Plum and posner’s diagnosis of stupor and coma fourth Edition series editor sid Gilman, md, frcp
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118 Plum and Posner’s Diagnosis of Stupor and Coma Chapter 4 Specific Causes of Structural Coma INTRODUCTION SUPRATENTORIAL COMPRESSIVE LESIONS EPIDURAL, DURAL, AND SUBDURAL MASSES Epidural Hematoma Subdural Hematoma Epidural Abscess/Empyema Dural and Subdural Tumors SUBARACHNOID LESIONS Subarachnoid Hemorrhage Subarachnoid Tumors Subarachnoid Infection INTRACEREBRAL MASSES Intracerebral Hemorrhage Intracerebral Tumors Brain Abscess and Granuloma INFRATENTORIAL COMPRESSIVE LESIONS EPIDURAL AND DURAL MASSES Epidural Hematoma Epidural Abscess Dural and Epidural Tumors SUBDURAL POSTERIOR FOSSA COMPRESSIVE LESIONS Subdural Empyema Subdural Tumors SUBARACHNOID POSTERIOR FOSSA LESIONS INTRAPARENCHYMAL POSTERIOR FOSSA MASS LESIONS Cerebellar Hemorrhage Cerebellar Infarction Cerebellar Abscess Cerebellar Tumor Pontine Hemorrhage SUPRATENTORIAL DESTRUCTIVE LESIONS CAUSING COMA VASCULAR CAUSES OF SUPRATENTORIAL DESTRUCTIVE LESIONS Carotid Ischemic Lesions Distal Basilar Occlusion Venous Sinus Thrombosis Vasculitis INFECTIONS AND INFLAMMATORY CAUSES OF SUPRATENTORIAL DESTRUCTIVE LESIONS Viral Encephalitis Acute Disseminated Encephalomyelitis CONCUSSION AND OTHER TRAUMATIC BRAIN INJURIES Mechanism of Brain Injury During Closed Head Trauma Mechanism of Loss of Consciousness in Concussion Delayed Encephalopathy After Head Injury INFRATENTORIAL DESTRUCTIVE LESIONS 119
BRAINSTEM VASCULAR DESTRUCTIVE DISORDERS Brainstem Hemorrhage Basilar Migraine Posterior Reversible Leukoencephalopathy Syndrome
INFRATENTORIAL INFLAMMATORY DISORDERS INFRATENTORIAL TUMORS CENTRAL PONTINE MYELINOLYSIS INTRODUCTION The previous chapter divided structural lesions causing coma into compressive and destruc- tive lesions. It further indicated that lesions could be supratentorial, compressing or destroy- ing the diencephalon and upper midbrain, or infratentorial, directly affecting the pons and cerebellum. A physician attempting to deter- mine the cause of coma resulting from a struc- tural lesion must establish first the site of the lesion, determining whether the lesion is supra- tentorial or infratentorial, and second whether the lesion is causing its symptoms by compres- sion or destruction or both. Those considera- tions were the focus of Chapter 3. This chapter discusses, in turn, the specific causes of supra- tentorial and infratentorial compressive and de- structive lesions that cause coma. Although these designations are useful for rapid bedside diagnosis, it is of course possible for a lesion such as an intracerebral hemor- rhage both to destroy and to compress normal tissues. Extracerebral mass lesions can also cause sufficient compression to lead to infarc- tion (i.e., tissue destruction). Thus, in some instances, the division is arbitrary. However, the types of conditions that cause the com- pression versus destruction of neural tissue tend to be distinct, and often they have distinct clinical presentations as well. The guide pro- vided in this chapter, while not exhaustive, is meant to cover the most commonly encoun- tered causes and ones where understanding their pathophysiology can influence diagnosis and treatment (Table 4–1). When any structural process impairs con- sciousness, the physician must find a way to halt the progression promptly or the patient will run the risk of irreversible brain damage or death. Beyond that generality, different struc- tural lesions have distinct clinical properties that govern the rate of progression, hint at the diagnosis, and may dictate the treatment. Structural causes of unconsciousness often cause focal signs that help localize the lesion, particularly when the lesion develops acutely. However, if the lesion has developed slowly, over a period of many weeks or even months, it may attain a remarkably large size without causing focal neurologic signs. In those cases, the first evidence of a space-occupying lesion may be signs of increased intracranial pressure (e.g., headache, nausea) or even herniation itself (see Patient 3–2). SUPRATENTORIAL COMPRESSIVE LESIONS The supratentorial compartments are domi- nated by the cerebral hemispheres. However, many of the most dangerous and difficult le- sions to diagnose involve the overlying me- ninges. Within the hemisphere, a compressive lesion may originate in the gray matter or the white matter of the hemisphere, and it may di- rectly compress the diencephalon from above or laterally (central herniation) or compress the midbrain by herniation of the temporal lobe through the tentorial notch (uncal herniation). In addition, there are a number of compressive lesions that affect mainly the diencephalon. EPIDURAL, DURAL, AND SUBDURAL MASSES Tumors, infections, and hematomas can oc- cupy the epidural, dural, and subdural spaces to eventually cause herniation. Most epidural tumors result from extensions of skull lesions that grow into the epidural space. Their growth is relatively slow; they mostly occur in patients with known cancer and are usually discovered long before they affect consciousness. Dural tu- mors, by contrast, are usually primary tumors of the meninges, or occasionally metastases. 120
