Plum and posner’s diagnosis of stupor and coma fourth Edition series editor sid Gilman, md, frcp
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481. Aldemir M, Ozen S, Kara IH, et al. Predisposing factors for delirium in the surgical intensive care unit. Crit Care 2001; 5(5), 265–270. 482. Bitsch M, Foss N, Kristensen B, et al. Pathogenesis of and management strategies for postoperative delirium after hip fracture: a review. Acta Orthop Scand 2004; 75(4), 378–389. 483. Wilson LM. Intensive care delirium. The effect of outside deprivation in a windowless unit. Arch Intern Med 1972; 130, 225–226. 296 Plum and Posner’s Diagnosis of Stupor and Coma Chapter 6 Psychogenic Unresponsiveness CONVERSION REACTIONS CATATONIA PSYCHOGENIC SEIZURES CEREBELLAR COGNITIVE AFFECTIVE SYNDROME ‘‘AMYTAL INTERVIEW’’ Differentiating psychogenic neurologic symp- toms from those caused by structural disease is often very difficult. The difficulty arises in part because many patients are very accurate in mim- icking neurologic signs (actors are often used to train medical students in the diagnosis of neurologic illnesses) and, in part, because many patients with psychogenic neurologic disorders (conversion reactions) also have somatic disease, the somatic illness representing a stressor that causes psychologic problems. Examples abound: approximately one-half of patients with psy- chogenic seizures also have epilepsy. 1 Of those who do not have epilepsy, over 20% show evi- dence of a brain disorder characterized either by epileptiform activity on electroencephalo- gram (EEG), magnetic resonance imaging (MRI) abnormalities, or neuropsychologic def- icits.
2 Psychogenic neurologic symptoms some- times complicate the course of multiple sclero- sis.
3 Merskey and Buhrich studied 89 patients with classic motor conversion symptoms and found that 48% had a cerebral disorder. 4 Of
tural disease, psychogenic unresponsiveness is among the most difficult to diagnose. With most psychogenic illnesses that mimic structural neurologic disease, the physician pursues a two- pronged diagnostic attack. He must first de- termine by the neurologic examination that the patient’s neurologic signs and symptoms are not in keeping with the anatomy and physiology of the nervous system (i.e., they are anatomically or physiologically impossible). Secondly, he must discern from the history and mental status examination that the patient’s emotional make- up and current psychologic problems are suf- ficient to explain the abnormal findings on a psychologic basis. Because in psychogenic un- responsiveness no history or mental status ex- amination from the patient is possible (a history should be obtained from relatives or friends), the physician is left with only the first portion of his diagnostic armamentarium (i.e., the demonstration that despite apparent uncon- sciousness, the patient is in fact physiologically awake). Thus, the diagnosis of psychogenic unresponsiveness must be approached with the greatest care. A careful neurologic examination, sometimes supplemented by caloric tests, EEG, 297
and an ‘‘Amytal interview,’’ as described below, will usually establish the diagnosis and obviate the need for extensive, potentially harmful lab- oratory investigations. However, if after such a meticulous examination of a patient with sus- pected psychogenic unresponsiveness any ques- tion remains about the diagnosis, a careful search for other causes of coma is obligatory. Psychogenic unresponsiveness is uncommon; it was the final diagnosis in only eight of our original 500 patients (Table 1–1). We have, how- ever, encountered the condition as a challenging diagnostic problem in several further patients at a rate of about one every other year since that time. In one study of conversion symptoms in 500 psychiatric outpatients, ‘‘unconsciousness’’ occurred in 17. 5 Two older series from London each report six patients with psychogenic un- responsiveness who were initially puzzling diag- nostically. 6,7
Over how long a period of time these cases were collected, or from how wide a patient population, is not stated. More recently, Lempert and colleagues found that 405 (9%) of 4,470 consecutive neurologic inpatients were found to have psychogenic rather than neuro- logic disorders 8 (Table 6–1). Among these only Table 6–1 Signs and Symptoms (N = 717) of 405 Patients With Psychogenic Dysfunction of the Nervous System* Pain Trunk and extremities 89 Headache
61 Atypical facial pain 13 Motor Symptoms Astasia/abasia 52 Monoparesis 31 Hemiparesis 20 Tetraparesis 18 Paraparesis 10 Paresis of both arms 2 Recurrent head drop 1 Tremor
11 Localized jerking 1 Stereotyped motor behavior 1 Hypokinesia 1 Akinesia
1 Foot contracture 1 Isolated ataxia of the upper extremities Sensory Symptoms Hypesthesia/anesthesia 81 Paresthesia/dysesthesia 63 Sensation of generalized vibration 1 Sensation of fever 1 Pressure in the ears 1 Seizures
With motor phenomena 47 Other (amnestic episodes, mental and emotional alterations) 34 Vertigo/Sizziness Attacks of phobic postural vertigo 47 Continuous dizziness 38 Ocular Symptoms Amblyopia 10 Amaurosis 6 Visual field defects 6 Color blindness 2 Double vision 2 Other visual phenomena 6 Ptosis
1 Convergence spasm 1 Unilateral gaze paresis 1 Alimentary Symptoms Dysphagia 4 Vomiting 4 Speech Disturbances Dysarthria 9 Slow speech 1 Aphonia
2 Mutism
1 Neuropsychologic Symptoms Cognitive impairment 2 Amnestic aphasia 1 Apathy
2 Coma
1 Other Symptoms Bladder dysfunction 11 Stool incontinence 1 Cough
1 From Lempert et al., 8 with permission. 298 Plum and Posner’s Diagnosis of Stupor and Coma one was comatose, although 34 had seizures described as consisting of ‘‘amnestic episodes, mental and emotional alterations.’’ How many of these had disorders of consciousness is un- clear. Another study conducted in the 566-bed tertiary care hospital identified a conversion dis- order in 42 patients over 10 years. 9 In 17 pa- tients, the presenting complaints were ‘‘seizure activity, syncope, or loss of consciousness.’’ Pa- tients admitted directly to the hospital with- out a definitive diagnosis were not included among the 42; how many there were was not stated.
