Veterinary Surgery, 20, 6, 41 3-41 7, 1991

Subdural Hematoma in a Dog ANDREW L. HOPKINS, BVSC. MVM, and SIMON J. WHEELER,

BVSc. PhD

A traumatic subacute subdural hematoma in a dog was diagnosed by computed tomography and treated successfully by craniectomy and surgical drainage.

NTRACRANIAL HEMORRHAGE CAUSED by trauma may be focal or multifocal, petechial, or frank, and it may be epidural, subdural, subarachnoid, or intraparenchymatous. Clinical signs may be immediate or delayed. Progressive hemorrhage and the development of cerebral edema may lead to increased intracranial pressure and herniation of the brain.'-' Other causes of intracranial hemorrhage in dogs include neoplasia and disorders of coagulation. In humans, other well-recognized causes include aneurysm, stroke, and hyperten~ion.~ In humans, subdural hematoma is usually caused by trauma and arises as blood collects between the dura mater and the arachnoid mater.'.'-' In the presence of a tear in the arachnoid mater, the hematoma extends into the subarachnoid space. To our knowledge, the diagnosis and treatment of subdural hematoma has not been reported in the dog.

I

Case Report

Hisr orjy An 8-year-old, spayed female mixed-breed dog was referred to North Carolina State University, College of Veterinary Medicine, Veterinary Teaching Hospital for evaluation of increasing signs of depression, ataxia. head pressing, and aimless wandering. Eight days earlier. head injuries sustained when the dog was hit by a car caused depression, disorientation, anisocoria and several minor lacerations. Treatment with intravenous fluids. mannitol. and glucocorticoids was followed by gradual improvement, and the dog was discharged from veterinary care on day 4. At home, the dog continued to improve and was only slightly lethargic on day 5. On day 6, the dog

appeared to be less aware of her surroundings and was depressed. These signs worsened over the next 24 hours, with intermittent head pressing, circling to the right, and aimless wandering. The dog was also sensitive to handling around the head.

Clinical Finding7 On admission, the dog was depressed and disoriented. It was reluctant to walk and had a tendency to stumble. There were mild. asymmetric, conscious propnoceptive deficits in all limbs, with the left side more severely affected than the right side. Spinal reflexes were exaggerated in all limbs. Cranial nerve functions and the ocular fundi were normal. The neurologic findings were indicative of a predominantly right-sided forebrain lesion. Differential diagnoses included intracranial (neoplasia, encephalitis, hemorrhage) and extracranial (metabolic, toxic) disorders. The dog's condition deteriorated to a profoundly stuporous state. Anisocoria with mydriasis of the right pupil developed. Pupillary light reflexes were intact, but direct and consensual responses in the right eye were sluggish. Menace responses disappeared bilaterally. On the basis of the marked deterioration and anisocoria, rising intracranial pressure with possible brain herniation was suspected. Mannitol(1 g/kg intravenously [IV] over 2 minutes) and. 15 minutes later, furosemide (0.7 mg/kg IV) were administered.* One hour later the dog was fully conscious and standing in its cage. The next morning a computed tomography (CT) scan was planned. A complete blood count was normal except for a stress leukogram with a mature neutrophilia of 48,000 neutrophils/pL. Serum biochemistry, including a fasting ammonia concentration, and a coagulation panel were normal.

From the Department of Companion Animal and Special Species Medicine, College of Veterinary Medicine. North Carolma State University, Raleigh, North Carolina The authors thank Margaret Hemingway, Sharon Eldridge, and Debra Collins for help in preparing the manuscript No reprints available

41 3

414

SUBDURAL HEMATOMA

The dog’s neurologic status began to deteriorate again, and a second dose of mannitol was administered. After sedation with diazepam (0.2 mg/kg IV), anesthesia was induced with thiamylal sodium (10 mg/kg 1V) and maintained with isoflurane in oxygen. Ventilation was controlled to maintain a low normal PaC02 (approximately 30 mm Hg) and a high PaOz. Acid-base status and arterial pressure were monitored regularly throughout the anesthetic period.