Plum and Posner’s Diagnosis of Stupor and Coma Epidural or subdural hematomas, on the other hand, may develop acutely or subacutely and can be a diagnostic problem. Epidural Hematoma Because the external leaf of the dura mater forms the periosteum of the inner table of the skull, the space between the dura and the skull is a potential space that accumulates blood only when there has been an injury to the skull itself. Epidural hematomas typically result from head trauma with a skull fracture that crosses a groove in the bone containing a meningeal vessel (see Figure 4–1). The ruptured vessel may be either arterial or venous; venous bleeding usually de- velops slowly and often is self-limiting, having a course more similar to subdural hematomas, which are discussed below. On rare occasions, epidural hematomas may result from bleeding into skull lesions such as eosinophilic granulo- ma,
1 metastatic skull or dural tumors, 2 or cra-
niofacial infections such as sinusitis. 3 Arterial bleeding is usually under high pres- sure with the result that the vessel may not seal and blood continues to accumulate. Thus, in- stead of causing symptoms that develop slowly or wax and wane over days or weeks, a patient with an epidural hematoma may pass from hav- ing only a headache to impairment of con- sciousness and signs of herniation within a few hours after the initial trauma. Although epidural hematomas can occur frontally, occipitally, at the vertex, 4 or even on the side opposite the side of trauma (contre- coup),
5 the most common site is in the lateral temporal area as a result of laceration of the middle meningeal artery. Trauma sufficient to cause such a fracture may also fracture the skull base. For this reason, it is necessary for the examiner to be alert to signs of basal skull fracture on examination, such as blood behind the tympanic membrane or ecchymosis of the skin behind the ear (Battle’s sign) or around the eyes (raccoon eyes). The epidural hemor- rhage pushes the brain medially, and in so do- ing stretches and tears pain-sensitive menin- ges and blood vessels at the base of the middle fossa, causing headache. However, the head- ache is often attributed to the original head injury, and unless the lesion causes sufficiently increased intracranial pressure (ICP) to pro- duce nausea and vomiting, the condition may Table 4–1 Examples of Structural Causes of Coma Compressive Lesions Destructive Lesions Cerebral hemispheres Cerebral hemispheres Epidural and subdural hematomas, tumors, and abscesses Subarachnoid hemorrhages, infections (meningitis), and tumors (leptomeningeal neoplasms)* Intracerebral hemorrhages, infarcts, tumors, and abscesses Hypoxia-ischemia Hypoglycemia Vasculitis Encephalitis Leukoencephalopathy Prion diseases Progressive multifocal leukoencephalopathy Diencephalon Diencephalon Basal ganglia hemorrhages, tumors, infarcts, and abscesses* Pituitary tumor Pineal tumor Thalamic infarct Encephalitis Fatal familial insomnia Paraneoplastic syndrome Tumor
Brainstem Brainstem Cerebellar tumor Cerebellar hemorrhage Cerebellar abscess Infarct
Hemorrhage Infection *Both compressive and destructive. Specific Causes of Structural Coma 121
not be recognized. Subsequently, the hema- toma compresses the adjacent temporal lobe and causes uncal herniation with gradual im- pairment of consciousness. Early dilation of the ipsilateral pupil is often seen followed by complete ophthalmoparesis and then impair- ment of the opposite third nerve as the herni- ation progresses. 6 Motor signs often occur late in such cases. In many patients the degree of head trauma is less than one might expect to cause a frac- ture. In Jamieson and Yelland’s series, for exam- ple, of 167 patients with epidural hematoma, nearly one-half had no initial loss of con- sciousness, 7 and in Gallagher and Browder’s equally large series, two-thirds of such patients had an initial injury too mild to command hospital attention. 8 This is particularly true in children, one-half of whom have suffered a fall of less than one-half meter, and many of whom complained of nonspecific symptoms. 9 Only 15% to 20% of patients had the ‘‘classic’’ his- tory of traumatic loss of consciousness, fol- lowed by a lucid interval and then a relapse into coma (patients who ‘‘talk and die’’). 10 Thus,