Because the diagnosis of psychogenic neu- rologic symptoms is often difficult, mistakes are sometimes made. Sometimes a structural dis- order is initially diagnosed as psychogenic, 10,11 but sometimes the opposite occurs. The latter is typically true when psychogenic coma com- plicates a physical illness. 12,13 Although errors were common in the past, a recent systematic review of misdiagnosis of conversion symptoms suggests an error rate of only 4% since 1970. 14 Among the 390 patients with a diagnosis of non- epileptic seizures and/or loss of consciousness, only nine were misdiagnosed. Several psychiatric disorders can result in psychogenic unresponsiveness. These include (1) conversion reaction, which may in turn be secondary to a personality disorder, severe de- pression, anxiety, or an acute situational reac- tion
15 ; (2) catatonic stupor, often a manifestation of schizophrenia; (3) a dissociative or ‘‘fugue’’ state; and (4) factitious disorder or malingering. The two major categories of psychogenic un- responsiveness are those that result from a con- version disorder (often called conversion hys- teria) and those that are part of the syndrome of catatonia (often thought to be a manifestation of schizophrenia). The two clinical pictures differ somewhat, but both may closely simulate de- lirium, stupor, or coma caused by structural or metabolic brain disease. The diagnosis of psy- chogenic unresponsiveness of either variety is made by demonstrating that both the cerebral hemispheres and the brainstem-activating path- ways can be made to function in a physio- logically normal way, even though the patient will seemingly not respond to his or her envi- ronment.
The physician must recognize that with the exception of factitious disorders and malinger- ing, psychologically produced neurologic symp- toms are not ‘‘imaginary.’’ The disorders are associated with measurable changes in brain function. Although routine tests including MRI, evoked potentials, and EEG are usually normal, measurement of cerebral metabolism is region- ally abnormal. 16 Using single photon emission computed tomography (SPECT), Vuilleumier and colleagues conducted a study in which se- ven patients with conversion symptoms mim- icking motor or sensory dysfunction revealed a consistent decrease of blood flow in the thala- mus and basal ganglia contralateral to the def- icit. These abnormalities resolved in those pa- tients who recovered. 17 Spence and colleagues studied two patients with psychogenic weakness affecting their left arms. They compared posi- tron emission tomography (PET) scans of these patients with normal individuals, and also with normal individuals who feigned paralysis of the left arm. The left dorsolateral prefrontal cor- tex was activated in the normal individuals and those feigning paralysis, but was hypofunctional in the patient’s with the conversion reaction. In- terestingly, those feigning paralysis exhibited hy- pofunction of the right anterior prefrontal cor- tex when compared with controls. 18 A study of four patients with ‘‘hysterical anesthesia’’ using functional MRI revealed that stimuli to the an- esthetic parts of the body did not activate areas in the thalamus, posterior region of the anterior cingulate cortex, or Brodmann’s areas 44 and 45. These are the areas activated by individuals who perceived the stimuli. A patient studied during catatonic stupor showed hypometabo- lism in a large area of the prefrontal cortex in- cluding anterior cingulate, medial prefrontal, and dorsolateral cortices when compared with controls. 16 The few other studies of functional imaging in patients with catatonia also showed hypometabolism in the frontal lobes. 19–21 Al-
though no patients with psychogenic coma have been studied by these techniques (the catatonic patient was stuporous), the data from patients with other conversion reactions suggests that one would find abnormalities of brain metabo- lism in these patients as well. CONVERSION REACTIONS A conversion reaction is the cause of most psy- chogenic comas. As used here, the term con- version reaction describes a psychogenic or nonphysiologic loss or disorder of neurologic function involving the special senses or the Psychogenic Unresponsiveness 299
voluntary nervous system. Many physicians as- sociate conversion reactions with a hysterical personality (conversion hysteria) but, in fact, conversion reactions may occur as a psycho- logic defense against a wide range of psychi- atric syndromes, including depressive states and neuroses. 22 Furthermore, as indicated on page 297, conversion symptoms, including psychogenic unresponsiveness, may be a re- action to organic disease, and thus occur in a patient already seriously ill. We find it impos- sible to differentiate conversion reactions, pre- sumably representing involuntary responses by patients to stress, from voluntary malingering except by the direct statement of the subject involved and perhaps by PET. 18 Patients suffering from psychogenic unres- ponsiveness, owing to either a conversion reac- tion or to malingering, usually lie with their eyes closed and do not attend to their surroundings. The respiratory rate and depth are usually nor- mal, but in some instances the patient may be overbreathing as another manifestation of the psychologic dysfunction (hyperventilation syn- drome). The pupils may be slightly widened, but are equal and reactive except in the instance of the individual who self-instills mydriatic agents. Oculocephalic responses may or may not be present, but caloric testing invariably produces quick-phase nystagmus away from the ice water irrigation rather than either tonic deviation of the eyes toward the irrigated ear or no response at all. It is the presence of normal nystagmus in response to caloric testing that firmly indicates that the patient is physiologically awake and that the unresponsive state cannot be caused by structural or metabolic disease of the nervous system. (A rare patient with pre-existing vestib- ular dysfunction may be awake, but not have caloric responses.) Henry and Woodruff de- scribed six patients with psychogenic unrespon- siveness in whom the eyes deviated tonically toward the floor when the patient lay on his side. 6
of the eyes was psychologically mediated as a way of avoiding eye contact with the examiner. In some patients, the eyes deviate upward (or sometimes downward) when the eyelids are passively opened. Upward eye deviation also occurs during syncopal attacks. 23 When one at- tempts to open the closed lids of a patient suf- fering from psychogenic unresponsiveness, the lids often resist actively and usually close rap- idly when they are released. The slow, steady closure of passively opened eyelids that occurs in many comatose patients cannot be mimicked voluntarily. Similarly, slow roving eye move- ments cannot be mimicked voluntarily. Patients suffering from psychogenic unresponsiveness as a conversion symptom usually offer no resis- tance to passive movements of the extremities although normal tone is present; if an extremity is moved suddenly, momentary resistance may be felt. The patient usually does not withdraw from noxious stimuli. Dropping the passively raised arm toward the face is a maneuver said to be positive when the patient’s hand avoids hit- ting the face. However, the weight of the upper arm sometimes pulls the hand away from the face, giving the appearance of voluntary avoid- ance. 24
mal, but they can be voluntarily suppressed in some subjects and thus may be absent or, rarely, asymmetric. The abdominal reflexes are usually present and plantar responses are invariably ab- sent or flexor. The EEG is that of an awake patient, rather than one in coma. Patient 6–1 A 26-year-old nurse with a history of generalized convulsions was admitted to the hospital after a night of alcoholic drinking ostensibly followed by generalized convulsions. She had been given 50% glucose and 500 mg sodium amobarbital intrave- nously. Upon admission she was reportedly unre- sponsive to verbal command, but when noxious stimuli were administered she withdrew, repeti- tively thrust her extremities in both flexion and extension, and on one occasion spat at the exam- iner. Her respirations were normal. The remainder of the general physical and neurologic examina- tion was normal. She was given 10 mg of diazepam intravenously and 500 mg of phenytoin intrave- nously in two doses 3 hours apart. Eight hours later, because she was still unresponsive, a neurologic consultation was requested. She lay quietly in bed, unresponsive to verbal commands and not with- drawing from noxious stimuli. Her respirations were normal; her eyelids resisted opening actively and, when they were opened, closed rapidly. The eyes did not move spontaneously, the doll’s eye responses were absent, and the pupils were 3 mm and reactive. Her extremities were flaccid with 300