Radiology Computed tomography of the head was performed before and after administration of 60% iothalamate meglumine ( 3 mL/kg, IV) for radiographic contrast (Figs. 13). There was a large region of decreased opacity over the right cerebral hemisphere, immediately under the calvarium. In the transverse images, there was a gradation of opacity in the abnormal region with the least opaque areas being dorsal (Fig. 2 ) . Collapse of the right ventricle and displacement of the falx cerebri to the left were evident. The contrast-enhanced CT images revealed a thin line of enhancement in the cerebral tissue, immediately underlying the hypo-opaque region. Differential diagnoses included cyst formation, lysing hematoma, abscess, and edema. Acute hemorrhage and

Fig. 2. Contrast-enhanced CT image. Image section is 10 rnm caudal to that in Figure 1. Findings are as in the nonenhanced image. Collapse of the right lateral ventricle, a line of increased opacity (hematoma membrane) medial to the hematoma, and the gradation in opacity of the abnormal region are visible.

organizing hematoma were less likely because their opacity is usually greater than or equal to the surrounding parenchyma on nonenhanced CT images.’ A cerebrospinal fluid (CSF) tap was not performed because of the clinical and radiologic indications of increased intracranial pressure and the attendant risk of brain herniation.

Surgery

Fig. 1. Computed tomographic (CT) image without contrast enhancement. Transverse image of the cranial vault just rostra1 to the diencephalon. There is a region of decreased opacity between the right calvarium and the brain parenchyma, and deviation of the falx cerebri to the left.

An exploratory craniectomy was performed. A lateral rostrotentorial approach was made over the right parietal lobe.’ An air-powered burr was used to excise a 4 cm X 4 cm bone flap from the calvarium. The dura mater was bulging, darkened, and purple-brown. Incision of the dura mater revealed a collection of watery, rust-brown floccular fluid containing many smzll, soft pieces of coagulum. The particulate components were more abundant in the ventral portion of the cavity. The underlying brain surface was mildly hyperemic and was separated from the calvarium by approximately l cm. The fluid was drained, and the subdural space was ir, ’ .ted thoroughly with sterile saline solution. The dura mater was partially closed with a continuous suture of size 4-0 absorbable polyglactin.* A remaining defect was covered with a fascia1 graft

*

Vicryl, Ethicon, Sornerville. New Jersey

41 5

HOPKINS AND WHEELER

One week after surgery, the dog showed signs of poorly localized pain by crying out when the thorax and abdomen were palpated. Despite this. the dog was alert and active, and ate and drank normally. Results of physical and neurologic examinations were normal. A moderately elevated alkaline phosphatase of 7 1 0 IU (normal 10-150 IU) was attributed to hepatic enzyme induction by elevated endogenous cortisol levels associated with stress, and perhaps to elevations in the bone isoenzyme due to the craniectomy. Thoracic and abdominal radiographs were normal. In the absence of a visceral abnormality to account for the pain. an aseptic meningitis or poorly defined posttraumatic "pain syndrome" were suspected.' A second CT scan was performed to evaluate the lesion and surgical site. The region of decreased density had disappeared. with brain parenchyma evident to the edge of the calvarium. A cerebrospinal fluid sample obtained from the cerebellomedullary cistern contained mildly elevated protein of 35 mg/dL (normal, < 25 mg/dL) with normal cytology. On the basis of the clinical signs of pain and the elevated cerebrospinal fluid protein, a mild nonseptic meningitis was suspected, although the previous surgical intervention could have accounted for the elevated protein. Aspirin (20 mg/kg orally, BID) was administered for the pain for 2 weeks. The dog was normal when examined at week 3, week 12. and year 1. Fig 3 Axial reconstruction of the contrast-enhanced CT scan made at the level of the horizontal solid white line in Figure 2 The region of decreased opacity over the right cerebral hemisphere that is the hematoma, the linear enhancementjust medial to the accumulation, and collapse of the right ventricle and displacement of the falx cerebri to the left are visible

obtained from the outer surface of the temporalis muscle. The bone flap was not replaced (surgeon's preference). and the muscle and skin incisions were closed. The fluid contained a predominance of crenated red blood cells, with occasional nondegenerate neutrophils and macrophages. The small pieces of coagulum appeared to be protein (possibly fibrin) mixed with degenerated erythrocytes. Aerobic and anaerobic cultures of the fluid were negative for growth. Postoperative therapy included cephalexin (22 mg/kg orally, TID) for 2 weeks and anticonvulsant medication (phenobarbital 2 mg/kg orally, BID) for 4 months. After a 4-month seizure-free period, anticonvulsant medication was gradually discontinued over 2 months. On the day after surgery, the dog was moderately depressed but would respond to its name, could stand, and was able to eat and drink. Symmetrical conscious propnoceptive deficits were present in all four limbs. Pupillary sizes and reflexes were normal. The dog's neurologic function improved over the following week.

