Plum and posner’s diagnosis of stupor and coma fourth Edition series editor sid Gilman, md, frcp
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scale is adequate for all patients; hence, the best policy in recording the results of the coma examination is simply to describe the findings. Nevertheless, the GCS is widely used, and still is probably the best for most trauma patients. 5 It is useful to obtain GCS scores, which can be compared against large databases to evaluate prognosis for specific etiologies of coma (see Chapter 9). FOUR Score (Full Outline of Unresponsiveness) 109
Eye Response 4 ¼ eyelids open or opened, tracking, or blinking to command 3 ¼ eyelids open but not tracking 2 ¼ eyelids closed but open to loud voice 1 ¼ eyelids closed but open to pain 0 ¼ eyelids remain closed with pain Motor Response 4 ¼ thumbs-up, fist, or peace sign 3 ¼ localizing to pain 2 ¼ flexion response to pain 1 ¼ extension response to pain 0 ¼ no response to pain or generalized myoclonus status Brainstem Reflexes 4 ¼ pupil and corneal reflexes present 3 ¼ one pupil wide and fixed 2 ¼ pupil or corneal reflexes absent 1 ¼ pupil and corneal reflexes absent 0 ¼ absent pupil, corneal, and cough reflex Respiration 4 ¼ not intubated, regular breathing pattern 3 ¼ not intubated, Cheyne-Stokes breathing pattern 2 ¼ not intubated, irregular breathing 1 ¼ breathes above ventilator rate 0 ¼ breathes at ventilator rate or apnea (continued) 41
make only nonspecific motor responses (winc- ing, restlessness, withdrawal reflexes) without a directed attempt to defend against the stim- ulus are considered to have a nonlocalizing re- sponse and are comatose. Patients who fail to respond at all are in the deepest stage of coma. This rough grading system, from verbal re- sponsiveness, to localizing responses, to non- localizing responses, to no response, is all that is needed for an initial assessment of the depth of unresponsiveness that can be used to follow the progress of the patient. If the initial eval- uation of the level of consciousness demon- strates impairment, it is essential to progress through the next steps of the coma examina- tion as rapidly as possible to safeguard that patient’s life. More elaborate coma scales are described in Box 2–1, but many of these de- pend upon the results of later stages in the examination, and it is never justified to de- lay attending to the basics of airway, breathing, and circulation while performing a more elab- orate scoring evaluation. ABC: AIRWAY, BREATHING, CIRCULATION It is critical to ensure that the patient’s airway is maintained, that he or she is breathing ad- Glasgow Coma Scale Eye Response 4 ¼ eyes open spontaneously 3 ¼ eye opening to verbal command 2 ¼ eye opening to pain 1 ¼ no eye opening Motor Response 6 ¼ obeys commands 5 ¼ localizing pain 4 ¼ withdrawal from pain 3 ¼ flexion response to pain 2 ¼ extension response to pain 1 ¼ no motor response Verbal Response 5 ¼ oriented 4 ¼ confused 3 ¼ inappropriate words 2 ¼ incomprehensible sounds 1 ¼ no verbal response A GCS score of 13 or higher indicates mild brain injury, 9 to 12 moderate brain injury, and 8 or less severe brain injury. AVPU ACDU
Is the patient Is the patient Alert and oriented? Alert and oriented? Responding to voice? Confused? Responding to pain? Drowsy?
