Plum and posner’s diagnosis of stupor and coma fourth Edition series editor sid Gilman, md, frcp
Yüklə 9,02 Mb. Pdf görüntüsü
|
|
8% 28%
24% Mod Disab Good Recov 0% 10% 75% No Yes No At least
localizing? At least
inappropriate words?
At least withdrawal? Figure 9–3. (A-D) The best 1-year outcome for 500 conventionally treated patients in coma from nontraumatic causes. For each time period following onset, the diagram correlates the degree of recovery with clinical signs. The numbers are, in most instances, sufficiently large to provide a basis for estimating prognosis among similarly affected patients in the future. (From Levy et al., 4 with permission.) Consciousness, Mechanisms Underlying Outcomes, and Ethical Considerations 351
CARDIOPULMONARY ARREST/ HYPOXIC-ISCHEMIC ENCEPHALOPATHY Several large studies have examined outcome in coma specifically following cardiac arrest. Data from 942 patients prospectively enrolled in the Brain Resuscitation Clinical Trials 35 (circa 1979 to 1994) demonstrated that loss of any of the cranial nerve reflexes following car- diac arrest significantly predicted poor out- come. Booth and associates 2 reviewed all avail- able large studies of coma following cardiac arrest from 1966 to 2003 to assess the precision and accuracy of the physical examination in prognosis. They found that five clinical signs were strongly predictive of death, VS, or severe disability (GOS 1, 2, or 3): absent corneal re- flexes, absent pupillary reflexes, absent with- drawal to painful stimuli, absent motor re- sponse at 24 hours, and absent motor response at 72 hours. Notably, no clinical examination finding strongly predicted a GOS of 4 or 5. In the aggregate, the data shown in Table 9–8 support the algorithms shown in Figure 9–3 and add further details as well as time points. It should be recognized that the Booth et al. pre- dictors aggregate severely disabled outcomes (GOS 3) with outcomes of death or permanent VS (GOS 1 and 2). Thus, careful explanation of the predicted outcomes is required if the physician uses these data to counsel families, as choices concerning severe disability may differ widely (see family dynamics and philosophic considerations, page 379). ELECTROPHYSIOLOGIC TESTING IN HYPOXIC-ISCHEMIC ENCEPHALOPATHY Although the physical examination gives a strong prediction of poor outcome, it does not accurately assess the extent of cortical injury. Electrophysiologic testing adds valuable data. SSEPs provide the best predictors of poor Table 9–7 Two-Week Outcome of Nontraumatic Coma and Coma Etiology Two-Week Outcome Coma Etiology No. (%)
% Awake % Dead
% Coma Hypoxic/ischemic 61 (36.1) 21.3
54.1 24.6
Metabolic or septic 37 (21.8) 32.4 48.7
18.9 Focal cerebral injury 38 (22.5) 34.2
47.4 18.4
Generalized cerebral injury 22 (13.0) 45.4 36.4
18.2 Drug induced 11 (6.5) 72.7
0 27.3
All 169 (100) 33.1 44.4
21.5 Modified from Sacco et al., 34 with permission. Table 9–6 Variables Correlated With Two-Month Mortality Two-Month Mortality, Number (%) Risk Factor Present on Day Three If Factor Present If Factor Not Present Abnormal brainstem function 88/99 (89) 83/136 (61) Absent verbal response 151/175 (86) 23/57 (40) Absent withdrawal to pain 122/136 (90) 52/96 (54) Creatinine !132.6 mmol/L (1.5 mg/dL) 82/94 (87) 99/153 (65) Age !70 93/111 (84) 88/136 (65) From Hamel et al., 33 with permission. 352 Plum and Posner’s Diagnosis of Stupor and Coma Table 9–8 Useful Clinical Findings in the Prognosis of Postcardiac Arrest Coma Organized by Time After Onset of Coma LR* of Poor Neurologic Outcome (95% Confidence Interval) Clinical Finding Positive Negative
Absent pupillary reflex 7.2 (1.9–28.0) 0.5 (0.4–0.6) Absent motor response 3.5 (1.4–8.6) 0.6 (0.4–0.7) Absent corneal reflex 3.2 (1.1–9.5) 0.7 (0.6–0.8) Absent oculocephalic reflex 2.5 (1.3–4.8) 0.4 (0.3–0.6) Absent spontaneous eye movement 2.2 (1.3–4.0) 0.4 (0.3–0.6) ICS <4
2.2 (1.1–4.5) 0.2 (0.1–0.6) GCS <5 1.4 (1.1–1.6) 0.3 (0.2–0.5) Absent verbal effort 1.2 (0.9–1.6) 0.1 (0.0–0.7) At 12 Hours Absent cough reflex 13.4 (4.4–40.3) 0.3 (0.2.-0.4) Absent corneal reflex 9.1 (3.9–21.1) 0.3 (0.2–0.4) Absent gag reflex 8.7 (4.0–18.9) 0.4 (0.4–0.5) Absent pupillary reflex 4.0 (2.5–6.6) 0.5 (0.5–0.6) GCS <5
3.5 (2.4–5.2) 0.4 (0.3–0.4) Absent motor response 3.2 (2.2–4.6) 0.4 (0.3–0.5) Absent withdrawal to pain 2.3 (1.9–3.1) 0.2 (0.1–0.2) Absent verbal effort 1.6 (1.4–1.9) 0.1 (0.0–0.1) At 24 Hours Absent cough reflex 84.6 (5.3–1342.0) 0.4 (0.3–0.5) Absent gag reflex 24.9 (6.3–98.3) 0.5 (0.4–0.5) GCS <5 8.8 (5.1–15.1) 0.4 (0.3–0.4) Absent eye opening to pain 5.9 (3.9–9.0) 0.3 (0.3–0.4) Absent spontaneous eye movement 3.5 (1.4–8.8) 0.5 (0.4–0.7) Absent eye opening to pain 3.0 (1.5–6.2) 0.4 (0.3–0.5) Absent oculocephalic reflex 2.9 (1.8–4.6) 0.5 (0.5–0.6) Absent spontaneous eye movement 2.7 (2.1–3.4) 0.3 (0.2–0.3) Absent verbal effort 2.4 (2.0–2.9) 0.1 (0.0–0.1) At 48 Hours GCS <6 2.8 (1.3–5.9) 0.3 (0.1–0.5) GCS <10