Plum and Posner’s Diagnosis of Stupor and Coma normal deep tendon reflexes, normal superficial abdominal reflexes, and flexor plantar responses. When 20 mL of ice water was irrigated against the left tympanum, nystagmus with a quick compo- nent to the right was produced. The examiner in- dicated to a colleague that the production of nys- tagmus indicated that she was conscious and an EEG would establish that fact. She immediately ‘‘awoke.’’ Her speech was dysarthric and she was unsteady on her feet when she arose from bed. An EEG was marked by low- and medium-voltage fast activity in all leads with some 8-Hz alpha activity and intermittent 6- to 7-Hz activity, a recording suggesting sedation owing to drugs. She recovered full alertness later in the day and was discharged a day later with her neurologic examination having been entirely normal. An EEG done at a subse- quent time showed background alpha activity of 8 to 10 Hz with a moderate amount of fast activity and little or no 5- to 7-Hz slow activity. Comment: This patient illustrates a common problem in differentiating ‘‘organic’’ from psycho- genic unresponsiveness. She had been sedated and had a mild metabolic encephalopathy, but the preponderance of her signs was a result of psy- chogenic unresponsiveness. The presence of nys- tagmus on oculovestibular stimulation, and an EEG that was only mildly slowed without other signs of neurologic abnormality, effectively ruled out or- ganic coma. The converse of Patient 6–1 is illustrated by Patient 5–3 (see page 194). In the latter, the initial examination suggested psychogenic un- responsiveness, but vestibular testing elicited tonic deviation of the eyes without nystagmus. The tonic eye deviation clearly indicated phys- iologic rather than psychologic unresponsive- ness. A rare patient with psychogenic unrespon- siveness is able to inhibit nystagmus induced by caloric testing (probably by intense visual fixa- tion), but in that instance there is no tonic de- viation of the eyes and the combination of other signs can establish the diagnosis. When a patient with severe organic illness, whether systemic or neurologic, becomes unre- sponsive, the physician sometimes fails to en- tertain the possibility that the unresponsiveness is psychogenic and represents a conversion re- action to a difficult psychologic situation. Patient 6–2 illustrates this. Patient 6–2 A 69-year-old woman was admitted to the coronary care unit complaining of chest pain. On examina- tion she was diaphoretic and the electrocardiogram (ECG) showed changes suggestive of an acute an- terior wall myocardial infarction. She was awake and alert at the time of admission and had a nor- mal neurologic examination. The following morn- ing she was found to be unresponsive. On ex- amination her respiratory rate was 16 and regular, pulse 92, temperature 37.5, and blood pressure 120/80. The general physical examination was un- remarkable, revealing no changes from the day before. On neurologic examination she failed to respond to either verbal or noxious stimuli. She held her eyes in a tightly closed position and ac- tively resisted passive eye opening, and the lids, af- ter being passively opened, sprung closed when released. Oculocephalic responses were absent. Cold caloric responses yielded normal, brisk nys- tagmus. Pupils were 4 mm and reactive. Tone in the extremities was normal. The deep tendon reflexes were equal throughout and plantar responses were flexor. The neurologist who examined the patient suggested to the cardiologist that the unrespon- siveness was psychogenic and that psychiatric con- sultation be secured. At the patient’s bedside the incredulous cardiologist began to discuss how the diagnosis of psychogenic unresponsiveness was made. When the decision was finally made to con- sult a psychiatrist, the patient, without opening her eyes, responded with the words, ‘‘No psychiatrist.’’ In this instance, the presence of severe heart disease led the patient’s physicians to refuse initially to entertain a diagnosis of psychogenic unresponsiveness. In Patient 6–3, the presence of severe organic neurologic disease masked the diagnosis for a considerable period. Patient 6–3 A 28-year-old man with hepatic carcinoma met- astatic to the lungs was admitted to the hospital complaining of abdominal pain. His behavior was noted to be inappropriate a few days after admis- sion, but this was believed secondary to the Psychogenic Unresponsiveness 301
opioids given for pain. The inappropriate behavior progressed to lethargy and then stupor. When first examined by a neurologist, he was unresponsive to verbal stimuli but grimaced when stimulated noxiously. He held his eyes open and blinked in response to a bright light. Nuchal rigidity and bi- lateral extensor plantar responses were present, but there were no other positive neurologic signs. A lumbar puncture revealed bloody cerebrospinal fluid (CSF) with xanthochromic supernatant fluid and a CSF glucose concentration of 15 mg/dL. The EEG consisted of a mixture of theta and delta ac- tivity, which was bilaterally symmetric. Carotid arteriography failed to reveal the cause of his symptoms, which were believed to be caused by leptomeningeal metastases. For the next 2 weeks his state of consciousness waxed and waned. When awake he continued to act oddly. Two weeks after the initial neurologic examination, he was noted to be lying in bed staring at the ceiling with no responses to verbal stimuli and with 6-mm pu- pils, which responded actively to light. Bilateral extensor plantar responses persisted. The EEG now was within normal limits, showing good alpha ac- tivity, which blocked with eye opening. Because of the confusion about the exact cause of his di- minished state of consciousness, an ‘‘Amytal inter- view’’ was carried out (see page 307). After 300 mg of intravenous Amytal was given slowly over sev- eral minutes, the patient awoke, was fully oriented, and was able to perform the serial sevens test without error. During the course of the discussion, when the problems of his cancer were broached, he broke into tears. Further history indicated that the patient’s brother had a history of hospitaliza- tions for both mania and depression. A diagnosis of psychogenic unresponsiveness superimposed on metastatic disease of the nervous system was made. The patient was started on psychotropic drugs and he remained alert and responsive through- out the remainder of his hospital stay. The two patients above illustrate the difficul- ties in making a diagnosis of psychogenic un- responsiveness in patients with organic disease. Merskey and Buhrich have stressed the fre- quency of conversion hysteria in patients suf- fering from structural disease. 4 Of 89 patients with hysterical conversion symptoms, 67% had some organic diagnosis; 48% of the group with organic diagnoses had either an organic cere- bral disorder or a systemic illness affecting the brain. The authors believe that organic cere- bral disease predisposes patients to the devel- opment of conversion reactions. CATATONIA The second major category of psychogenic un- responsiveness is catatonia. Catatonia is a symp- tom complex characterized by either stupor or excitement accompanied by behavioral distur- bances that include, among others, mutism, pos- turing, rigidity, grimacing, waxy flexibility (a mild but steady resistance to passive motion, which gives the examiner the sensation that he is bend- ing a wax rod), and catalepsy (the tonic main- tenance for a long period of time of a limb in a potentially uncomfortable posture where it has been placed by an examiner). Tables 6–2 and 6–3 list the signs of catatonia and some of its causes.
