Altered Mental Status (Case 52)

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Chapter 60
Altered Mental Status (Case 52)

Nils Petersen MD

Case: The patient is a 25-year-old man without significant past medical history. His girlfriend had called his private physician earlier this morning because he was confused and agitated overnight. He awakened her from sleep at around 2 AM after he fell over a chair and soon after urinated in the corner of their bedroom. He appeared confused and was complaining of a headache. He finally went back to sleep. This morning she was unable to awaken him, and he is warm to the touch.

Differential Diagnosis

Meningitis/encephalitis	Subarachnoid hemorrhage (SAH)	Trauma
Hypoglycemia	Intracranial hemorrhage	Intoxication

Speaking Intelligently

In evaluating a patient with altered mental status (AMS), determine whether the patient’s level of consciousness is impaired, whether this is a disorder of thought content, and the time course of the illness. In derangements in level of consciousness that are acute and severe, it may be necessary to act faster to prevent permanent neurologic damage or even death. When assessing level of consciousness, it is essential to be able to very clearly pinpoint the patient’s response to stimulus level; in this sense, it is more important to describe the patient’s state of consciousness according to how he or she is acting or responding (e.g., sleepy, not responding to painful stimuli) than using nonspecific medical jargon such as “lethargic” or “confused.” Such early, rapid assessments of severity and time course help to direct the rest of the examination, workup, and management.

PATIENT CARE

Tests for Consideration

Diagnostic testing can be extremely helpful in many cases, but your clinical findings should guide your workup and not vice versa. As a result, there is no one algorithm for evaluating patients with AMS, and each case should be considered individually. The common indications and utility of various tests are discussed below.

• A fingerstick glucose test is more accurate than the glucose measurement on a complete metabolic profile and is very quick, easy, and cheap. It should be done first to check for either hypoglycemia or hyperglycemia, which both can cause altered consciousness and even mimic symptoms of stroke. Keep in mind that many patients with AMS receive a bolus of dextrose 50% in water (D50) by emergency medical services (EMS) before coming to the ED.	$5
• Laboratory studies: A complete blood count (CBC) is commonly performed for elevated white blood cell (WBC) count in infections or low WBC count suggesting immunocompromised status or sepsis. Thrombocytopenia and AMS may result from thrombotic thrombocytopenic purpura (TTP). Complete metabolic profile may reveal important electrolyte abnormalities such as hyponatremia, hypoglycemia, hypocalcemia, hypercalcemia, or uremia. Acute changes in these values are more important than absolute numbers and are more likely to cause AMS. Abnormal liver function tests may also suggest hepatic encephalopathy. A thyroid-stimulating hormone (TSH) value does not come back as rapidly from the lab, but thyroid abnormalities can definitely cause altered consciousness in patients with either hyperthyroidism or hypothyroidism.	$11, $12, $12, $24
• A urine toxicology/drug screen is always a good idea, especially in those with a psychiatric history or when polypharmacy is suspected. Remember that a blood alcohol concentration should be obtained in addition to the urine toxicology.	$21
• Chest radiograph and urinalysis can be useful for confirming a source of infection (pneumonia or urinary tract infection [UTI]) because elderly people cannot always mount an immune response and this is a common cause of delirium.	$45, $4
• An electrocardiogram (ECG) is important, especially because confusional states can sometimes be the only manifestation of an acute myocardial infarction.	$27
• Lumbar puncture (LP) with cerebrospinal fluid (CSF) analysis is useful in both diagnosis of infection, SAH, and, rarely, leptomeningeal carcinomatosis. Keep in mind that the LP should be done before the introduction of antibiotics, because the results will be indispensable in tailoring your antimicrobial therapy. However, if you suspect that your patient has bacterial meningitis and there is a delay in performing the LP, emergent empirical antibiotics (and dexamethasone) should be administered before CSF analysis. Opening pressure should be measured and CSF sent for cell count and differential, Gram stain, and cultures, as well as glucose and protein concentrations. Further specific microbiology and nucleic acid amplification testing, such as polymerase chain reaction (PCR), can be pursued if other etiologies are suspected.	$272
• Electroencephalography (EEG) can be used to assess for epileptiform (seizure) activity as in complex partial seizures of nonconvulsive status. It might also give clues in cases of toxic metabolic encephalopathy and herpes simplex encephalitis.	$170

IMAGING CONSIDERATIONS

→ CT of the head without contrast is often the first test in acute confusional state. It is immediately available and can identify structural brain damage or hemorrhage. It is not indicated as a routine test for patients with AMS and should be reserved for patients with new focal deficits, those who are stuporous or comatose, those who have history or evidence of head trauma, and, finally, those without a plausible etiology of their symptoms despite thorough history, physical examination, and basic lab tests and radiography.