1.3 (1.0–1.7) 0.0 (0.0–0.7) At 72 Hours Absent withdrawal to pain 36.5 (2.3–569.9) 0.3 (0.2–0.4) Absent spontaneous eye movement 11.5 (1.7–79.0) 0.6 (0.5–0.7) Absent verbal effort 7.4 (2.0–28.0) 0.3 (0.2–0.5) Absent eye opening to pain 6.9 (1.8–27.0) 0.5 (0.4–0.6) At 7 Days Absent withdrawal to pain 29.7 (1.9–466.0) 0.4 (0.3–0.6) Absent verbal effort 14.1 (2.0–97.7) 0.4 (0.2–0.6) GCS, Glasgow Coma Scale; ICS, Innsbruck Coma Scale; LR, likelihood ratio. *Clinical findings that have a positive LR >2 and a lower confidence interval boundary >1 are presented with the corresponding negative LR. Modified from Booth et al., 2 with permission. 353 outcomes and are relatively insensitive to metabolic derangements and drug effects. 36 Bilateral loss of primary cortical somatosensory responses has been repeatedly confirmed to have a 100% specificity for outcomes no better than a permanent VS following anoxic in- juries.
37,38 A recent review 23 found that of 176 patients with absent bilateral primary somato- sensory responses (N20), none recovered past a permanent VS (Table 9–9). The robust cor- relation of bilateral loss of SSEPs and poor outcome reflects a close connection with the underlying degree of anoxic injury as indicated by autopsy studies. 39 Of 10 patients examined at autopsy who had SSEP measurements ob- tained within 48 hours of cardiac arrest, all seven with bilateral absence of the SSEPs had extensive anoxic-ischemic destruction of the cerebral cortex (with acute ischemic changes in patients with short survival, and frank necrosis of the pseudolaminar type in those patients with longer survival times). Two additional patients (one with delayed SSEPs and one with normal-latency SSEPs) showed patchy neuro- nal loss in the cerebral cortex. Importantly, although an index of better outcomes, preser- vation of normal-latency SSEPs following car- diac arrest is not a definite predictor of positive outcomes. Death or vegetative outcomes may occur in as many as 40% of cases where a normal N20 response is measured. 38 Other electrophysiologic techniques, includ- ing EEG, brainstem auditory-evoked responses (BAERs), and transcranial motor-evoked re- sponses, also have predictive value (see 23 for detailed review). EEG patterns are often sup- pressed early following anoxic injuries and a variety of signal abnormalities 22 correlate with poor outcomes; these include burst suppres- sion, alpha-theta patterns, and generalized sup- pression or periodic patterns. The BAER test can identify severe brainstem injury, but does not address the outcome of cerebral cortical injury. Preservation of longer latency auditory- evoked responses that involve contributions from larger cerebral cortical networks may pre- dict recovery of cerebral function with greater specificity. Both a late auditory response (N100) and the mismatch negativity (MMN) response have value in predicting outcome from coma following anoxic injury. 40 Other longer latency evoked responses such as the P300 and N400 have also been studied (see 22 for review). PITFALLS IN THE EVALUATION OF COMA FOLLOWING CARDIOPULMONARY ARREST Although prognosis in coma following cardio- pulmonary arrest is generally accurate, pitfalls do exist. The following case illustrates an ex- treme, although not isolated, example from the literature. 41 Patient 9–1 A 25-year-old asthmatic man collapsed at home and stopped breathing. The patient received car- diopulmonary resuscitation (CPR) from a family member for 6 minutes until emergency medical personnel arrived to find the patient without re- spiratory effort or palpable pulse. Electrocardio- gram (ECG) showed a rate of 24 bpm; CPR and tracheal intubation were performed. Three min- utes later the pulse was 107 bpm and spontaneous respirations were noted. Initial GCS was 3. In the Table 9–9 Somatosensory-Evoked Potentials in Anoxic- Ischemic Encephalopathy: Absent N20 Response Series Day
Proportion With Sign Proportion Recovering Brunko and Zegers De Byl, 1987 < 8 hours
30/50 0/30
Rothstein, 2000 < 2 hours
19/40 0/19
Madl et al., 2000 < 2 hours
22/66 0/22
Chen et al., 2000 1–3
12/34 0/12
