Plum and posner’s diagnosis of stupor and coma fourth Edition series editor sid Gilman, md, frcp
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surgery. Intraparenchymal hemorrhages, trau- matic brain injury, or infarctions are best trea- ted by careful supportive care if the ICP can be controlled and the patient is not in danger of herniation. 70,71 Monitor the patient’s vital signs and the neu- rologic examination constantly during therapy. An endotracheal tube should be in place, and the patient ventilated to PaO 2 at greater than 100 mm Hg. After initial hyperventilation, ad- just the PaCO 2 between 35 and 40 mm Hg. Mannitol may be repeated as often as every 4 to 6 hours, depending on the patient’s clinical state, but it is important to maintain intravascu- lar volume by monitoring the inputs and out- puts, and to watch for rebound increased ICP. In patients suffering from cerebral tumors or abscess, continue dexamethasone (typically 4 mg 322
Plum and Posner’s Diagnosis of Stupor and Coma every 6 hours, although doses up to 24 mg every 6 hours may be used if clinically necessary) or an equivalent steroid. The head of the bed should probably be slightly elevated. Insert a Foley catheter and record urine output each hour. Measure electrolytes frequently if man- nitol or saline is being given, because the use of these drugs can result in severe electrolyte im- balance. Once in the intensive care unit, ICP should be monitored. Some investigators have advocated barbitu- rate anesthesia to treat severe intracranial hy- pertension from head injury. 72 The drug usually employed is pentobarbital (although thiopental works faster) given intravenously. In one pro- tocol, a loading dose of 10 mg/kg is given over 30 minutes followed by 5 mg/kg over 60 minutes for three doses. The patient is then maintained at 1 to 3 mg/kg/hour to maintain the pentobar- bital level at 3 to 4 mg/dL. 73 The level of coma is also monitored by EEG, to produce a burst suppression pattern at about three to five bursts per minute. 74 The effect of this treatment on long-term outcome is not dramatic and the fre- quent monitoring of EEG, drug levels, and po- tential cardiopulmonary complications make it extremely labor intensive. With such therapy, the ICP decreases rapidly and usually remains low as long as the patient is anesthetized. This technique requires extremely careful monitoring of vital signs and should be carried out only in an intensive care unit. There are reports of de- creases in mortality with the use of barbiturate anesthesia in head injuries, drownings, cerebral infarction, and other supratentorial mass le- sions. 75
is unknown. It is not simply through anesthesia, since in experimental animals gas anesthesia ap- pears to have no such salutary effect. The clini- cal usefulness of barbiturate therapy for coma must be regarded as still in the stage of experi- mental evaluation. Midazolam and propofol are also used to lower ICP, but like barbiturate coma, it is un- clear if they result in an improved outcome. 76 Another second-tier therapy to control intract- able intracranial hypertension is decompres- sive craniectomy. 77 The procedure is being used in patients with severe traumatic brain injury and also those with massive cerebral infarction. It may improve outcome in the former, 77 but while it may be lifesaving in the latter, func- tional outcome is often poor especially in the elderly. 78 Infratentorial Mass Lesions Infratentorial lesions fall into two groups: those that are intrinsic to the brainstem and those that compress it. In patients with infratentorial mass or destructive lesions causing coma, one may elicit a history of occipital headache or com- plaints of vertigo, diplopia, or other symptoms and signs suggesting brainstem dysfunction. Frequently, however, the onset of the coma is sudden and headache occurs only moments before the patient loses consciousness. If the onset of the headache is accompanied by vo- miting, one should suspect an infratentorial le- sion, as acute vomiting is less common with supratentorial masses in adults. Characteristic oculovestibular abnormalities including skew deviation, dysconjugate gaze, fixed gaze palsies, or dysconjugate responses to oculocephalic and oculovestibular testing are strong presump- tive evidence of an infratentorial lesion. Cranial nerve palsies are often present and abnormal respiratory patterns usually are present from onset. The major problem in differential diag- nosis arises when a patient with a supratentorial mass lesion has progressed far enough to arrive at the pontine or medullary level of coma. In this instance, it is virtually impossible to dis- tinguish by physical examination between the effects of supratentorial and infratentorial masses. Metabolic coma can usually be distin- guished from destructive or compressive lesions because the pupils remain reactive. A CT scan distinguishes between supra- and infratentorial masses and often establishes the diagnosis de- finitively. A hyperdense basilar artery strongly suggests brainstem infarction even when the infarct cannot be seen on CT. MRI, particularly with diffusion-weighted imaging, is much better at identifying brainstem infarcts. At times it is impossible to distinguish on clinical grounds an intrinsic brainstem lesion (such as infarction from basilar artery occlusion) from an extrinsic compressive lesion (such as cerebellar hematoma), but the treatment is dif- ferent: surgery for compressive lesions 73 and