In a retroprospective clinical study of patients admitted to a psychiatric unit with catatonic symptoms, only four of 55 were schizophrenic; 39 had affective disorders, three had reactive psychoses, and nine suffered from organic brain diseases, which included toxic psychosis, en- cephalitis, alcoholic degeneration, and drug- induced psychosis. 27 Patients with catatonic stupor usually give the appearance of being ob- tunded or semi-stuporous rather than coma- tose. This state is compatible with normal pu- pillary and oculovestibular function even when the obtundation has a structural origin. In ad- dition, catatonic stupor is accompanied by a va- riety of autonomic and endocrine abnormalities that give the patient a particularly strong ap- pearance of organic neurologic disease. Catatonia occurs in two forms: retarded and excited. The patient in a catatonic stupor who presents a problem in the differential diagnosis of stupor or coma usually appears unresponsive to his or her environment. Severe and prolonged catatonic stupor, as described below, is uncom- mon, since such patients are usually treated early with psychotropic medications before the full picture develops. The patient in catatonic stu- por usually lies with the eyes open, apparently unseeing. The skin is pale and frequently mar- red by acne and has an oily or greasy appear- ance. The patient’s pulse is rapid, usually be- tween 90 and 120, and may be hypertensive. Respirations are normal or rapid. The body temperature is often elevated 1.08C to 1.58C above normal. Such patients usually do not 302 Plum and Posner’s Diagnosis of Stupor and Coma move spontaneously and appear to be unaware of their surroundings. They may not blink to visual threat, although optokinetic responses are usually present. The pupils are dilated and there is frequently alternating anisocoria; they are, however, reactive to light. Some patients hold their eyes tightly closed and will not permit passive eye opening. Doll’s eye movements are absent and caloric testing produces normal oc- ular nystagmus rather than tonic deviation. At times there is increased salivation, the patient allowing the saliva either to drool from the mouth or to accumulate in the back of the phar- ynx without being swallowed. Such subjects may be incontinent of urine or feces or, on the contrary, may retain urine requiring catheteri- zation. Their extremities may be relaxed, but more commonly are held in rigid positions and are resistant to passive motion. Many patients Table 6–2 Signs of Catatonia Excitement Nonpurposeful hyperactivity or motor unrest Immobility Extreme hypoactivity, reduced response to stimuli Mutism Reduced or absent speech Stupor/coma Unresponsive to all stimuli; eyes closed, flaccid, or rigid Staring
Fixed, nonreactive gaze, reduced blinking Posturing Spontaneous maintenance of posture (the posture itself may or may not be abnormal) for longer than is usual Grimacing Maintenance of odd facial expressions Echolalia Mimicking of examiner’s speech (may be delayed) Echopraxia Mimicking of examiner’s movements (may be delayed) Stereotypy Repetitive, non-goal-directed movements Mannerisms Odd, purposeful voluntary movements Verbigeration Repetition of meaningless phrases or sentences Rigidity
Maintenance of position despite efforts to be moved Negativism Apparently motiveless resistance to instructions or attempts to make contact Waxy flexibility During reposturing there is initial resistance, then the new posture is maintained Withdrawal Refusal to eat, drink, or make eye contact Impulsivity Sudden inappropriate behaviors with no explanation Automatic Exaggerated cooperation with request or continuation of obedience movement requested Mitgehen
Raising of arm in response to light finger pressure (like an angle-poise lamp) despite instructions to the contrary Gegenhalten Resistance to passive movement in proportion to strength of stimulus Ambitendency Indecisive, hesitant movement Grasp reflex Reflex grasping movement of hand in response to stroking palm Perseveration Repeatedly returns to same topic or persists with movement Combativeness Usually undirected aggression or violent behavior Modified from Bush et al. 25 Table 6–3 Some Reported Causes of Catatonia Category
Association Idiopathic Perhaps nearly 50% of patients Psychiatric Affective disorders, dissociative disorders, schizophrenia, drug-indued and other psychoses, obsessive compulsive disorder, personality disorder Neurologic Cerebral tumors, subarachnoid hemorrhage, subdural hemorrhage, hemorrhagic infarcts, closed head injury, multiple sclerosis, narcolepsy, tuberous sclerosis, epilepsy, Wernicke’s encephalopathy, Parkinsonism, systemic lupus erythematosus Metabolic Addison’s disease, Cushing’s disease, diabetic ketoacidosis, hypercalcemia, acute intermittent porphyria, Wilson’s disease Drugs and toxins
Alcohol, anticonvulsants, disulfiram, neuroleptics, amphetamines, mescaline, phencyclidine, aspirin, l -dopa, steroids Infections Encephalitis (especially herpes), malaria, syphilis, tuberculosis, typhoid, acquired immuno- deficiency mononucleosis, viral hepatitis Modified from Philbrick and Rummans. 26 Psychogenic Unresponsiveness 303 demonstrate waxy flexibility. Catalepsy is pres- ent in about 30% of retarded catatonics. Cho- reiform jerks of the extremities and grimaces are common. The deep tendon reflexes are usu- ally present and there are no pathologic re- flexes.