Total < 3 83/190 0/83 From Young et al., 23 with permission. 354 Plum and Posner’s Diagnosis of Stupor and Coma emergency room the patient was unresponsive with dilated pupils that were responsive to light; spontaneous decorticate posturing was noted. The patient was sedated with propofol, given atracur- ium, and transferred to the intensive care unit (ICU). In the ICU the patient required mild pressor support and was noted to exhibit frequent myo- clonic jerks of the head and all four limbs. EEG recordings revealed generalized status epilepticus. Theophylline levels were within the normal ther- apeutic range. Seizures were uncontrolled with phenytoin, midazolam, clonazepam, valproate, and MgSO 4 , so that thiopental infusion producing burst suppression was required. After cessation of the thiopental drip, generalized alpha frequency activity was noted. On the sixth day the patient was extubated, given a Do Not Resuscitate (DNR) status, and transferred to the general neurology floor still with a GCS of 3. He subsequently grad- ually improved and had a GCS of 10 by day 16 with the recovery of head nodding and verbali- zation. His GCS reached 15 by the 19th week following the respiratory arrest. While EEG exam- inations showed progressive improvements, the patient continued to exhibit frequent myoclonic jerks and epileptiform activity despite multiple an- tiepileptic medication trials. Ultimately, this pa- tient regained independent function. This patient’s case highlights the potential complexity of prognosis in coma even in circum- stances that appear to predict poor outcome following cardiac arrest and severe hypoxic in- jury. A retrospective review of the history sug- gests several points for consideration. While the patient’s young age, initial presence of pu- pillary light responses, and early return of spon- taneous respiration were positive predictors, the presence of myoclonus and seizures with no history of epilepsy suggested severe hypoxic injury. As reviewed above, postanoxic myoclo- nus usually predicts a dismal prognosis, 42 but
this is not invariably the case. 43 The early se- dation and paralysis of the patient due to the seizure activity may have masked improve- ment in level of consciousness within the first 6 hours, and the extensive use of different an- tiepileptic medications may have mimicked the pattern of alpha coma, a finding that otherwise carries a greater than 90% mortality in the setting of anoxic injury. 44 This patient demonstrates the limitations of obtaining complete information from events in the field and unequivocal separation of the effects of primary injury versus potential con- founds introduced by methods of treatment. A pulseless patient may still have some unde- tected circulatory activity, or have lost perfu- sion just prior to evaluation, making accurate estimate of duration of hypoxia problematic. A similar case involving seizures and myoclonus following a cardiac arrest has been reported, with lateimprovement onday16 after remaining at a GCS of 5 until that point. 45 Finally, a postictal state can severely depress brainstem function, and tonic seizures can sim- ulate flexion or extension posturing, whereas single epileptic jerks can be difficult to distin- guish from myoclonus. Cardiac arrest from a seizure-induced cardiac arrhythmia 46 can fur- ther complicate the picture. Vascular Disease STROKE Prognosis in coma following stroke depends on the arterial territory affected by the stroke that produces bilateral hemispheric dysfunction as detailed in Chapter 4. Wijdicks and Rabin- stein
47 surveyed the literature of prognostic factors for severe stroke from 1966 to 2003. They found no evidence-based studies better than class III to indicate prognosis, although several suggestive clinical and radiologic fea- tures were identified. Large proximal vessel occlusions causing diffuse hemispheric edema and midline shift carry a grave prognosis with a nearly 90% mortality when the shift of the septum pellucidum was greater than 12 mm. 48 Patients with coma caused by acute basilar oc- clusions may recover 49 (see Chapter 2), whereas those with coma due to hypertensive pontine hemorrhages usually do not. 50 SUBARACHNOID HEMORRHAGE Coma resulting from spontaneous subarach- noid hemorrhage (SAH) has a grave prognosis. The World Federation of Neurological Sur- geons (WFNS) grades SAH using the GCS 51 (see also 52 ) (Table 9–10). Although brief loss of consciousness is common, coma is a rela- tively uncommon sign in patients who reach the hospital with SAH; two-thirds present with WFNS grade III examinations or better. Consciousness, Mechanisms Underlying Outcomes, and Ethical Considerations 355
