History
Head CT
• Neurologic consultation
• Lumbar puncture
• EEG
• MRI brain
Neurologic examination, vital signs, glucose level (exclude pain and agitation).
Urine, blood, and sputum cultures, CXR, lumbar puncture
Mannitol, neurosurgical evaluation, treat elevated intracarinal pressure
• Medication review
• Correct environmental factors
• CBC, CMP, magnesium, phosphorus serum, and urine toxicology screen, drug levels, urinalysis
• ECG, CXR
• Thyroid profile, RPR, B12 level, ammonia
Chronic dementia or psychiatric illness
New delirium
Chronic Acute
Focal findings or history of head
trauma Low-glucose
trauma
Seizures Thiamine and D50
Fever, meningismus
Nonfocal examination
Signs of herniation
No cause found
EEG
CT, computed tomography; EEG, electroencephalography; CXR, chest radiography; CBC, complete blood cell count; CMP, complete metabolic panel; electrocardiography; RPR, rapid plasma regain; MRI, magnetic resonance imaging.
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TABLE 57.1 Risk Factors for Delirium Age
Baseline dementia or cognitive impairment Psychiatric comorbidity
History of alcohol or drug abuse Low albumin/malnutrition
Psychosocial stress (e.g., death of spouse) Hearing or visual impairment
Sleep deprivation
History of multiple medical problems
W O R K - U P
The work-up of altered mental status in the ICU begins with knowledge of their baseline cognitive function, including known dementia and level of functional inde- pendence. Dementia is highly underdiagnosed; often people’s living arrangement and activity level can be useful data. The time line of the delirium is of course essential to distinguish the cause from a primary neurologic insult to the sequelae of medications, abnormal sleep patterns, and metabolic disturbance. It is essential to see delirium as both an indication of an evolving pathology and a problem in itself that needs to be treated; giving a sedative without consideration of etiology may lead to masking a developing crisis.
The general and neurologic examinations guide the search for insults that cause delirium. Some causes may be obvious when you walk in the patient’s room: fever, hypoxemia, or hypotension is easily assessed on any continuous ICU monitor. Hypo- glycemia can likewise be rapidly assessed. The goal of the neurologic assessment is similar to that of coma in that discovery of focal signs helps differentiate a structural neurologic cause from a metabolic or infectious cause. Any asymmetry should raise concern for a focal lesion and may constitute an emergency. Subtle signs of seizure (eye or head deviation, rhythmic movements of the face or extremities) are sought.
See Chapter 55 on coma for further explanation of the relevant neurologic examina- tion.
The differential diagnosis of delirium is broad (Table 57.2). A careful examina- tion, medication review, and basic laboratory studies will address most causes. Medi- cations are among the most common causes of delirium in the ICU (Table 57.3). In addition to current medications potentially causing cognitive dysfunction, recently dis- continued medicines with a withdrawal potential, new drug interactions, or change in the metabolism of previously well-tolerated medications should be addressed. Always be willing to reconsider a change in a patient’s physiology; do not assume that a patient’s cognition is drifting down just because of his or her presence in the ICU. Liver and renal dysfunction may alter medication levels; elderly patients may become delirious even with “therapeutic” levels.
Basic studies include chemistries, blood counts, electrolytes, urine and blood toxicology, ammonia, drug levels, urine analysis, electrocardiography, and chest radio- graphy. Thyroid testing and checking of vitamin B12and rapid plasma reagin levels are done to establish the reversible causes of dementia. Any suspicion for infection such as fever, meningismus, or leukocytosis should be pursued with blood cultures and lumbar
Neurologic Disorders rDelirium and Sedation 4 6 1
TABLE 57.2 Causes of Delirium
Vascular Stroke, hemorrhage, reversible posterior leukoencephalopathy, vasospasm, migraine
Toxins Medications, alcohol, illicit drugs, occupational exposures, withdrawal
Seizures Aura, ictal state, nonconvulsive status epilepticus, postictal state Other organs Hepatic, uremia, cardiac disease, lung disease
Electrolytes Hypoglycemia, hyponatremia, hypocalcemia, hypomagnesemia Neoplastic Primary tumor, metastases, carcinomatous meningitis,
paraneoplastic syndromes
Infection Urinary tract infection, pneumonia, meningitis/encephalitis, sepsis
Trauma Direct trauma, edema, diffuse axonal injury, postconcussive syndrome
Autoimmune Neuropsychiatric lupus, Hashimoto encephalopathy, CNS vasculitis, limbic encephalitis
Endocrine Hypo/hyperthyroidism, hypopituitary state, hyper/
hypoparathyroidism
Nutritional Vitamin B12deficiency, Wernicke encephalopathy (thiamine deficiency), Machiafava–Bignami disease
CNS, central nervous system.
