579
(Accepted: October 12, 2010)
Abstract : An 18-month-old intact male Pomeranian dog was presented because of traumatic head injury from a fall.
Based on physical and neurological examination, brain injury was suspected. On plain skull radiographs, bony fragment following fracture was identified in the region of the right occipital bone. On computed tomography (CT) images, there were specific findings associated with an intracranial hemorrhage. The patient expired few hours after diagnosis, and performed necropsy. On gross findings, intracerebral hemorrhage and edema was detected and those were consistent with CT images. This report describes the clinical findings, CT imaging characteristics, necropsy findings, and histopathologic features of severe traumatic brain injury in a dog.
Key words : computed tomography, dog, traumatic brain injury.
Introduction
Traumatic brain injury (TBI) refers to an injury to the intrac- ranial structures following a physical trauma to the head (1,4,6,8). Severe TBI is one of the leading causes of death and disability in human medicine (9,11). TBI is also frequently seen in small animals (1,2,4). TBI in small animals is often caused by automobile trauma, kick or bite injuries, penetrat- ing wounds, and falls (1,2,4,6). Road accidents and falls from a height, to be exact, are the most common cause of brain trauma in small animals (1,5,6). The brain is so well pro- tected by the skull and the overlying muscle that only a severe trauma can cause brain injury (1,5). Pathophysiologically, the external force causes a destruction of the blood-brain barrier and brain cells (1,4,10). The swelling of the cells (brain edema) increases ischemia and hypoxia (1,4,5,9). The prog- nosis depends on the severity of the neurological deficits, the extent of the lesion and the time of treatment (5).
In this report, we describe the clinical findings, radiographic and computed tomographic (CT) imaging characteristics, nec- ropsy findings, and histopathological features of severe TBI in a dog.
Case Report
An 18-month-old intact male Pomeranian dog was pre-
sented 16 hours after traumatic head injury from a fall. The patient exhibited neurological signs such as head tilt, nystag- mus, tetraparesis and seizure after trauma. Physical and neuro- logical examinations revealed severe depression and lethargic status, jerk nystagmus of both eyes, head tilt to the right side, bilaterally dilation of the pupils, absent menace response, and delayed postural reactions in all limbs. These results sug- gested that the clinical signs were caused by the lesions in the brain. Modified Glasgow Coma Scale (MGCS) score of the patient was 7, suggestive of a grave prognosis. (Motor activity- Recumbent, intermittent extensor rigidity; score 4 / Brain stem reflexes- Bilateral, unresponsive mydriasis with reduced oculo- cephalic reflexes; score 1 / Level of consciousness- Semicoma- tose, responsive only to repeated noxious stimuli; score 2)
The results of complete blood count (CBC) and serum chem- ical analysis were within the normal ranges.
Plain skull radiographs revealed a widened suture line. In addition, an approximately 1.3 cm length, long ovoid shaped bony fragment was identified in the region of the right occipital bone (Fig 1).
CT of the head was performed just after patient stabiliza- tion. CT scanning was progressed without anesthesia, because the patient couldn’t move voluntarily. In noncontrast images, the right lateral ventricle and the third ventricle were filled with hyperattenuating materials (58 Hounsfield units [HU]).
Additionally, there was an ill-defined hyperattenuating lesion (59 HU) in the region of the right temporo-occipital lobe. This ill-defined lesion was surrounded by an irregularly hypoatten- uating region (22 HU) at the level of the sellar. On bony win-
1Corresponding author.
E-mail: [email protected]
dow, it was seen that the bony fragment was distracted to outward in the region of right temporo-occipital bone. The falx cerebri was shifted to the left around the ill-defined hyper-
attenuating lesions in the contrast-enhanced CT images. The hyperattenuation of the lesions on noncontrast images, sur- rounded by a hypoattenuating area, was consistent with hem- orrhage and surrounding edema in the noncontrast images.
On the basis of the results of radiography and CT scan, the patient was diagnosed with an intracerebral hemorrhage caused by TBI.
To establish euvolemia and to maintain hydration, normal saline (30 ml/kg/hr CRI) was administered for 1 hour. Then, to reduce secondary injuries, we administered 15% mannitol (1 g/
kg CRI for 30 min; Daehan Pharm, Korea) with furosemide (1 mg/kg IV; Handok Phama, Korea) and methylprednisolone sodium succinate (MPSS; 30 mg/kg CRI for 30 min; Sam- chundang Phama, Korea) to the patient. Oxygen was supplied via a facial mask.