However, as many as one-half of the patients presenting with grades I or II deteriorate from vasospasm, rebleeding, hydrocephalus, or brain edema. About 10% (range 3% to 17%) of patients die before reaching medical atten- tion and another 10% prior to hospital evalu- ation. The overall mortality is 40% to 50%. 53 GCS is a good predictor of outcome from SAH if the patient’s age, the amount of blood on CT scan, the location of the aneurysm (worse for posterior circulation sites compared with anterior circulation), 53 and secondary compli- cations following the initial rupture are also fac- tored in. A high percentage of patients with grades IV and V die from secondary complica- tions if they remain in coma for 2 weeks or more. Rebleeding of an aneurysm causing coma and depression or loss of brainstem reflexes carries a mortality rate of 50%. In one study, bilateral loss of pupillary responses carried a 95% mortality rate. Electrophysiologic mea- surements have also shown some utility in the prognosis of SAH; loss of BAERs and SSEPs correlate with poor grades on examination. 54,55 Central Nervous System Infection Coma was present on admission in 14% of 696 patients with bacterial meningitis 56 (see also page 262). Obtundation on admission was a significant risk factor for death or a GOS less than 4, as were age older than 60 years, hy- potension, seizures within 24 hours (often as- sociated with a low serum sodium), and cere- brospinal fluid (CSF) abnormalities including decreased glucose concentration or elevation of the CSF protein (greater than or equal to 250 mg/dL). In most cases, death was a result of herniation, occasionally following an ill- advised lumbar puncture. Some investigators have suggested that the presence of coma is the best predictor of morbidity from acute meningitis. 57 Coma is often the result of in- creased ICP resulting from alteration of the blood-barrier by toxins (vasogenic edema), im- paired resorption of CSF (interstitial edema), or venous or arterial occlusions (infarction with cytotoxic edema). 58 A brain abscess caus- ing coma also has a poor prognosis (GOS less than 4)
59 ; herniation is the principal cause of coma with a 60% mortality rate. 60 Acute Disseminated Encephalomyelitis Acute disseminated encephalomyelitis (ADEM) (see also page 366) is a monophasic autoimmune demyelinating disease most commonly affect- ing children and young adults that follows viral or bacterial illnesses or may arise postvacci- nation. 61
historically been considered poor, current ex- perience reflects that most patients (range 55% to 90% across studies) will recover fully or with minor neurologic disabilities. The improved prognosis may reflect either the increased fre- quency of diagnosis of relatively mild cases, which often can be demonstrated on magnetic resonance imaging (MRI), or perhaps the ten- dency to treat patients with corticosteroids. Most patients with ADEM improve within 6 months, although many documented cases showed lon- ger recovery times. Hepatic Coma Hepatic coma develops either as an inexor- able stage in progressive hepatic failure or as a more reversible process in patients with portal systemic shunts when increased loads of ni- trogenous substances are suddenly presented into the circulation (see Chapter 5). Prognosis in hepatic coma depends on the cause, the acuteness and severity of the liver failure, and the presence or absence of dysfunction of other organs. The prognosis is far worse in fulminant Table 9–10 Grading System for Subarachnoid Hemorrhage Grade
GCS Score Presence of any Motor Deficit I 15 None II 14–15 None III
14–13 Present
IV 12–7
Present or absent V 6–3 Present or absent World Federation of Neurological Surgeons score is in- dexed by Glasgow Coma Scale (GCS) and evidence of identifiable motor deficits. From the World Federation of Neurological Surgeons, 51 with permission 356 Plum and Posner’s Diagnosis of Stupor and Coma hepatic failure than in coma associated with chronic cirrhosis or portacaval shunting. Among patients with nontraumatic coma, those with hepatic encephalopathy demonstrated the best chance for recovery (33%). 4 Survival also correlates with age in patients with infectious and serum hepatitis. Patients with chronic hepatocellular disease often drift in and out of encephalopathy, a situation that can be managed by correction of intercurrent processes such as infection or reduction of cir- culating nitrogenous load. If no exogenous fac- tor can be identified, the presence of enceph- alopathy is far more ominous and correlates with high mortality; approximately 50% of pa- tients with cirrhosis die within 1 year of dem- onstrating encephalopathy. 62 Depressant Drug Poisoning Most fatal intentional depressant drug poi- sonings occur outside the hospital. Once such Yüklə 9,02 Mb. Dostları ilə paylaş:
|