TABLE 57.3 Medications that Can Cause Delirium
During use Withdrawal
Anticholinergic agents Appetite suppressants
Sedatives Cough/cold remedies
Antiemetics Alcohol (even without delirium tremens) Antipsychotics Selective serotonin reuptake inhibitors
Antispasmodics Nicotine
Tricyclic antidepressants Baclofen Muscle relaxants
Digoxin Cimetidine Anticonvulsants Corticosteroids Lithium
Benzodiazepines Barbiturates Opioids
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TABLE 57.4 Nonmedication Causes of Delirium
Cause Treatment
Disorientation Frequent reorientation
Sleep cycle change Provide stimulating activity, keep out of bed during day, no interruptions at night
Sensory deficits Put on glasses, hearing aids Poor communication Communication devices
Catheters, restraints Remove catheters, tubes, and restraints as early as possible
Dehydration Assess for dehydration and hydrate Malnutrition Feed with parenteral nutrition if needed
Pain Assess for and treat pain
Immobility Remove restraints early, range-of-motion exercises, keep out of bed
Urinary retention Place a bladder catheter or start scheduled catheterizations
Constipation Disimpact if needed, start bowel routine Fever Antipyretics, scheduled if necessary Infection Search for and treat underlying infection Hypoxemia, hypercarbia Check arterial blood gases, ventilate or oxygenate
as needed
puncture. Other causes of delirium (Table 57.4) should also be sought and corrected, if possible.
If the cause of delirium is not found, neurologic consultation should be obtained.
Serious conditions can exhibit subtle findings or even nonfocal examination. For instance, strokes in the nondominant hemisphere can cause delirium in the absence of hemiparesis, or fluent aphasia may be mistaken for delirium. Nonconvulsive status epilepticus may have no symptoms except delirium (see Chapter 51). Lumbar punc- ture, electroencephalography, brain imaging, and more specific laboratory studies are usually needed at this point.
T R E A T M E N T O F D E L I R I U M
A methodical and thorough approach will help identify the cause of delirium in most cases and should guide the treatment. However, a useful technique to combat the contribution of delirium that is due simply to the routine of being in the ICU include family members bringing in familiar objects (glasses, hearing aids, clocks, calendars, photographs of friends, and family) and regular reorientation of the patient. Placing patients in rooms with natural light helps restore normal sleep–wake cycles, and if pos- sible, limit stimulation at night. Next, approach the differential systematically. After a neurosurgical or neurologic cause has been evaluated and the remaining possibili- ties are metabolic and pharmacologic, eliminate any potential inciting medications.
Likewise, address the metabolic dysfunction if possible.
Neurologic Disorders rDelirium and Sedation 4 6 3
If delirium persists despite treating possible causes or if treating of causes is not feasible, consider treating symptoms pharmacologically. This should not be the first choice, redirection is always the first option followed by soft restraints. If more exten- sive physical restraints leave the patient agitated and uncomfortable, then escalate to pharmacologic treatment. The goal should not be to make the patients unconscious but to treat them to the point that they are not a danger to themselves. Although hypoactive delirium should be monitored and evaluated, we would not recommend trying to improve level of consciousness in the acute setting with activating medica- tions. Although no randomized controlled trials have been done to prove efficacy of any one agent for delirium, clinical experience has shown relative efficacy and superior- ity of antipsychotic medications. Although atypical antipsychotics are becoming more popular, haloperidol is still the most commonly used medication. It is given at 1 to 10 mg intravenously or intramuscularly repeated every 30 minutes until effect and then continuing at 25% of the effective dose every 6 hours. A scheduled regimen is more effective than as-needed dosing; elderly or small patients receive a smaller dose. Newer antipsychotics include quetiapine, risperidone, and olanzapine, all of which are given orally or enterally, and ziprasidone, which is also available in an intramuscular form.
Patients treated with antipsychotics need to be carefully monitored for fever or rigidity (indicating neuroleptic malignant syndrome), extrapyramidal symptoms (tremors, stereotypic movements, dystonia), and QT interval prolongation, which can lead to fatal arrhythmias. All patients should have a baseline and daily electrocar- diogram. Benzodiazepines may be effective but are not the first-line sedative, as they tend to have lingering affects and disturb sleep architecture, which can worsen delir- ium. The exception is delirium caused by withdrawal from long-term use of alcohol, benzodiazepines, or barbiturates. An unfortunately common habit in the ICU is to overmedicate patients with sedatives and analgesics while undertreating delirium. A more prudent approach is to evaluate for delirium, pain, and anxiety separately and treat each specifically.