Unresponsive? Unresponsive? Box 2–1 Coma Scales (cont.) 42 Plum and Posner’s Diagnosis of Stupor and Coma equately, and that there is sufficient arterial perfusion pressure. The first goal must be to correct any of these conditions if they are found inadequate (Chapter 7). In addition, blood pres- sure, heart rate, and respiration may provide valuable clues to the cause of coma. Circulation It is critical first to ensure that the brain is receiving adequate blood flow. Cerebral per- fusion pressure is the systemic blood pressure minus the intracranial pressure. The physician can measure blood pressure but in the ini- tial examination can only estimate intracranial pressure. Over a wide range of blood pres- sures, cerebral perfusion remains stable be- cause the brain autoregulates its blood flow by mechanisms described in the paragraphs be- low and illustrated in Figure 2–2. If the blood pressure falls too low or becomes too high, autoregulation fails and cerebral perfusion fol- lows perfusion pressure passively; that is, it falls as the blood pressure falls and rises as the blood pressure rises. In this situation, both too low (ischemia) and too high (hypertensive en- cephalopathy; see Chapter 5) a blood pres- sure can damage the brain. To ensure adequate brain perfusion, the physician should attempt to maintain the blood pressure at a level nor- mal for the individual patient. For example, a patient with chronic hypertension autoregu- lates at a higher level than a normotensive pa- tient. Lowering the blood pressure to a ‘‘normal level’’ may deprive the brain of an adequate blood supply (see Figure 2–2). Conversely, the cerebral blood flow (CBF) in children and pregnant women, who normally run low blood pressures, is regulated at lower levels and may develop excessive perfusion if the blood pres- sure is raised (e.g., pre-eclampsia). The perfusion pressure of the brain may be influenced by the position of the head. In a normal individual, as the head is raised, the systemic arterial pressure is maintained by blood pressure reflexes. At the same time, the arterial perfusion pressure to the head is re- duced by the distance the head is raised above the heart, but the intracranial pressure is also reduced because of the improved venous and cerebrospinal fluid (CSF) drainage. The net effect is that there is very little change in brain perfusion pressure or CBF. On the other hand, in a patient with stenosis of a carotid or ver- tebral artery, the perfusion pressure for that vessel may be much lower than systemic arte- rial pressure. If the head of the bed is raised, Figure 2–2. Cerebral autoregulation in hypertension. Schematic representation of autoregulation of cerebral blood flow (CBF) in normotensive (solid line) and hypertensive (dashed line) subjects. In both groups, within a range of about 100 mm Hg, increases or decreases in mean arterial pressure are associated with maintenance of CBF due to appropriate changes in arteriolar resistance. Changes in pressure outside this range are eventually associated with loss of autoregu- lation, leading to a reduction (with hypotension) or an elevation (with marked hypertension) in CBF. Note that hyper- tensive encephalopathy (increased blood flow with pressures exceeding the autoregulatory range) may occur with a mean arterial pressure below 200 mm Hg in the normotensive individual, but may require a much higher mean arterial pressure in patients who have sustained hypertension. Conversely, lowering blood pressure to the ‘‘normal range’’ of a mean arterial pressure of 80 mm Hg (equivalent to 120/60) may produce a clinically significant fall in CBF, particularly if there is a pre- existing cerebrovascular stenosis. Examination of the Comatose Patient 43
perfusion pressure may fall below the thresh- old for autoregulation, and blood flow may be diminished below the level needed to support neurologic function. Such patients may show improvement in neurologic function when the head of the bed is flat. Conversely, in cases of head trauma where there is increased intra- cranial pressure, it may be important to raise the head of the bed 15 to 30 degrees to im- prove venous drainage to maximize cerebral perfusion pressure. 6 Similarly, it is necessary to remove tight neckwear and ensure that a cervical spine collar is not applied too tightly to a victim of head injury to avoid diminishing venous outflow from the brain. In a patient with impaired consciousness, the blood pressure can give important clues to the level of the nervous system that has been damaged. Damage to the descending sympa- thetic pathways that support blood pressure may result in a fall to levels seen after spinal transaction (mean arterial pressure about 60 to 70 mm Hg). Blood pressure is supported by a descending sympathoexcitatory pathway from the rostral ventrolateral medulla to the spinal cord, and so damage along the course of this pathway can result in spinal levels of blood pressure. The hypothalamus in turn provides a descending sympathoexcitatory input to the medulla and the spinal cord. 7,8