Although appearing comatose, the patient is fully conscious. This normal level of conscious- ness is attested to both by a normal neurologic examination at the time the patient appears stuporous and by the fact that when he or she recovers, the patient is often (but not always) able to recall all the events that took place during the ‘‘stuporous’’ state (Patient 6–4). Patient 6–4 A 74-year-old woman with a history of hyperten- sion and hypothyroidism, but otherwise in good health, was admitted to the hospital for replace- ment of her left hip. She had a previous replace- ment of the right hip several years before. She re- covered well from the surgery, but 3 days later at 4:30 a.m., she was found unresponsive in bed. She lay quietly with eyes closed but did not respond to voice or noxious stimuli. She was seen by a neu- rologist at 7:30 a.m. She was unresponsive to voice, her eyes were open, and she would direct her eyes to sound and would blink to threat, but would not follow commands and did not respond to noxious stimuli. Tone was normal, as was the remainder of the neurologic exam. Ninety minutes later she ‘‘awoke’’ and responded entirely appro- priately. She reported that at 4:30 a.m., unable to sleep, she had the sudden feeling that she had died. Physicians whom she recognized entered the room, but she was unable to respond to them. She reported that the noxious stimuli were very pain- ful, but she could not move, nor could she respond to questions. She continued to think that she was dead until somewhat later in the morning, when a nurse whom she knew well sat by the bedside and talked to her gently. Because the nurse was being so nice she thought she had to respond and she began to talk. There had been no history of pre- vious psychologic disorder nor was there any hint during the rest of her hospitalization of a psycho- logic abnormality. Comment: It is hard to classify this patient with psychogenic coma, but the patient’s mutism and inability or unwillingness to move suggest a form fruste of catatonia. That this disorder can be tran- sient and occur in people without other underlying psychologic difficulty is well known and is per- haps illustrated by this patient. While the patient with the retarded form of catatonia may be difficult to distinguish from a patient with stupor caused by structural disease, the patient with the excited type of catatonia may be difficult to distinguish from a patient with an acute delirium. Both may be wildly ag- itated and combative, and such behavior may make it impossible to test for orientation and alertness. Hallucinatory activity can be caused by either organic or psychologic disease, al- though pure visual hallucinations are usually due to structural or metabolic disease, and pure auditory hallucinations to psychologic disease. The segmental neurologic examination, insofar as it can be tested in a delirious or excited pa- tient, may be normal with either structural or organic disease. Grimacing, stereotypic motor behavior, and posturing suggest catatonia ra- ther than metabolic delirium. Although the passage of time usually resolves the diagnostic problem, the only immediately distinguishing feature between psychogenic and organic delirious reactions is seen on the EEG. In patients with an acute toxic delirium caused by hepatic encephalopathy, encephalitis, alco- hol, or other sedative drugs, slow EEG activity predominates. The EEG of the patient with the delirium of withdrawal from alcohol or barbi- turates is dominated by low-voltage fast activity. The EEG is usually normal in patients with cat- atonia unless there is an underlying medical illness. 28,29
Thus, an entirely normal EEG with good background alpha activity that responds to eye opening and noise suggests that an either unresponsive or excessively excited patient is suffering from catatonia rather than structural or metabolic disease of the nervous system. If the EEG is dominated by high-voltage slow ac- tivity in the case of a stuporous patient, or low- voltage fast activity in the case of an excited patient, the likelihood is that the disorder is met- abolic or structural rather than psychogenic. PSYCHOGENIC SEIZURES More difficult than identifying psychogenic coma is differentiating a psychogenic seizure from an epileptic seizure. 30 Psychogenic 304 Plum and Posner’s Diagnosis of Stupor and Coma seizures are common; in one population study, psychogenic seizures affected 4% of the pop- ulation. 1 The patient often presents in the emergency room having symptoms that may mimic a generalized tonic-clonic seizure or a complex partial seizure. 31 There is often no history available and the patient may be unre- sponsive, or appear to be stuporous or coma- tose. Because 50% of such patients also have epilepsy, differentiating a psychogenic from an epileptic seizure in a particular episode may be very difficult. Some clues both from the history and examination are given in Table 6–4. As indicated in the table, the physician should sus- pect a psychogenic seizure when the patient’s motor movements are unusual, particularly when the seizure lasts a long time. An EEG is usually unavailable and even if available, is often so marred by movement artifact as to not be interpretable. Furthermore, some EEGs in patients with complex partial seizures are nor- mal. The physician should draw a prolactin level. An elevated prolactin level strongly sug- gests that a generalized tonic-clonic or com- plex partial seizure is epileptic. 32 A normal pro- lactin level does not rule out a nongeneralized seizure. Because the diagnosis is often uncer- tain and because, as indicated below, intrave- nous benzodiazepines treat psychogenic alter- ations of consciousness as well as epilepsy, Table 6–4 Findings That Can Help Distinguish Psychogenic From Epileptic Seizures Psychogenic Seizures Epileptic Seizures History
Started <10 years of life Unusual
Common Seizures in presence of doctors Common Unusual
Recurrent ‘‘status’’ Common
Rare Multiple unexplained physical symptoms Common Rare
Multiple operations/invasive tests Common
Rare Psychiatric treatment Common Rare
Sexual and physical abuse Common
Rare Observation Situational onset Occasional Rare Gradual onset Common Rare
Precipitated by stimuli (noise, light) Occasional Rare Purposeful movements Occasional Very rare Opisthotonus, ‘‘arc de cercle’’ Occasional Very rare Tongue biting (tip) Occasional Rare
Tongue biting (side) Rare
Common Prolonged ictal atonia Occasional Very rare Vocalization during ‘‘tonic-clonic’’ phase Occasional Very rare Reactivity during ‘‘unconsciousness’’ Occasional Very rare Rapid postictal reorientation Common
Unusual Undulating motor activity Common Very rare Asynchronous limb movements Common
Rare Rhythmic pelvic movements Occasional Rare
Side-to-side head shaking Common
Rare Ictal crying Occasional Very rare Closed mouth in ‘‘tonic phase’’ Occasional Very rare Closed eyelids Very common Rare
Convulsion >2 minutes Common
Very rare Resisted lid opening Common Very rare Pupillary light reflex Usually retained Commonly absent Lack of cyanosis Common Rare
Modified from Reuber and Elger. 31 Psychogenic Unresponsiveness 305 one can often stop the episode with intrave- nous benzodiazepines. However, if there is a strong suspicion that the seizures are psycho- genic, anticonvulsants should not be given. In most instances, a definitive diagnosis will re- quire evaluation in an epilepsy unit, often with a video-EEG. CEREBELLAR COGNITIVE AFFECTIVE SYNDROME At times mistaken for catatonia, the cerebellar cognitive affective syndrome 33 was originally described in children following surgery to the vermis of the cerebellum. Because the children were awake but mute, the disorder was called the cerebellar mutism syndrome. 34 Cerebellar mutism also occurs in adults either after surgery involving the posterior fossa or as a result of lesions affecting the vermis and posterior lobes of the cerebellum. Such patients are awake, but may be somnolent. Whatever their level of alert- ness, they do not speak and often behave abnor- mally, either by not responding to the examiner or by behaving inappropriately. Patients may re- fuse to swallow food although they are not dys- phagic. In children the syndrome characteris- tically occurs after a period of normality in the postoperative period. The mutism begins hours to days after awakening from anesthesia. The syndrome is largely reversible, but neuropsycho- logic tests given long after apparent recovery demonstratedefectsinexecutivefunction,affect, and language. 34 Patient 6–5 A 32-year-old man with a cerebellar ependymoma complained of headache and mild imbalance. He had been operated on twice 2 years before with a vermis splitting operation that removed most of the lesion, but left residual tumor in the lateral wall of the fourth ventricle. An operation was under- taken to remove the residual tumor. The surgeon did not invade the vermis but lifted the cerebel- lar tonsil to successfully resect the residual tumor. Neurologic consultation was sought in the imme- diate postoperative period when the patient ap- peared to be ‘‘unresponsive.’’ He was lying in bed with his eyes open. He was still intubated, so that he could not speak, but he did not appear to re- spond to any verbal commands. He moved sponta- neously and sometimes appeared to withdraw from noxious stimuli but never would look at the examiner or regard the examiner in any way. When the patient was extubated he did not speak. Gradually over the next 24 to 36 hours, the patient began to respond by closing his eyes to command, but rarely looking at the examiner. He would carry out some commands, particularly grasping the examiner’s hand. However, he had difficulty with commands involving the lips or tongue (oral buc- cal apraxia). Transiently, he demonstrated cata- lepsy. He would say his name, but to other ques- tions he would only repeat his name. Later, when one of us asked him his name he responded ‘‘George Bush.’’ It turned out that the nurse had asked him who the president was about 10 min- utes before and he had responded appropriately. Over time he made a good recovery and was discharged from the hospital. However, even at dis- charge his affect seemed flat and he himself re- ported that he was not the same as prior to surgery, Figure 6–1. (A) A fluid-attenuated inversion recovery sequence demonstrating hyperintensity in the vermis, a result of the first two operations, with residual tumor. (B) A 24-hour postoperative film done during the time when the patient was responding poorly. The hyperintensity in the vermis is more marked and there is new hyperintensity in the right posterior lobe of the cerebellum. 306
Plum and Posner’s Diagnosis of Stupor and Coma although he could not describe what the changes were.