Discussion Subdural hematomas, in which blood accumulates between the dura mater and arachnoid mater, are thought to arise from rupture of small veins traversing the subdural space.'.'" In the present case, the hematoma was clearly beneath the dura mater when observed at surgery, but the relationship of the fluid accumulation to the subarachnoid space could not be defined. The term subdural hematoma is used here because of the gross location and the striking similarity of all the case details with those of human subacute or chronic subdural hematoma. In humans, subdural hematomas are broadly classified into three categories according to the time elapsed between the traumatic incident and the onset of clinical signs. In acute subdural hematoma, the signs develop in less than 72 hours. In subacute subdural hematoma, the interval is 72 hours to 3 weeks, and in chronic subdural hematoma, it is more than 3 weeks after trauma.6.i',i2 The time between trauma and the development of signs of intracranial dysfunction is inversely related to the seventy of cerebral and vascular damage sustained at the time of Acute subdural hematoma is often accompanied by cerebral contusion and laceration.'." These lesions can be rapidly life threatening and are often difficult to distinguish on the basis of clinical signs. Chronic subdural hematoma is often associated with a minor traumatic episode that

416

SUBDURAL HEMATOMA

may have been forgotten by the time the patient develops clinical signs. Subacute subdural hematomas have an intermediate pattern of development of clinical signs. The exact pathogenesis of subacute and chronic subdural hematomas is unknown. Hematoma formation is associated initially with the formation of delicate surrounding membranes. The initial size of the hematoma is thought to determine its fate, with small accumulations undergoing spontaneous resorption with fibrous organization of the new membranes. Larger hematomas start to undergo clot lysis, become encysted, and may subsequently show a tendency to e ~ p a n d . ~Several . ‘ ~ observations suggest that the genesis of a local hyperfibrinolytic state leads to the development of an expanding hematoma. High levels of plasminogen activator in the membranes” and a plasmin complex in the fluid space16 have been observed, raising the possibility of increased plasmin production and subsequent fibrinolysis. Eosinophils in the membranes may secrete plasminogen into the fluid space.” Elevated fluid levels of fibrinogen degradation products (known anticoagulants) have been demon~ t r a t e d . ’ ~ ,Blood ’ ~ . ’ ~vessels in the membranes are poorly formed and leak erythrocytes into the fluid space.20This low-gradehemorrhage is perpetuated by the anticoagulant, fibrinolytic environment. Daily hemorrhage of up to 10% of the existing hematoma volume has been demonstrated.I8 Expansion of a subdural hematoma is thus primanly a result of persistent hemorrhage. Inflammatory mediators released by the hemorrhagic, clotting, and fibrinolytic processes may cause edema in surrounding neural tissue, contributing to this expansion. The permeability of the vessels of the membranes allows the latter to be visualized on contrast-enhanced CT images (Fig. 2). The clinical signs of subdural hematoma are largely related to increasing intracranial pressure, which gives rise to nonspecific signs of forebrain disease. Common signs in humans are headache, vomiting, and altered state of consciousness, which may vary from mild mental impairment to ~ o m a . ~ .Signs ~ . ’ of asymmetric involvement may include ipsilateral or contralateral hemiparesis, ipsilateral mydriasis, and p t ~ s i s .The ~ ocular signs are thought to be related to compression of the oculomotor nerve against the floor of the skull and, in humans, they are a more reliable indicator of the side of the lesion than the postural deficits.’ ‘ , I 2 Asymmetric transtentorial herniation and midbrain compression would also result in identical signs. The clinical signs of progressive forebrain disease with the development of lateralizing mydriasis in this dog are compatible with those reported in humans. Cephalic pain may have been the reason for the apparent increase in sensitivity to handling around the head. Because of the nonspecific clinical signs, there are many differential diagnoses to consider and subdural hematoma has been referred to as the “great neurological imitator.”2’



Consideration should be given to intracranial and extracranial brain disorders. Diagnosis of subdural hematoma in humans is usually made by CT scan, arteri~graphy,~.~-’ or, more recently, magnetic resonance imaging. Arteriography reveals displacement of meningeal vessels from the inner surface of the skull. In a CT scan, fresh hemorrhage is usually more opaque than the surrounding parenchyma, while organizing hematoma often has the same opacity. In the latter case, the presence of an expanding lesion is suggested by a shift of midline structures, which is referred to as mass effect.’ In chronic and subacute subdural hematoma, there is often much lysis of the hematoma, and the fluid becomes less opaque. The CT images in this case are identical to those of humans with subacute or chronic subdural hematoma. The features of importance are decreased opacity of the lesion, enhancement of the surrounding membranes by the contrast medium, and the evidence of mass effect (collapse of the lateral ventricle and shift of midline structures). The accumulation of cellular and proteinaceous debris at the ventral aspect of the lesion providing the gradation in density is also seen in humans and may be referred to as the “hematocrit” effect. Subdural hematomas are most often located over the frontal or parietal lobes. Lateral craniectomy was performed in this dog because the exact diagnosis was not clear from the CT images (mainly because of unfamiliarity of this problem in veterinary neurology), and the dog’s neurologic status was deteriorating despite attempts to lower the intracranial pressure. While the images were suggestive of a hematoma, other lesions might have been present. Anticonvulsant medication was administered to reduce the likelihood of postoperative seizures. A long course was used because about half of all humans who develop posttraumatic epilepsy suffer their first seizure within the first 6 months of the i n ~ i d e n t . ~ Treatment of subdural hematoma in humans usually involves evacuation of the fluid through burr holes, although in more severe cases a large craniotomy may be performed to assess and control persistent bleeding sites.5 The postoperative prognosis in patients with subacute or chronic subdural hematoma is usually favorable, but, because of the severity and coexistence of other lesions, acute subdural hematoma carries a much poorer prognosis. This case is an example of an unusual late sequela to cranial trauma in dogs. The possibility of such a development should be considered il, the management of head injury. Computed tomographic scanning is an appropriate diagnostic technique for the evaluation of head trauma in animals. In view of the favorable prognosis after surgical treatment, the recognition of subdural hematoma is important.