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→ Brain MRI allows a more detailed examination of the brain and may be useful for visualizing parenchymal infections, acute strokes in the posterior fossa, or brainstem lesions. However, it is costly, may take up to days to acquire, and is not universally available.

$534

Clinical Entities

Medical Knowledge

Meningitis/Encephalitis (see also Chapter 64, Headache)
Pφ	Meningitis and encephalitis are usually caused by hematogenous spread of a systemic bacterial or viral infection. The course of the disease, from a more localized benign infection to disseminated and lethal, depends on the type and aggressiveness of the organism as well as on the immune status of the host.
TP	Clinical manifestations typically include fever, decreased level of consciousness, pain or difficulty with flexing the neck, and, in the case of encephalitis, focal neurologic signs and possibly seizures.
Dx	Clinical suspicion and diagnosis are confirmed by CSF analysis. In the case of encephalitis, MRI and/or EEG might be helpful. Blood cultures should also be drawn to assess for systemic infection.
Tx	Early, empirical antibiotic and/or antiviral therapy is the treatment of choice. Corticosteroids, in addition to antibiotics, may improve prognosis for certain etiologies of bacterial meningitis. See Cecil Essentials 97.

Intoxication or Substance Withdrawal
Pφ	The mechanism of intoxication is drug-specific, but many common medications and recreational drugs can alter neurotransmitter levels and therefore affect mental status. Similarly, sudden discontinuation of sedative or psychotropic medication, or of alcohol, can cause an acute change in mental status, as this causes a relative shift in neurotransmitter levels from baseline.
TP	Signs include rebound tachycardia and hypertension, in combination with acute delirium or seizure.
Dx	Diagnosis is based on history and clinical suspicion, evidence of intoxication/withdrawal on physical exam (e.g., abnormal vital signs, dilated or constricted pupils, and diaphoresis), and abnormal lab results (e.g., anion gap acidosis, elevated salicylate level), and is confirmed by urine toxicology screen and/or blood alcohol concentration.
Tx	Treatment consists of ABCs and substance-specific interventions. For some drug intoxications, an antidote may be available, while others may require treatment with activated charcoal or gastric lavage, depending on the scenario. Still others may require dialysis, though only some substances can be removed by this method. For many substances the patient will require supportive care until the drug effects abate. Patients with withdrawal often need supportive care: medication tapering or, for alcoholics, treatment with benzodiazepines to prevent delirium tremens. See Cecil Essentials 135.

Systemic Infection
Pφ	Systemic infections such as sepsis, pneumonia, UTI, infected decubitus ulcers, and spontaneous bacterial peritonitis (to name a few) can diffusely affect cerebral neurochemical functioning and are probably among the most common causes of acute confusional states.
TP	Delirious patients exhibit signs of acute change in mental status that may manifest as either hyperactivity or hypoactivity, usually accompanied by inattention and cognitive deficits that cannot be accounted for by a preexisting condition. By definition, delirium lasts only for a short time. It is important to note that delirium may be the only manifestation of systemic infection or other illness in an older patient, so it is critically important to always search for an infectious or cardiac source in this patient population!
Dx	Diagnosis is clinical, based on the above symptoms. CBC, blood cultures, chest radiograph, and urinalysis may be helpful in the initial approach.
Tx	Treatment consists of antibiotics for any underlying illness and supportive care with or without symptomatic treatment with psychotropic medications for agitation. Remember that once patients have an in-hospital episode of delirium from any cause, their mortality significantly increases, so be aggressive in finding the source and initiate treatment. See Cecil Essentials 96.