Comment: The cerebellar cognitive affective syndrome is rare in adults and can easily be mis- taken for catatonia or psychogenic unresponsive- ness. This patient had suffered modest damage to the vermis of the cerebellum from the first two operations (Figure 6–1A), and suffered further tran- sient damage to both a vermis and the right pos- terior lobe of the cerebellum as a result of the trauma of the third operation (Figure 6–1B). In- terestingly, the surgeon noted that when she first interviewed him his affect seemed ‘‘flat.’’ She re- ferred him to a psychiatrist, who noted that his behavior had changed after the first operation in that he found himself ‘‘apathetic’’ and ‘‘not happy with the way I am.’’ She found impaired memory, and language ‘‘adequate, but not descriptive of his feelings and emotions.’’ These changes were probably a result of the vermis damage from the first two operations. ‘‘AMYTAL INTERVIEW’’ In many instances, an immediate distinction between organic and psychologic delirium or stupor cannot be made on the basis of the neu- rologic examination or the EEG, and in these instances an Amytal interview is often helpful. Although historically we have used Amytal, clin- ical evidence suggests that a benzodiazepine such as lorazepam works just as well and is more available. 35 We use the term Amytal in- terview loosely to describe the slow intrave- nous injection of an anxiolytic agent. The Am- ytal interview is conducted by injecting the drug intravenously at a slow rate while talking to the patient and doing repeated neurologic examinations. It is important that the discus- sion remain fairly neutral and not represent a direct challenge of the patient’s veracity. Pa- tients with structural or metabolic disease of the nervous system usually show immediately increasing neurologic dysfunction as the drug is injected. Neurologic signs not present prior to the injection of amobarbital (such as ex- tensor plantar responses or hemiparesis) may appear after only a small dose has been intro- duced, and behavioral abnormalities, especially confusion and disorientation, grow worse. On the other hand, patients with psychogenic un- responsiveness or psychogenic excitement fre- quently require large doses of amobarbital be- fore developing any change in their behavior, and the initial change is toward improvement in behavioral function rather than worsening of abnormal findings. Thus, a patient appar- ently stuporous may fully awaken after several hundred milligrams of Amytal and carry out a rational conversation (see Patient 6–3). A stu- porous and withdrawn patient who is catatonic may become fully rational. An excited patient may calm down and demonstrate that he or she is alert, is oriented, and has normal cognitive functions. Patients in nonconvulsive status epi- lepticus may also awaken (see page 281). In a few instances, even the Amytal interview does not make a distinction between organic and psychologic delirium. In such instances, the patient must be hospitalized for observation while a meticulous search for a metabolic cause of the delirium is made. In one of our patients, a diagnosis of catatonic stupor, al- though strongly suspected, did not make itself certain until the patient fully awoke after a thorough diagnostic evaluation had proved un- informative and electroshock therapy was ini- tiated. 35
sponsiveness is established, a more extensive developmental and psychiatric history must be obtained to determine the type of psychiatric Figure 6–1. (B) (continued ). Psychogenic Unresponsiveness 307
disturbance. The exact psychiatric diagnosis will determine the treatment. While the Amytal in- terview is a relatively safe procedure for diag- nostic purposes, and is the first line treatment for catatonia, 35 most psychiatrists do not rec- ommend it for treatment if the patient relapses into psychogenic unresponsiveness after the diagnosis has been made. Intravenous barbitu- rates given with the assumption that they will remove a symptom can be hazardous, because the patient who has resolved his or her conflict by developing the conversion symptom may develop more serious psychologic disturbances should the symptom abruptly be removed. 36 REFERENCES 1. Sigurdardottir KR, Olafsson E. Incidence of psycho- genic seizures in adults: a population-based study in Iceland. Epilepsia 1998; 39, 749–752. 2. Reuber M, Fernandez G, Helmstaedter C, et al. Ev- idence of brain abnormality in patients with psycho- genic nonepileptic seizures. Epilepsy Behav 2002; 3, 249–254. 3. Caplan LR, Nadelson T. Multiple sclerosis and hyste- ria. Lessons learned from their association. JAMA 1980; 243, 2418–2421. 4. Merskey H, Buhrich NA. Hysteria and organic brain disease. Br J Med Psychol 1975; 48, 359–366. 5. Guze SB, Woodrugg RA, Clayton PJ. A study of conversion symptoms in psychiatric outpatients. Am J Psychiatry 1971; 128, 643–646. 6. Henry JA, Woodruff GH. A diagnostic sign in states of apparent unconsciousness. Lancet 1978; 2, 920–921. 7. Hopkins A. Pretending to be unconscious. Lancet 1973; 2, 312–314. 8. Lempert T, Dieterich M, Huppert D, et al. Psycho- genic disorders in neurology: frequency and clinical spectrum. Acta Neurol Scand 1990; 82, 335–340. 9. Dula DJ, DeNaples L. Emergency department pre- sentation of patients with conversion disorder. Acad Emerg Med 1995; 2, 120–123. 10. Slater E. Diagnosis of ‘‘hysteria.’’ Br Med J 1965; 5447, 1395–1399. 11. Shraberg D, D’Souza T. Coma vigil masquerading as psychiatric illness. J Clin Psychiatry 1982; 43, 375– 376.