thrombolysis for acute vascular occlusions. 79 Hematomas of the cerebellum or the subdural space should be evacuated if the patient is stu- porous or comatose, if the state of conscious- ness is progressively becoming impaired, or if other signs indicate progressive brainstem compression (see Chapter 4). 80 A cerebellar Approach to Management of the Unconscious Patient 323
infarct causing stupor or coma from brainstem compression appears on CT scan as a hypo- dense area and likewise may require surgical decompression by removal of infarcted tissue. Some reports describe successful surgical evac- uation of brainstem hematomas, 81 particularly when the hemorrhage is due to a cavernous angioma. Primary pontine hemorrhages (those due to hypertension) usually are not treated surgically, particularly when the patient is co- matose. 82
masses are similar to those for supratentorial masses, discussed above. Metabolic Encephalopathy Metabolic coma (Table 7–1) is usually charac- terized by a history of confusion and disorien- tation having preceded the onset of stupor or coma, usually in the absence of any motor signs. When motor signs (decorticate or decerebrate rigidity) appear, they are usually symmetric. If the patient is stuporous rather than comatose, asterixis, myoclonus, and tremor are common, and in comatose patients the presence of repet- itive seizures, either focal or generalized, provide presumptive evidence of metabolic dysfunction. Many patients with metabolic coma either hy- per- or hypoventilate, but it is rare to see the ab- normal respiratory patterns that characterize in- fratentorial mass or destructive lesions (see page 50). There are two major errors in the diagnosis of metabolic coma. The first is in dif- ferentiating patients with the diencephalic stage of supratentorial masses from those with meta- bolic coma. In the absence of focal motor signs, one may initially suspect metabolic coma even in patients who have a supratentorial mass le- sion with early central herniation. The second error occurs in those occasional patients with metabolic coma (e.g., hepatic coma or hypogly- cemia) who have strikingly asymmetric motor signs with hyperventilation and deep coma. In this instance, the preservation of intact and sym- metric pupillary and oculovestibular responses provides strong presumptive evidence for meta- bolic rather than structural disease. It is stupor and coma caused by metabolic brain disease that most challenges the internist, neurologist, or general physician likely to be reading this monograph. If patients suffer from major damage caused by supra- or infratentorial mass lesions or destructive lesions, specific treat- ment often involves a surgical or intravascular procedure. If psychogenic unresponsiveness is the problem, the ultimate management of the patient rests with a psychiatrist. In metabolic brain disease, however, the task of preserving the brain from permanent damage rests with the physician of first contact. The physician should first evaluate the vital signs, provide adequate ventilation and arterial pressure, and then draw blood for metabolic studies. Metabolic studies that should be secured from the first blood drawing are indicated in Table 7–5. Because drug ingestion is a common cause of coma, procure blood and urine for toxicologic study on all patients (see Table 7–6). Those metabolic encephalopathies that are most likely to pro- duce either irreversible brain damage or a quick demise but are potentially treatable in- clude drug overdose, hypoglycemia, metabolic or respiratory acidosis (from several causes), hyperosmolar states, hypoxia, bacterial men- ingitis or sepsis, and severe electrolyte imbal- ance. It is important to secure an arterial sample for blood gas analysis, although emergency management may have to begin even before laboratory results are returned. Both acidosis and alkalosis can cause cardiac arrhythmias, but acute metabolic acidosis is more likely to be lethal; however, pH is not an independent predictor of mortality in critically ill patients with metabolic acidosis. 83 Whether sodium bi- carbonate should be given to treat severe aci- dosis is controversial. 84–86 The agent is not indicated in the treatment of diabetic acidosis and may not be helpful in treating acidosis from other causes. Instead, urgent treatment of the underlying cause of the acidosis is probably the best approach. Relieve hypoxia immediately by ensuring an adequate airway and delivering sufficient oxygen to keep the blood fully oxy- genated. Even in the presence of a normal PaO 2