As a conse- quence, bilateral diencephalic lesions result in a fall in sympathetic tone, including mei- otic pupils (see below), decreased sweating re- sponses, and a generally low level of arterial pressure. 9 However, persistent hypotension below these levels in a comatose patient is almost never caused by an acute neurologic injury. One of the most common mistakes seen in evaluation of a comatose patient with a mean arterial pres- sure below 60 mm Hg is the assumption that a neurologic event may have caused the hypo- tension. This is almost never the case. A mean arterial pressure at or above 60 mm Hg is gen- erally sufficient in a supine patient to support cerebral and systemic function. On the other hand, acute hypotension, due to cardiogenic or vasomotor shock, is a common cause of loss of consciousness and a threat to the patient’s life. Thus, the initial evaluation of a comatose pa- tient with low blood pressure should focus on identifying the cause of and correcting the hypotension. On the other hand, lesions that result in stim- ulation of the sympathoexcitatory system may cause an increase in blood pressure. For exam- ple, pain is a major ascending sympathoexcit- atory stimulus, which acts via direct collaterals from the ascending spinothalamic tract into the rostral ventrolateral medulla. The elevation of blood pressure in response to a painful stim- ulus applied to the body (pinch of skin, ster- nal rub) is evidence of intact medullospinal connections. 10,11 In a patient who is still semi- wakeful after subarachnoid hemorrhage, blood pressure may be elevated as a response to head- ache pain. Each of these conditions is associ- ated with a rise in heart rate as well. Direct pressure to the floor of the medulla can activate the Cushing reflex, an increase in blood pressure and a decrease in heart rate. 12 In children, the Cushing reflex may be seen when there is a generalized increased intracra- nial pressure, even above the tentorium. How- ever, the more rigid compartmentalization of intracranial contents in adults usually prevents this phenomenon unless the expansile mass is in the posterior fossa. Activation of descending sympathoexcita- tory pathways from the forebrain may also ele- vate blood pressure. Irritative lesions of the hy- pothalamus, such as occur with subarachnoid hemorrhage, may result in an excess hypotha- lamic input to the sympathetic and parasym- pathetic control systems. 13 This condition can trigger virtually any type of cardiac arrhythmia, from sinus pause to supraventricular tachycar- dia to ventricular fibrillation. 14 However, the most common finding in subarachnoid hemor- rhage is a pattern of subendocardial ischemia. Such patients may in fact have enzyme evi- dence of myocardial infarction, and at autopsy demonstrate contraction band necrosis of the myocardium. 15 Sympathoexcitation is also seen in patients who are delirious. The infralimbic and insular cortex and the central nucleus of the amygdala provide important inputs to sympathoexcit- atory areas of the hypothalamus and the me- dulla. 8
ception of stimuli in the environment causing emotional responses such as fear or anger may result in hypertension, tachycardia, and en- larged pupils. Stokes-Adams attacks are periods of brief loss of consciousness due to lack of adequate 44 Plum and Posner’s Diagnosis of Stupor and Coma cerebral perfusion. These almost always oc- cur in an upright position. In recumbent po- sitions, when the head is at the same height as the heart, it takes a much steeper fall in blood pressure (below 60 to 70 mm Hg mean pres- sure) to cause loss of consciousness. The fall in blood pressure during a Stokes-Adams attack may reflect a failure of the baroreceptor reflex arc on assuming an upright posture (in which case it can be reproduced by testing orthostatic responses). Alternatively, hyperactivity of the baroreceptor reflex nerves may occasionally cause hypotension (e.g., in patients with carotid sinus hypersensitivity or glossopharyngeal neu- ralgia, where brief bursts of activity in barore- ceptor nerves trigger a rapid fall in heart rate and blood pressure). 16,17
In other patients, the fall in blood pressure may be caused by an in- termittent failure of the pump (i.e., cardiac ar- rhythmia). Thus, careful cardiologic evaluation is required if a neurologic cause is not identified. PATHOPHYSIOLOGY The brain ordinarily tightly controls the cir- culation to provide an adequate level of cere- bral perfusion. It does this in two ways. First, across a wide range of arterial blood pressures, it autoregulates its own blood flow. 18–21
The mechanism for this remarkable stability of blood flow is not entirely understood, although it appears to be due to intrinsic innervation of the cerebral blood vessels and may also be regulated by local metabolism. 20,22 In general, local increases in CBF correspond to increases in local metabolic rate, allowing the use of blood flow (in positron emission tomography [PET] imaging) or local blood volume (in functional magnetic resonance imaging [MRI]) to approx- imate neuronal activity. However, there are also neuronal networks that regulate cerebral perfu- sion distinct from metabolic need. The two sys- tems normally act in concert to ensure sufficient blood supply to allow normal cerebral function over a wide range of blood pressures but are dysregulated following some brain injuries. Second, the brain acts through the auto- nomic nervous system to acutely adjust sys- temic arterial pressure in order to maintain a pressure head that is within the range that al- lows cerebral autoregulation. Blood pressure is the product of the cardiac output times the total vascular peripheral resistance. Cardiac output in turn is the product of heart rate and stroke volume. Both heart rate and stroke vol- ume are increased by beta-1 adrenergic stim- ulation from sympathetic nerves (or adrenal catechols), which play a key role in regulating cardiac output. Heart rate is slowed by mus- carinic cholinergic action of the vagus nerve, and hence, increased vagal tone decreases car- diac output. Peripheral resistance is regulated mainly by the level of alpha-1 adrenergic tone in small arterioles, the most important resis- tance vessels. Therefore, the blood pressure is regulated by the balance of sympathetic tone, which increases both cardiac output and vaso- constrictor tone, versus parasympathetic tone, which slows heart rate and therefore decreases cardiac output. The cardiac vagal tone is main- tained by the nucleus ambiguus in the medulla, which contains most of the cardiac parasym- pathetic preganglionic neurons. 