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32. Chen DK, So YT, Fisher RS. Use of serum prolactin in diagnosing epileptic seizures: report of the Ther- apeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology 2005; 65, 668–675. 33. Schmahmann JD, Sherman JC. The cerebellar cog- nitive affective syndrome. Brain 1998; 121, 561–579. 34. Robertson PL, Muraszko KM, Holmes EJ, et al. Incidence and severity of postoperative cerebellar mutism syndrome in children with medulloblastoma: a prospective study by the Children’s Oncology Group. J Neurosurg 2006; 105, 444–451. 35. Bush G, Fink M, Petrides G, et al. Catatonia. II. Treatment with lorazepam and electroconvulsive therapy. Acta Psychiatr Scand 1996; 93, 137–143. 36. Menza MA. A suicide attempt following removal of conversion paralysis with amobarbital. Gen Hosp Psychiatry 1989; 11, 137–138. 308 Plum and Posner’s Diagnosis of Stupor and Coma Chapter 7 Approach to Management of the Unconscious Patient A CLINICAL REGIMEN FOR DIAGNOSIS AND MANAGEMENT PRINCIPLES OF EMERGENCY MANAGEMENT Ensure Oxygenation, Airway, and Ventilation Maintain the Circulation Measure the Glucose Lower the Intracranial Pressure Stop Seizures Treat Infection Restore Acid-Base Balance Adjust Body Temperature Administer Specific Antidotes Control Agitation Protect the Eyes EXAMINATION OF THE PATIENT Verbal Responses Respiratory Pattern Eye Opening Pupillary Reactions Spontaneous Eye Movement Oculocephalic Responses Caloric Vestibulo-Ocular Responses Corneal Responses Motor Responses Tendon Reflexes Skeletal Muscle Tone GUIDES TO SPECIFIC MANAGEMENT Supratentorial Mass Lesions Infratentorial Mass Lesions Metabolic Encephalopathy Psychogenic Unresponsiveness A FINAL WORD A CLINICAL REGIMEN FOR DIAGNOSIS AND MANAGEMENT Of the acute problems in clinical medicine, none is more challenging than the prompt diagnosis and effective management ofthe patient in coma. The challenge exists in part because the causes of coma are so many and the physician pos- sesses only a limited time in which to make the appropriate diagnostic and therapeutic judg- ments. Coma caused by a subdural or epidural hematoma may be fully reversible when the patient is first seen, but if treatment is not promptly undertaken, the brain injury may be- come either irreparable or fatal within a very short period of time. A comatose patient suf- fering from diabetic ketoacidosis or hypoglyce- mia may rapidly return to normal if appropriate treatment is begun immediately, but may die or be rendered permanently brain damaged if treatment is delayed. In extradural hematoma, meticulous evaluation of acid-base balance and substrate availability is not only useless, but it is 309
also dangerous, because precious time may be lost. In untreated diabetic coma, time spent per- forming imaging is meddlesome, fruitless, and potentially dangerous. The physician evaluating a comatose patient requires a systematic approach that will allow directing the diagnostic and therapeutic en- deavors along appropriate pathways. The pre- ceding chapters of this text presented what may appear to be a bewildering variety of dis- ease states that cause stupor or coma. However, these chapters have also indicated that for any disease or functional abnormality of the brain to cause unconsciousness, it must either (1) produce bilateral dysfunction of the cerebral hemispheres, (2) damage or depress the phys- iologic activating mechanisms that lie along the central core of the upper brainstem and dien- cephalon, or (3) metabolically or physiologically damage or depress the brain globally. Condi- tions that can produce these effects can be divided into (1) supratentorial mass lesions that compress or displace the diencephalon and brainstem, (2) infratentorial destructive or ex- panding lesions that damage or compress the reticular formation, or (3) metabolic, diffuse, or multifocal encephalopathies that affect the brain in a widespread or diffuse fashion. In ad- dition, the clinician must be alert to unre- sponsiveness of psychiatric causes. Conditions associated with loss of motor response but in- tact cognition must be excluded as etiologies (e.g., brainstem infarction, degenerative loss of motor nerves, or acute peripheral neuropathy [Guillain-Barre´ syndrome] producing a locked- in state
1 ). Using these physiologic principles, one may considerably narrow the diagnostic possibilities and start specific treatment rap- idly enough to make a difference in outcome. This chapter outlines a clinical approach that in most instances allows the physician to assign the cause of unresponsiveness promptly into one of the above four main categories while preventing irreversible damage to the patient’s brain. The key to making a categorical clinical di- agnosis in coma consists of two steps: first, the accurate interpretation of a limited number of physical signs that reflect the integrity or im- pairment of various levels of the brain, and sec- ond, the determination of whether structural or metabolic dysfunction best explains the pat- tern and evolution of these signs. As Table 7–1 indicates, each of these pathophysiologic cate- gories causes a characteristic group of symptoms and signs that usually evolve in a predictable manner. Once the patient’s disease can be as- signed to one of the three main categories, spe- cific radiographic, electrophysiologic, or chem- ical laboratory studies can be employed to make disease-specific diagnoses or detect conditions that potentially complicate the patient’s man- Table 7–1 Differential Characteristics of States Causing Sustained Unresponsiveness I. Supratentorial mass lesions compressing or displacing the diencephalon or brainstem Signs of focal cerebral dysfunction present at onset Signs of dysfunction progress rostral to caudal Neurologic signs at any given time point to one anatomic area (e.g., diencephalon, midbrain-pons, medulla) Motor signs often asymmetric II. Subtentorial masses or destruction causing coma History of preceding brainstem dysfunction or sudden onset of coma Localizing brainstem signs precede or accompany onset of coma Pupillary and oculomotor abnormal findings usually present Abnormal respiratory patterns common and usually appear at onset III. Metabolic, diffuse, or multifocal coma Confusion and stupor commonly precede motor signs Motor signs are usually symmetric Pupillary reactions are usually preserved Asterixis, myoclonus, tremor, and seizures are common Acid-base imbalance with hyper- or hypoventi- lation is frequent IV. Psychiatric unresponsiveness Lids close actively Pupils reactive or dilated (cycloplegics) Oculocephalic responses are unpredictable; oculovestibular responses physiologic for wakefulness (i.e., nystagmus is present) Motor tone is inconsistent or normal Eupnea or hyperventilation is usual No pathologic reflexes are present Electroencephalogram is normal 310 Plum and Posner’s Diagnosis of Stupor and Coma agement. Once diagnosis is made and treatment started, changes in these same clinical signs and laboratory tests can be used serially to extend or supplement treatment (medical or surgical), to judge its effect, and, as indicated in Chapter 9, to estimate recovery and prognosis. Many efforts have been made to find an ideal clinical approach to the unconscious patient. Most such approaches repeat or even enlarge upon the complete neurologic examination, which makes them too time consuming for practical daily use. A few are admirably brief and to the point (Chapter 2) (e.g., Glasgow Coma Scale), but have been designed for lim- ited purposes, such as following patients with head injury; generally they provide too little information to allow diagnosis or the monitor- ing of metabolic problems. The recently de- scribed FOUR score scale (Chapter 2) gives more information, but is still limited. 2 The
