and treatment of strangulation-induced bilateral dissection of the cervical internal carotid artery. J Neurosurg 92:481, 2000.
32. Eisenstat SA, Bancroft L: Domestic violence. N Engl J Med 341:886, 1999.
33. Ohkawa S, Yamadori A: CT in hanging. Neuroradiology 35:591, 1993.
34. Rao P, Carty H, Pierce A: The acute reversal sign: comparison of medical and non-accidental injury patients. Clin Radiol 54:495, 1999.
35. Ozkan U, Kemaloglu S, Ozates M, et al.: Analysis of 107 civilian craniocerebral gunshot wounds. Neurosurg Rev 25:231, 2002.
36. Brancatelli G, Sparacia G, Midiri M: Brain damage in hanging: a new CT finding. Neuroradiology 42:209, 2000.
37. Penney DJ, Stewart AHL, Parr MJA: Prognostic outcome indicators following hanging injuries. Resuscitation 54:27, 2002.
38. Kaki A, Crosby ET, Lui AC: Airway and respiratory management following non-lethal hanging. Can J Anaesth 44:445, 1997.
39. Hori A, Hirose G, Katoaka S, et al.: Delayed postanoxic encephalopathy after strangulation. Serial neuroradiological and neurochemical studies. Arch Neural 48:871, 1991.
40. Kalita J, Mishra VN, Misra UK, et al.: Clinicoradiological observation in three patients with suicidal hanging. J Neurol Sci 198:21, 2002.
41. Feldhaus KM, Houry D, Utz A, et al.: Physician's knowledge of and attitudes toward a domestic violence mandatory reporting law. Ann Emerg Med 41:159, 2003.
42. Sekula-Perlman A, Tobin JG, Pretzler E, et al.: Three unusual cases of multiple suicidal gunshot wounds to the head. Am J Forensic Med Pathol 19:23, 1998.
43. Hagemann G, Willig V, Fitzek C, Witte OW. Gunshot-induced artery dissection with twelfth nerve palsy. Arch Neurol 60:280, 2003.
44. Helling TS, McNabney WK, Whittaker CK, et al.: The role of early surgical intervention in civilian gunshot wounds to the head. J Trauma 32:398, 1992.
45. Grahm TW, Williams FC Jr, Harrington T, et al.: Civilian gunshot wounds to the head: a prospective study. Neurosurgery 27:696, 1990.
46. Aldrich EF, Eisenberg HM, Saydjari C, et al.: Predictors of mortality in severely head-injured patients with civilian gunshot wounds: a report from the NIH Traumatic Coma Data Bank. Surg Neurol 38:418, 1992.
47. Gonul E, Baysefer A, Erdogan E, et al.: Tension pneumocephalus after frontal sinus gunshot wound. Otolaryngol Head Neck Surg 118:559, 1998.
48. Aferzon M, Aferzon J, Spektor Z: Endoscopic repair of tension pneumocephalus. Otolarygol Head Neck Surg 124:688, 2001.
49. Gardner WJ, Shannon EW: Pneumocranium from gunshot wound of brain. JAMA 214:2333, 1970.
50. Shaffrey ME, Polin RS, Phillips CD, et al.: Classification of civilian craniocerebral gunshot wounds: a multivariate analysis predictive of mortality. J Neurotrauma 9(Suppl 1):S279, 1992.
51. Selden BS, Goodman JM, Cordell W, et al.: Outcome of self-inflicted gunshot wounds of the brain. Ann Emerg Med 17:247, 1988.
52. Aarabi B, Alden TD, Chesnut RM, et al.: Neuroimaging in the management of penetrating brain injury. J Trauma 51(Suppl):S7, 2001.
53. Aarabi B, Alden TD, Chesnut RM, et al.: Management and prognosis of penetrating brain injury: introduction and methodology. J Trauma 51(Suppl):S3, 2001.