23 Sympathetic vascular and cardiac sympathetic tone is set by neurons in the rostral ventrolateral medulla that provide a tonic activating input to the sym- pathetic preganglionic neurons in the thoracic spinal cord. 24 When in a lying position, the brain is at the same level as the heart, but as one rises, the brain elevates to a position 20 to 30 cm above the heart. This drop in perfusion pressure (ar- terial pressure minus intracranial pressure) is equivalent to 15 to 23 mm Hg, and it may be sufficient to cause a drop in cerebral perfusion pressure that would make it difficult to main- tain CBF necessary to allow conscious brain function. To defend against such a precipitous fall in perfusion pressure, the brain maintains reflex mechanisms to compensate for the hydrody- namic consequences of gravity. The level of arterial pressure is measured at two sites, the aortic arch (by the aortic depressor nerve, a branch of the vagus nerve) and the carotid bi- furcation (by the carotid sinus nerve, a branch of the glossopharyngeal nerve). These two nerves terminate in the brain in the nucleus of the solitary tract, which is the main relay for all visceral sensory information in the brain. 25,26
The nucleus of the solitary tract then provides an excitatory input to the caudal ventrolateral medulla. 27 The caudal ventrolateral medulla in turn pro- vides an ascending inhibitory input to the tonic vasomotor neurons in the rostral ventrolateral Examination of the Comatose Patient 45
medulla. 28 In addition, the nucleus of the soli- tary tract provides both direct and relayed excit- atory inputs to the cardiac decelerator neurons in the nucleus ambiguus. 27 Thus, a rise in blood pressure results in a reflex fall in heart rate and vasomotor tone, re-establishing a normal arte- rial pressure. Conversely, a fall in blood pres- sure causes a reflex tachycardia and vasocon- striction, re-establishing the necessary arterial perfusion pressure. As a result, on assuming an upright posture, there is normally a small in- crease in both heart rate and blood pressure. On occasion, loss of consciousness may re- sult from failure of this baroreceptor reflex arc. In such patients, measurement of standing and supine blood pressure and heart rate discloses a fall in blood pressure on assuming an upright posture that is clinically associated with symp- toms of insufficient CBF. Rigid criteria for di- agnosing orthostatic hypotension (e.g., a fall in blood pressure of 10 or 15 mm Hg) are not useful, as systemic arterial pressure is usually measured in the arm but the symptoms are produced by decreased blood flow to the brain. A pressure head that is adequate to perfuse the arm (which is at the same elevation as the heart) will be reduced by 15 to 23 mm Hg at the brain in an upright posture, and if perfu- sion pressure to the brain falls even a few mm Hg below the level needed to maintain auto- regulation, the drop in cerebral perfusion may be precipitous. The most common nonneurologic causes of orthostatic hypotension, including low intravas- cular volume (often a consequence of diuretic administration or inadequate fluid intake), car- diac pump failure, and medications that impair arterial constriction (e.g., alpha blockers or di- rect vasodilators), do not impair the tachycardic response. Most neurologic cases of orthostatic hypotension, including peripheral autonomic neuropathy or central or peripheral autonomic degeneration, impair both the heart rate and the blood pressure responses. Put in other words, the hallmark of baroreceptor reflex fail- ure is absence of the elevation of heart rate when arterial pressure falls in response to an orthostatic challenge. Respiration The brain cannot long survive without an ad- equate supply of oxygen. Within seconds of being deprived of oxygen, brain function be- gins to fail, and within minutes neurons begin to die. The physician must ensure that respi- ration is supplying adequate oxygenation. To do this requires examination of both respiratory exchange and respiratory pattern. Listening to the chest will ensure that there is adequate movement of air. A normal patient at rest will regularly breathe at about 14 breaths per min- ute and the exchange of air can be heard at both lung bases. The physician should estimate from the rate and depth of respiration whether the patient is hypo- or hyperventilating or whether respiration is normal. The patient’s color is a gross indicator of oxygenation: cya- nosis indicates deficient oxygenation; a cherry red color may also indicate deficient oxygena- tion because of CO intoxication. A better esti- mate of oxygenation can be achieved by plac- ing an oximeter on the finger; many intensive care units and some emergency departments also measure expired CO 2 , which correlates well with PCO 2 . This section considers the neuroanatomic basis of respiratory abnormalities that accom- Table 2–2 Neuropathologic Correlates of Breathing Abnormalities Forebrain damage Epileptic respiratory inhibition Apraxia for deep breathing or breath holding ‘‘Pseudobulbar’’ laughing or crying Posthyperventilation apnea Cheyne-Stokes respiration Hypothalamic-midbrain damage Yüklə 9,02 Mb. Dostları ilə paylaş:
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