S E D A T I O N I N T H E I N T E N S I V E C A R E U N I T
In critical care medicine, sicker patients are becoming more dependent on invasive devices, frequently necessitating pharmacologic sedation for patient comfort. Titrating to a predefined goal and avoiding oversedation is imperative. The risk of delirium after sedation is proportional to the amount of medications used. The modified Ramsey sedation scale (Table 57.5) is a commonly used tool in the ICU setting; another scale focusing more on agitation is the Richmond Agitation Sedation Scale Sedationag (Table 57.6). Having a sedation goal with frequent titration of medicines as part of institutional protocols eases communication between medical personnel and helps to avoid inappropriate over sedation.
TABLE 57.5 Modified Ramsey Sedation Scale 1 Patient anxious and agitated or restless or both 2 Patient cooperative, oriented, and tranquil 3 Patient responds to commands only
4 Asleep, brisk response to a light glabellar tap or loud auditory stimulus 5 A sluggish response to a light glabellar tap or loud auditory stimulus 6 No response to a light glabellar tap or loud auditory stimulus
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TABLE 57.6 Richmond Agitation Sedation Scale +4 Combative, violent, danger to staff
+3 Pulls or removes tube(s) or catheters; aggressive +2 Frequent nonpurposeful movement, fights ventilator +1 Anxious, apprehensive but not aggressive
0 Alert and calm
−1 Awakens to voice (eye opening/contact)>10 sec
−2 Light sedation, briefly awakens to voice (eye opening/contact)<10 sec
−3 Moderate sedation, movement or eye opening. No eye contact
−4 Deep sedation, no response to voice, but movement or eye opening to physical stimulation
−5 Unarousable, no response to voice or physical stimulation
Usual sedation protocols combine benzodiazepines and opioids. Continuous infusions may be beneficial in avoiding oversedation and withdrawal, but they may not be available in all situations. Propofol, with a very short half-life, is advantageous in situations in which frequent neurologic examinations are needed. However, because of the lipid components of propofol formulation and subsequent infection risk, propofol should only be used for the short term. The central alpha-2 agonist dexmedetomi- dine (Precedexr) allows for patients to be aroused for examinations but otherwise keeps them comfortably sedated. Sedation protocols differ and should be targeted to the specific patient population (neurologic, medical, or surgical ICU), in addition to having a built-in sedation target with parameters for modification for each individual patient. Our approach to neurologic patients requires that the minimum amount of sedation be used always, as the serial neurologic examination is the most important indicator of changes in cerebral physiology. However, a patient may be so ill from sepsis, acute respiratory distress syndrome, or recent surgery that any activity could worsen their condition, at which point a deeper level of sedation is needed. Although this will increase the likelihood of a longer time of awakening, the first priority is keeping the patient alive. Any paralyzed patient must also be kept on continuous sedation.
Sedation should be weaned as soon as possible. Daily weaning trials have been shown to decrease ventilation time; they also allow for better neurologic examinations.
Ideally, to avoid withdrawal, patients should be switched to scheduled dosing of longer- acting drugs before discontinuing continuous sedation and should be slowly tapered thereafter.
S U G G E S T E D R E A D I N G S
Jacobi J, Frasier GL, Coursin DB, et al. Clinical practice guidelines for the sustained use of sedatives and analgesics in the critically ill adult.Crit Care Med.2002;30:119–141.
Updated (original version published in 1995) practice guidelines for sedation of adult patients in the intensive care setting with comprehensive review of literature.
Lacasse H, Perreault MM, Williamson DR. Systematic review of antipsychotics for the treatment of hospital-associated delirium in medically or surgically ill patients.Ann Pharmacother.
2006;40:1966–1973.
Comprehensive review of data on available antipsychotics for the treatment of delirium.
58 Acute Spinal Cord Disorders
Michael A. Rubin
Acute spinal cord injury (SCI) results from numerous traumatic causes such as motor vehicle collisions, recreational activities, sports injuries, and work-related falls. In addi- tion, many nontraumatic causes of myelopathy have been described (Table 58.1). SCI may lead to devastating life-long disability with major health, emotional, and financial impact, especially if one considers that injuries most commonly occur in the 20–30s when people have young families and are in their most financially productive years.