cient to supply the brain’s needs for several reasons: (1) the hemoglobin may be abnor- mal(carboxyhemoglobinemia,methemoglobine- mia, or sulfhemoglobinemia). Methemoglobin or sulfhemoglobin are diagnosed by the typical chocolate appearance of oxygenated blood, and patients are treated with methylene blue (1 to 2 mg/kg IV over 5 minutes). 87,88 Topical
anesthetic agents such as benzocaine used in endoscopy can cause acute methemoglobi- 324 Plum and Posner’s Diagnosis of Stupor and Coma nemia. 89 (2) Carbon monoxide binds hemo- globin with 200 times the affinity of oxygen and thus displaces oxygen and yields carboxyhe- moglobin. The PaO 2 is normal and the pa- tient’s color is pink or ‘‘cherry red,’’ but he or she is hypoxic because insufficient hemoglobin is available to deliver oxygen to the tis- sue. Such patients should be given 100% oxy- gen and hyperventilated to increase blood oxygenation. Hyperbaric oxygenation may im- prove the situation, and if a hyperbaric cham- ber is available, it should probably be utilized for patients with life-threatening exposure. 90 (3) Severe anemia itself will not cause coma, but lowers the oxygen-carrying capacity of the blood even when the PaO 2 is normal, and thus decreases the oxygen supply to the brain. In patients with other forms of hypoxia, anemia may exacerbate the symptoms. Severe anemia (hematocrit less than 25) in a comatose patient should be treated with transfusion of whole blood or packed red cells. (4) Tissues can be hypoxic even when the PaO 2 and O 2 content is normal if they cannot metabolize the oxy- gen(e.g.,cyanide poisoning).Hydroxocobalamin administered as a one-time dose of 4 to 5 g IV is a safe and effective method of treating poi- soning. 91
febrile, whether or not nuchal rigidity and/or other signs of meningeal irritation (e.g., posi- tive Kernig or Brudzinski signs or jolt accen- tuation; see page 133) are present, consider acute bacterial meningitis. As described above, initial treatment includes antibiotic and steroid administration, followed as soon as possible by CT scan and lumbar puncture if no mass is seen that would threaten herniation. It is often useful to do a Gram stain of the centrifuged sediment, as this may yield an organism that can guide therapy; additional CSF should be sent for culture; polymerase chain reaction (PCR) analysis for bacteria and viruses, espe- cially herpes viruses; and additional tests as may be dictated by the clinical situation. The absence of cells in the spinal fluid does not rule out acute bacterial meningitis; if there is a high index of suspicion, the lumbar puncture can be repeated in 6 to 12 hours. The centrifuged sed- iment should also be examined by Gram stain, as occasionally organisms may be seen even before there is pleocytosis. Severe potassium imbalance usually affects the heart more than the brain. Accordingly, an electrocardiogram often suggests the diagnosis before serum electrolytes are returned from the Table 7–6 Stat Toxicology Assays Required to Support an Emergency Department Quantitative Serum Toxicology Assays Qualitative Urine Toxicology Assays Acetaminophen (paracetamol) Cocaine Lithium
Opiates Salicylate Barbiturates Co-oximetry for oxygen saturation, carboxyhemoglobin, and methemoglobin Amphetamines Theophylline Propoxyphene Valproic acid Phencyclidine (PCP) Carbamazepine Tricyclic antidepressants (TCAs) Digoxin
Phenobarbital (if urine barbiturates are positive) Iron Transferrin (or unsaturated iron-binding capacity [UIBC] assay if transferrin is not available) Ethyl alcohol Methyl alcohol Ethylene glycol From Wu et al., 93 with permission. Approach to Management of the Unconscious Patient 325
laboratory. It usually is advisable to adjust both electrolyte and acid-base imbalances slowly, since too rapid correction often leads to over- shoot or intracellular-extracellular imbalances and worsens the clinical situation. 92 Drug overdose is a common cause of coma in patients brought to an emergency room. Many emergency departments can provide a rapid assessment of toxic drugs (Table 7–6). 93 Most of these drugs are not rapidly lethal but, because they are respiratory depressants, they risk pro- ducing respiratory arrest or circulatory depres- sion at any time. Therefore, no stuporous or comatose patient suspected of having ingested sedative drugs should ever be left alone. This is particularly true in the minutes immediately following the initial examination; the stimula- tion delivered by the examining physician may arouse the patient to a state in which he or she appears relatively alert or his or her respiratory function appears normal, only to lapse into coma with depressed breathing when external stimulation ceases. The management of specific drug poisonings is beyond the scope of this chapter,