However, the patient expired few hours after the diagnosis and necropsy was performed. Necropsy findings revealed intracerebral hematoma and parenchymal necrosis (Fig 4).
Gross findings were consistence with the CT findings. Micro- scopically, hemorrhage was markedly seen in the subarachnoid space and cerebral cortex (Fig 5A). Lesions also revealed neu- ronal necrosis, neuronal loss, neuronal vacuolation, neuronal edema, and astrogliosis. Neuronal necrosis caused neuronal cytoplasmic eosinophilia, and pyknotic nuclei were observed (Fig 5C). Edema was seen in the perivascular spaces, which had widened as a result of fluid leakage and spongy degenera- tion characterized by small clear vacuoles of varied sizes pri- marily in the gray matter (Fig 5B). Moreover, gemistocytes, increased glial filaments, and enlarged nuclei were seen in the cerebral cortex around the damaged lesion (Fig 5D).
Discussion
TBI is usually classified into primary and secondary inju- ries. Primary brain injury occurs immediately following the Fig 1. Lateral (A) and dorsoventral (B) skull radiographs show the bony fragment (arrows) in the region of right temporo-occipital bone. In addition, widen of suture lines (arrowheads) throughout the skull is identified.
Fig 2. Noncontrast CT images of neurocranium show the right lateral ventricle, the third ventricle, and some part of cerebral pa- rencyma were filled with hyperattenuating materials (black arrows).
Additionally, there was a ill-defined hyperattenuating lesion which was surrounded by irregular hypoattenuating region (white arrow- heads) at the level of sellar. On bony window, it was shown that bony fragment (white arrow) was distracted to outward in the region of right temporo-occipital bone.
impact and initiates a number of biochemical processes that result in secondary brain injury. Primary injury involves dam- age to the intracranial structures at the time of initial impact.
Such injury can cause intracranial hemorrhage leading to mass compression, direct neuronal damage, and cerebral lacerations caused by skull fractures (1,6). In addition to hemorrhage and edema, the damage caused by the primary injury activates a number of interrelated biochemical pathways that act in con- cert to perpetuate further brain parenchymal damage and sub- sequent increase in intracranial pressure (ICP). These phenom- ena are secondary brain injuries (1,6). This classification is important because secondary injuries are potentially prevent- able, whereas primary injuries have already occurred by the time the patient first presents for medical attention. The pre- vention and treatment of secondary brain injury can decrease mortality and improve the outcome. To achieve the best out- come, attention must be focused on blood pressure optimiza-
tion and brain tissue oxygenation, maintenance of adequate cerebral perfusion pressures, and prevention of seizures (1,6,7).
Clinical classification of the severity of TBI is usually based on the Glasgow Coma Scale (GCS) in human medicine (9). A modification of the GCS has been proposed by Shores for use in veterinary medicine (8). This scoring system enables grad- ing of the initial neurological status and serial monitoring of the patient after head trauma. A MGCS score was evaluated in this case on the basis of the scoring system proposed pre- viously (4,8). According to previous reports (4,8), MGCS scores could be an indication of the severity of brain injury and help in the prognosis. Actual MGCS scores of 3-8, 9-14, and 15-18 indicate prognosis as grave, guarded, and good, respectively. The score of the present patient was 7 and that suggested grave prognosis (4,8).
Neuroimaging should be considered early in the manage- ment of patients with head injury and marked impairment of consciousness or neurological deficits that progressively worsen despite initial medical therapy (1,10). Previously, skull radiog- raphy was limited imaging examination of head trauma patients for the detection of fractures (10). However, plain radiography cannot identify traumatic brain lesions including hemorrhage and brain edema (3,10). In other words, skull radiography provides only limited diagnostic information in head trauma cases (3,10). Generally, CT is the diagnostic method of choice for initial evaluation in head trauma patients, because it can be completed quickly and is sensitive enough to detect acute hemorrhage (10). CT also provides fine anatomic detail of the bone when viewed on a wide window allowing accurate characterization of any skull fractures. Although magnetic res- onance imaging (MRI) is slightly more sensitive than CT for the detection of hematomas, those that are not seen on CT are usually small (3,10). A disadvantage of MRI is the longer examination time and the difficulty in monitoring unstable patients in the MRI environment. Despite the advances in MRI technology, as discussed above, CT continues to be the modal- ity of choice for the evaluation of acute injury because it is Fig 4. Necropsy findings reveals the intracerebral hematoma and
parenchymal necrosis (thin arrows), hemorrhages in right lateral and third ventricles (big arrows), and swelling of right side cere- bral parenchyma (arrow heads).