Despite extensive public education campaigns, licensing requirements, and weapon control laws, SCI continues to increase in its prevalence.
Certain types of myelopathy can be reversed if addressed in a timely fashion;
therefore, prompt recognition of clinical symptoms is imperative. The usual clinical presentation involves a triad of motor impairment (may be asymmetric), sensory loss, and sphincter dysfunction (urine retention, incontinence of stool and/or urine) with preservation of cerebral function (unless there is concomitant traumatic brain injury).
Pain at the corresponding level of the spine is not always present. A group of syndromes has been well described that help localize the level of the injury (Table 58.2). Algorithm 58.1 presents a detailed initial approach to this serious medical emergency. In addition to surgical care and medical interventions for improving neurologic outcome, intensive care unit (ICU) management may be necessary for the systemic complications of SCI.
T R A U M A T I C S P I N A L C O R D I N J U R Y
Cervical cord injury is the most common type of traumatic SCI. Traumatic brain injury is found in up to a half of these patients; just as many may have injuries to other organs. Almost 50% of victims of cord trauma will present in spinal shock with flaccid areflexic paralysis and lack of sensation in all modalities, but it usually resolves within 48 hours. Spine stability is assessed with multiple-view radiography, computed tomog- raphy, and often magnetic resonance imaging (to evaluate for ligamentous injury) to direct surgical interventions or the use of a cervical collar for stabilization. Surgery may have to be done urgently or may be delayed if there is concern for cord edema.
The surgical plan and the stability of the spine are important for critical care man- agement, as limitations of movement while in bed and the ability to extend the neck are important to airway management. Immobilization, performed to limit secondary cord damage due to improper positioning of the unstable spine, carries its own risks, including increased intracranial hypertension, airway compromise, diminished chest wall mobility, pressure sores, and pain.
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TABLE 58.1 Causes of Spinal Cord Injury
rTraumatic and degenerative (compression fractures, disc herniation) rVascular (infarcts, epidural hematoma, arteriovenous malformations) rInfections (abscesses, myelitis, empyema, tuberculosis)
rInflammatory/demyelinating (transverse myelitis, acute disseminating encephalomyelitis, multiple sclerosis)
rNeoplastic (tumors and metastases, postradiation)
rOther (vitamin B12deficiency, syringomyelia, amyotrophic lateral sclerosis, spinal canal stenosis, spondylosis)—usually more chronic course
Neuroprotection
For those patients who present within 3 hours of traumatic injury, methylprednisolone infusion at 30 mg/kg followed by 5.4 mg/kg/hr for 24 hours may improve neurologic function. The infusion may be continued for 48 hours if the injury is 3 to 8 hours old;
however, there is an increased risk of gastrointestinal bleeding and infection associated with prolonged infusion. Review of the studies supporting the use of methylpred- nisolone has led many to question the methodology; therefore, this protocol is con- sidered a therapeutic option and no longer the standard of care. Other interventions have been studied such as GM-1 ganglioside and thyrotropin-releasing hormone.
Cardiovascular Management
Many patients with cervical or upper thoracic cord injury may develop neurogenic shock because of the interruption of the spinal sympathetic chain. Decreased sympa- thetic innervation to the heart and blood vessels results in cardiovascular depression with bradycardia, hypotension, and low systemic vascular resistance. Hemodynamic monitoring is advised, and treatment with fluids and vasopressors to preserve organ per- fusion is essential. Vasopressors with chronotropic/inotropic features (norepinephrine, dopamine) are preferred to augment cardiac function as well as to increase vascular tone.
The optimal blood pressure goal is unclear; experimental data show that hypotension further worsens SCI due to hypoperfusion. We recommend targeting mean arterial
TABLE 58.2 Spinal Cord Syndromes
rComplete transection—loss of bilateral motor and sensory function below level rHemisection—Brown–Sequard syndrome—loss of ipsilateral motor and
proprioception/vibration; contralteral loss of pain and temperature rCentral cord—impairment of hands and arms more than legs rAnterior cord—loss of all modalities except proprioception/vibration rPosterior cord—preservation of motor and pain/temperature, loss of
proprioception/vibration
rCauda equina—extremely painful, asymmetric, lower motor neuron findings, late urinary retention
rConus medularus—less painful, symmetric, mixed upper and lower motor neuron findings, early urinary retention
Neurologic Disorders rAcute Spinal Cord Disorders 4 6 7