even though most epidural hematomas are identified by computed tomography (CT) scans performed acutely in emergency departments on trauma patients by using current evidence- based decision paradigms, 11,12
the examiner must remain alert to the possibility of an epi- dural hematoma that develops or rapidly en- larges after an apparently negative CT. It is therefore important to review the CT scan of trauma patients with attention directed to whether there is a skull fracture that crosses the middle meningeal groove. The hematoma appears as a hyperdense, lens-shaped mass be- tween the skull and the brain (i.e., the hema- toma is convex on both surfaces; subdural he- matomas, by comparison, are concave on the surface facing the brain; see Figure 4–1). A vertex hematoma may be missed on a routine axial CT scan, 13 but a coronal reconstruction should identify the lesion. 4 A magnetic reso- nance imaging (MRI) scan is not required for evaluation of an epidural hematoma, but may be necessary to evaluate contusions and edema in the underlying brain. In addition, mass le- sions outside the brain may cause hyperdensity Figure 4–1. A pair of computed tomography scans showing an epidural hematoma. The image in (A) shows the lens- shaped (biconvex), bright mass along the inner surface of the skull. In (B), the skull is imaged with bone windows, showing a fracture at the white arrow, crossing the middle meningeal groove. 122 Plum and Posner’s Diagnosis of Stupor and Coma of subarachnoid cisterns that may be mistaken for subarachnoid hemorrhage on CT, but is probably an artifact of partial volume averag- ing.
14 In these instances, MRI helps rule out subarachnoid hemorrhage. In those circumstances where CT scan is not readily available, a plain skull film can often identify the fracture. Certainly, all patients with head trauma should be cautioned that it is im- portant to remain under the supervision of a family member or friend for at least 24 hours; the patient must be returned to the hospital immediately if a lapse of consciousness occurs. Careful follow-up is required even in patients in whom the original CT was negative, as oc- casionally the development of the hematoma is delayed. 15 In comatose patients with epidural hemato- mas, the treatment is surgical evacuation. The surgery is an emergency, as the duration from time of injury to treatment is an important determinant of the prognosis. 16 Other factors in determining outcome are age, depth of coma, degree of midline shift, and size of the hema- toma. 17
recover, even those whose pupils are dilated and fixed before surgery. 18 Rarely, acute epi- dural hematomas resolve spontaneously, prob- ably a result of tamponade of the bleeding vessel by underlying edematous brain. 19 Subdural Hematoma The unique anatomy of the subdural space also can produce much slower, chronic subdural hematomas in patients in whom the history of head trauma is remote or trivial. The potential space between the inner leaf of the dura mater and the arachnoid membrane (subdural space) is traversed by numerous small draining veins that bring venous blood from the brain to the dural sinus system that runs between the two leaves of the dura. These veins can be dam- aged with minimal head trauma, particularly in elderly individuals with cerebral atrophy in whom the veins are subject to considerable movement of the hemisphere that may occur with acceleration-deceleration injury. When focal signs are absent, these cases can be quite difficult to diagnose. A useful rule when faced with a comatose patient is that ‘‘it could always be a subdural,’’ and hence imaging is needed even in cases where focal signs are absent. Subdural bleeding is usually under low pres- sure, and it typically tamponades early unless there is a defect in coagulation. Acute subdural bleeding is particularly dangerous in patients who take anticoagulants for vascular throm- botic disease. Continued venous leakage over several hours can cause a mass large enough to produce herniation. Warfarin inhibits the syn- thesis of vitamin K-dependent clotting factors II, VII, IX, and X and the anticoagulant pro- teins C and S. The conventional treatment in- cludes administering fresh frozen plasma and vitamin K. However, these measures take hours to days to become effective and are too slow to stop subdural bleeding. Hence, in the case of a subdural (or epidural) bleed in a patient on warfarin, it is important to administer pooled cryoprecipitate of factors II, VII, IX, and X immediately. Recombinant factor VII has also been used, 20 but data are lacking as to its ef- fectiveness. Acute subdural hematomas, which are usu- Yüklə 9,02 Mb. Dostları ilə paylaş:
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