clinical profile described in Chapter 2, which has been employed extensively by ourselves and others, has advantages. The examination judges the normal and abnormal physiology of functions described earlier in Chapter 2: arousal, pupillary responses, eye movements, corneal responses, the breathing pattern, skel- etal muscle motor function, and deep tendon reflexes. Most of these functions undergo pre- dictable changes in association with localizable brain abnormalities that can locate the lesion or lesions. The constellation and evolution of these abnormal functions in a given patient can determine the cause of altered consciousness, whether supratentorial (focal findings start ros- trally and evolve caudally), infratentorial (focal findings start in the brainstem), metabolic (lacks focal findings, but evidence of diffuse fore- brain dysfunction), or psychiatric (lacks focal or diffuse signs of brain dysfunction). PRINCIPLES OF EMERGENCY MANAGEMENT No matter what the diagnosis or the cause of coma, certain general principles of manage- ment apply to all patients and should be ad- dressed as one pursues the examination and undertakes definitive therapy (Table 7–2). Al- gorithms describing the initial management of the comatose patient have also been published (Figure 7–1). Ensure Oxygenation, Airway, and Ventilation The brain must have a continuous supply of oxy- gen, and adequate blood oxygenation depends on sufficient respiration. Scrupulous attention must be given to the airway and the lungs them- selves. Check the airway. If the airway is ob- structed, attempt to clear it by suctioning and then arrange for a cuffed endotracheal tube to be placed by a skilled practitioner. Prior to plac- ing the tube, extend the head gently, elevate the jaw, and ventilate the patient with 100% oxygen using a mask and bag to ensure maximal possi- ble blood oxygenation during the procedure. Tracheal irritation usually produces a sympa- thetic discharge with hypertension, tachycardia, and occasional premature ventricular contrac- tions. The increase in heart rate and mean arte- rial pressure transiently raises intracranial pres- sure, possibly worsening outcome, 4 an effect that can be mitigated by lidocaine administra- tion (either topically or IV), IV thiopental, or propofol. Detailed reviews of rapid sequence intubation address these and several other phar- macologic agents used to ease intubation and prevent complications. 5–7 The choice depends on the specific clinical situation. 8,9
Rarely, par- ticularly in hypoxemic patients, a vagal discharge leading to bradycardia or cardiac arrest occurs. Maximal oxygenation helps prevent cardiac ar- rhythmias that otherwise may result from the vagal stimulation. To place an endotracheal tube usually requires the physician to extend the neck, raising concern that the procedure may Table 7–2 Principles of Management of Comatose Patients 1. Ensure oxygenation 2. Maintain circulation 3. Control glucose 4. Lower intracranial pressure 5. Stop seizures 6. Treat infection 7. Restore acid-base balance and electrolyte balance 8. Adjust body temperature 9. Administer thiamine 10. Consider specific antidotes (e.g., naloxone, flumazenil, etc.) 11. Control agitation Approach to Management of the Unconscious Patient 311
further damage an already injured cervical spine. In any patient who may have suffered a traumatic injury (obvious or suspected) requir- ing intubation, the neck should be manipulated as little as possible and fixed in a cervical collar. (The same principle applies to testing oculoce- phalic reflexes.) Several techniques exist for intubating patients with suspected cervical cord injuries. These include nasotracheal intubation, the use of a laryngeal mask, 10 and fiberoptic en- doscopic intubation. 11 However, in one series, as many as 12% (37 of 308) of patients intubated by physicians in one emergency department were subsequently shown to have cervical spine injuries, 12 but none suffered worsening neuro- logic injury. 13 Whatever technique is used, the most important point is that a skilled physician should perform the procedure. EVALUATE RESPIRATORY EXCURSIONS Arterial blood gas measurement is the most re- liable method of determining adequate venti- lation but, as a rule of thumb, if breath sounds can be heard at both lung bases, and if the re- spiratory rate is greater than 8 per minute, ven- tilation is probably adequate. A pulse oximeter placed on the finger allows continuous record- ing of blood oxygenation and pulse rate, but may slightly overestimate oxygen saturation in dark- skinned individuals and is falsely elevated with carbon monoxide intoxication. Noninvasive CO 2 monitoring, if available, is also useful. Patients comatose from drug overdose or who are hy- pothermic have depressed metabolism and re- quire less ventilation than awake individuals. The comatose patient ideally should maintain a PaO 2
2 between 35 and 40 mm Hg. After initial management, patients with metabolic coma who are not intubated should be kept in a semiprone Trendelenburg posi- tion and turned from side to side each hour. Others, particularly those with increased in- tracranial pressure (ICP), are kept supine with the head of the bed elevated 15 to 30 degrees. It is necessary to perform chest physical ther- apy frequently and to suction the airway using a sterile technique. The inspissation of dried mu- AIRWAY: intubate if GCS ≤ 8 and
pCO2 > 45 torr BREATHING: maintain Sa02 > 90% pCO2 < 40torr CIRCULATION: maintain MAP > 70 mmHg Check fingerstick glucose and administer glucose if < 45 mg/dl; draw blood sample for electrolytes, arterial blood gas, liver and thyroid function tests, complete blood count, toxicology screen (blood & urine), ECG Hyperventilation, mannitol 0.5–1.0 g/kg if clinical evidence of increased ICP/herniation (some prefer 30ml 23.4% NaCl) Yüklə 9,02 Mb. Dostları ilə paylaş:
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