HOPKINS AND WHEELER

41 7

12. Echlin FA. Sordillo SVR. Carve) TQ. .Acute. subacute and chronic subdurai hematoma. J Am Med Assoc 1956: I6 I:1345- 1350. Oliver, JE. Jr. Intracranial injury. In: Kirk RW. ed. firrrcwr l'Philadelphia: . WB Saunders Co. 1987:470-492. 10. Yamashima T. Friede RL. Why do bridging veins rupture into virtual subdural space? J Neurol Neurosurg Psychiatry 19x4: 47: I 2 I -

127. 1 I. McKissock W. Richardson A. Bloom WH. Subdural haematoma.

A review of 389 cases. Lancet 1960: 2: 1365-1 369.

200. 16. Saito K, Ito H. Hasegawa T. Yamamoto S. Plasmin-02-plasmin inhibitor complex and (ul-plasmin inhibitor in chronic subdural hematoma. J Neurosurg 1989: 70:68-72. 17. Yamashima 1.Kubota P. Yarnomoto S. Eosinophil degranulation in the capsule of chronic subdural hematornas. J Neurosurg 1985: 62:257-260. 18. Ito H. Yamarnoto S. Kornai T. Miiukoshi H. Role of local hyperfibrinolqsis in the etiology ofchronic subdural hematoma. J Neurosurg 1976: 45:26-31. 19. Weir B. Gordon P. Factors affecting coagulation: Fibrinolysis in chronic subdural fluid collections. J Neurosurg 1983: 58:142245. 20. Yamashima 1.Yarnarnoto S. Friede RI-. The role of endothelial gap junctions in the enlargement of chronic subdural hematomas. J Neurosurg 19x3: 59:298-303. 21. Black DW. Subdural hematoma: A retrospective study ofthe "great neurological imitator." Postgrad Med 1985: 78: 107-1 14.

Abstract of Current Literature PENTOXIFYLLINE. A METHY LXANTHINE DERIVATIVE. PREVENTS POSTSURGICAL ADHESION REFORMATION IN RABBITS Steinleitner A, Lambert H. Kazensky C. Danks P. Roy S Obstetrics & Gjwcolog!' 1990; 75:926-928 Previous studies from our laboratory have demonstrated pentoxifylline to be a potent inhibitor of primary post-traumatic adhesion formation in a rodent model. To evaluate pentoxifylline in a situation more closely mimicking the events encountered in infertility surgery. we developed a model for adhesion reformation after lysis of pelvic adhesions. New Zealand White rabbits received a standardized primary traumatic lesion to the left uterine horn. One week later. a laparotomy was performed for evaluation (prescore) and subsequent lysis of adhesions. After closure, the animals were randomized to treatment with vehicle or subcutaneous pentoxifylline, 2.5 mg/kg, administered at 1 '-hour intervals for six doses. Seven days later, the rabbits were euthanatized and evaluated in a blinded manner to quantify adhesion reformation (postscore). Using a scoring scale from 0 = no adhesions to 4+ = most severe, the mean prescore was not different between pentoxifylline-treated and control rabbits (3.8 v t v x f s 3.9, respectively). However, the mean postscore (.7 wrszis 3.7, respectively) was markedly reduced by pentoxifylline ( p < .OO I ). These data demonstrate a marked inhibition of adhesion reformation after lysis of pelvic adhesions under the influence of pentoxifylline in rabbits.

Subdural hematoma in a dog.

A traumatic subacute subdural hematoma in a dog was diagnosed by computed tomography and treated successfully by craniectomy and surgical drainage...
940KB Sizes 0 Downloads 0 Views