88,94 but certain general principles ap- ply to all patients suspected of having ingested sedative drugs. The type of medication influ- ences the treatment and its duration. Accord- ingly, search the patient and ask relatives or the police to search the patient’s living quarters for potentially toxic agents, or empty medication vials that might have contained sedative drugs. Both respiratory and cardiovascular failure may occur with massive sedative drug overdose. An- ticipation and early treatment of these compli- cations often smooth the clinical course. Insert an endotracheal tube in any stuporous or coma- tose patient suspected of drug overdose and be certain that an apparatus for respiratory support is available in case of acute respiratory failure. The placement of a central venous line allows one to maintain an adequate blood volume without overloading the patient. Give generous amounts of fluid to maintain blood volume and blood pressure, but avoid overhydrating oli- guric patients. Place a pulse oximeter on the fin- ger, but also measure arterial blood gases; a dif- ference between the two (oxygen saturation gap) may indicate poisoning. Carbon monoxide, methemoglobin, cyanide, and hydrogen sulfide cause an increased oxygen saturation gap. Once the vital signs have been stabilized, one should attempt to remove, neutralize, or reverse the effects of the drug. Attempts to remove poi- son from the gastrointestinal tract and thus prevent absorption have included inducing vo- miting with syrup of ipecac, 95 gastric lavage, 96 cathartics, 97 activated charcoal ingestion, 98 and
whole bowel irrigation. 99 Position papers from the American Academy of Clinical Toxicology and the European Association of Poison Cen- ters and Clinical Toxicologists indicate a lack of evidence that inducing vomiting is helpful; it is contraindicated in patients with a decreased level or impending loss of consciousness. 95 They
concluded that gastric lavage should not be employed routinely, but could be considered in patients who have ingested a potentially life- threatening amount of a poison within an hour of the time they are to be treated. 96 However, aspiration is a common complication, and so patients with impaired consciousness should be intubated first. Cathartics have no role in the management of the poisoned patient. 97 A single
dose of activated charcoal (50 g) can be ad- ministered to a patient with an intact or pro- tected airway but it will not efficiently adsorb acid, alkali, ethanol, ethylene glycol, iron, lith- ium, or methanol. Multiple doses of charcoal administered at an initial dose of 50 to 100 g, and then at a rate of not less than 12.5 g/hour via nasogastric tube, may be indicated when patients have ingested a life-threatening amount of carbamazepine, dapsone, phenobarbital, qui- nine, or theophylline. In addition to eliminating drugs from the small bowel, the agents may interrupt the enteroenteric and, in some cases, the enterohepatic circulation of drugs. 100 Whole
bowel irrigation using polyethylene glycol elec- trolyte solutions may decrease the bioavailability of ingested drugs, particularly enteric-coated or sustained-release drugs. 99 Intravenous sodium bicarbonate in amounts sufficient to produce a urine pH of 7.5 promotes the elimination of salicylate, phenobarbital, and chlorpropamide. 101
For very severe poisoning with barbiturates, glutethimide, salicylates, or alcohol, hemodialysis or hemoperfusion may be necessary. 100,101 Although acetaminophen does not by itself cause impaired consciousness, it may be included in opioid combinations (e.g., acetaminophen with codeine or oxycodone), and is often included in polydrug overdoses. Doses above 5 g in adults may cause acute hepatic in- jury, especially if combined with other hepato- toxins such as ethanol, and when acetamino- phen overdose is suspected, the patient should be treated with N-acetylcysteine as well. 103
326 Plum and Posner’s Diagnosis of Stupor and Coma Psychogenic Unresponsiveness Psychogenic unresponsiveness is characterized by a normal neurologic examination, including normal waking oculocephalic and oculovestibu- lar responses. Once one has considered the pos- sibilityofpsychogenicunresponsivenessandper- formed the appropriate neurologic examination, little difficulty arises in making the definitive diagnosis. If the patient meets the clinical cri- teria for psychogenic unresponsiveness, no fur- ther laboratory tests are required. If, however, there is still some question after the examination, an EEG is the most helpful diagnostic test. An EEG that shows normal alpha activity inhib- ited by eye opening and other stimuli strongly supports the diagnosis of psychogenic unre- sponsiveness. The Amytal interview (see Chap- ter 6) may be both diagnostic and therapeutic. In Yüklə 9,02 Mb. Dostları ilə paylaş:
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