Fig 3. On contrat CT images, the falx cerebri was shifted to the left around ill-defined hyperattenuating lesions.
fast, widely available, and highly sensitive to acute bleeding and can more easily accommodate life support and monitoring equipment (4,10,11). Therefore, MRI is indicated for patients with acute TBI when the neurological findings are unex- plained by CT (3).
The present patient was admitted in a recumbent and semico- matose state. Thus, CT scanning was conducted without anes- thesia and whole CT scan was conducted in less than 10 minutes. The CT findings of this patient were suggestive of bleeding into the lateral ventricle, third ventricle, and cerebrum.
Within hours of brain hemorrhage, the CT attenuation values within the hematoma increase up to 60-80 HU. This is due to the formation of a meshwork of fibrin and globulin molecules.
An acute hematoma may be surrounded by a hypoattenuating region corresponding to edema (10). Fluid begins to collect immediately in the region around the hematoma (11), and edema usually persists for up to 5 days and in some instances, for as long as 2 weeks (12). In this case, we could easily detect these findings, which were associated with brain hemorrhage in CT images.
Many patients suffering from severe head trauma present to the clinician in a state of hypovolemic shock, and the most common causes of death after head trauma are hypovolemia and hypoxia (1,7). Therefore, initial aggressive intravenous fluid therapy to counteract hypotension in the traumatically injured brain is necessary to improve the shock status. We administered isotonic crystalloid fluid (normal saline) rapidly to correct the shock status and supplied oxygen to prevent
hypoxia. Mannitol is an osmotic diuretic that has demon- strated efficacy in reducing brain edema and ICP in cases of severe TBI, and high-dose MPSS therapy should be consid- ered as an adjunctive treatment in patients with TBI who do not respond to fluid and oxygen therapy and mannitol admin- istration (1,7). MPSS was also used in the present patient for obtaining a positive outcome. However, the patient expired few hours after presentation despite adequate management.
This case report demonstrated correspondence between CT images and necropsy gross findings in a severe TBI patient.
In addition, histopathological features of the present case revealed the process of neuronal cell changes after severe TBI.
Accordingly, these TBI findings may be clinically useful information for veterinary clinicians.
References
1. Dewey CW. Head trauma management. In: A practical guide to canine and feline neurology, 2nd ed. USA: Wiley-Blackwell.
2008: 221-235.
2. Jung DI, Park C, Kang BT, Yoo JH, Kim JW, Kim HJ, Lim CY, Lee SY, Gu SH, Heo RY, Jeon HW, Kim JH, Eom KD, Park JI, Park HM. Identification of intracerebral hematoma using ultrasonography in a dog. Korean J Vet Res 2007; 47:
127-129.
3. Le TH, Gean AD. Neuroimaging of traumatic brain injury.
Mount Sinai J Med 2009; 76: 145-162.
4. Platt SR, Radaelli ST, McDonnell JJ. The prognostic value of the modified glasgow coma scale in head trauma in dogs. J Fig 5. Histopathological findings of the present case. Hemorrhage (A) and edema (B) are showed markedly in the cerebral cortex (arrows). Gliosis (C) and gemistocytes (D: arrows) induced by TBI are showed in the cerebral cortex around damaged lesion.
포메라니언 종에서 발생한 외상성 뇌손상 증례보고;
임상적, 전산화 단층촬영, 부검 소견
이희천·최을수·조규완·강병택**·김주원*·유치호*·서정향*·정동인1
경상대학교 수의과대학, *건국대학교 수의과대학, **미국 국립 보건원
요 약 : 18년 령의 수컷 포메라니언견이 낙상으로 인한 외상성 머리 손상으로 내원하였다. 신체검사 및 신경검사 후 뇌손상이 의심되었다. 두부 방사선 쵤영에서 우측 후두골 부위에 골절로 인한 뼈조각이 관찰되었다. 전산화 단층촬영 상에서 두개 내 출혈 소견이 확인되었다. 두부 외상에 대한 처치에도 불구하고 환자는 내원 수 시간 후 폐사하였고 부 검을 실시하였다. 육안 검사 상 대뇌 피질의 출혈 소견과 부종이 확인되었으며 이는 전산화 단층 촬영 결과와 일치하 였다. 본 증례보고는 개에서 발생한 심한 외상성 뇌손상의 임상적 특성, 전산화 단층촬영 영상적 특징, 부검 소견, 그 리고 조직학적 변화를 잘 보여주고 있다.
주요어 : 전산화 단층촬영, 개, 외상성 뇌손상