Intracranial Hemorrhage (see also Chapter 64, Headache)
Pφ	Epidural, subdural, or intraparenchymal bleeding in the brain leads to focal neurologic deficits by direct impact at the site of bleeding as well as by suddenly increasing intracranial pressure, thereby causing bilateral cerebral dysfunction. This, in turn, may cause an alteration in consciousness. Further swelling and mass effect might eventually lead to herniation and brain death, depending on the initial size of the hemorrhage.
TP	Severe headache, focal neurologic deficits, and decreased level of consciousness can all be seen. Patients may also present with hypertension as either a cause or an effect of the hemorrhage.
Dx	CT scan will reliably detect an acute intracranial hemorrhage.
Tx	Neurosurgical intervention depends on localization of the hemorrhage (e.g., subdural vs. epidural vs. intraparenchymal), size of the hemorrhage, and presence of midline shift. Otherwise, supportive care is provided, with reversal of any anticoagulation and management of increased intracranial pressure and blood pressure. See Cecil Essentials 127.

Subarachnoid Hemorrhage (see also Chapter 64, Headache)
Pφ	Sudden rupture of a saccular intracranial aneurysm with bleeding into the subarachnoid space causes cytokine release and inflammation that can diffusely impair brain metabolism as well as cause brain edema. Vasospasm may also occur within 3–7 days and result in acute ischemic stroke, causing further brain edema and worsened consciousness. In addition, SAH can cause acute hydrocephalus as CSF drainage is obstructed.
TP	Symptoms consist of sudden onset of an extremely severe headache (“worst headache of my life”), with or without nuchal rigidity or impaired level of consciousness.
Dx	CT scan usually reveals blood in the subarachnoid space, but if CT is negative and clinical suspicion is high, LP may show fresh blood or xanthochromia (yellow CSF from degraded red blood cells [RBCs]) in the case of a small hemorrhage.
Tx	Cerebral angiogram is both diagnostic and therapeutic to find the source of bleeding and coil the aneurysm. Otherwise, supportive care is provided with reversal of any anticoagulation or antiplatelet therapy and management of increased intracranial pressure and blood pressure. Administration of IV calcium channel blockers can prevent vasospasm; occasionally aggressive neurosurgical intervention is necessary to treat hydrocephalus. See Cecil Essentials 124.

Metabolic Encephalopathy
Pφ	Failure of different organ systems such as liver, kidneys, lungs, pancreas, thyroid, pituitary, or adrenal glands can lead to metabolic encephalopathy (brain dysfunction). Depending on the organ involved, this can be caused by accumulating toxins, electrolyte disturbances, changes in acid–base metabolism, endocrine effects, hypoxia, hypercapnia, or a combination of these factors. Eventually there may be to changes in neurotransmission or brain metabolism, brain edema, and decreased brain perfusion.
TP	Metabolic derangements cause changes in level of consciousness without other focal neurologic signs. Depending on the severity of the metabolic abnormality, this can range from mild clouding of consciousness to stupor or coma. Sometimes the additive effect of multiple mild abnormalities can lead to severe encephalopathy.
Dx	Clinical suspicion and examination will lead to the diagnosis, which is often confirmed with basic laboratory testing. Imaging with either CT or MRI will help to exclude other etiologies. An EEG may be helpful in showing diffuse cerebral dysfunction.
Tx	The primary concern here consists of the ABCs; treatment of the underlying abnormality and supportive care are essential. See Cecil Essentials 113.

a. Paraneoplastic limbic encephalitis: An immune response directed against antigens of some types of cancer, especially small cell lung cancer, can lead to antibody formation. These antibodies then attack structures in the central nervous system (CNS) limbic system, causing various neurologic symptoms including profound memory impairment, acute confusional state, seizures, and other psychiatric or neurobehavioral manifestations. These neurologic symptoms often precede the diagnosis of the underlying malignancy.

b. TTP: Caused by an immune-mediated deactivation of a von Willebrand factor–cleaving protease, eventually leading to platelet activation. This multisystem disorder causes thrombocytopenia, microangiopathic hemolytic anemia, fever, renal dysfunction, and/or neurologic dysfunction.

c. Leptomeningeal carcinomatosis: Diffuse metastatic spread of a systemic cancer to the leptomeninges can cause a variety of neurologic symptoms such as headache, gait disturbance, and/or cranial nerve dysfunction, as well as AMS.

Practice-Based Learning and Improvement: Evidence-Based Medicine

Title
A multicomponent intervention to prevent delirium in hospitalized older patients

Authors
Inouye SK, Bogardus ST, Jr, Charpentier PA, et al.

Institution
Department of Medicine, Epidemiology and Public Health, Yale University School of Medicine, New Haven, Connecticut

Reference
N Engl J Med 1999;340:669–676

Problem
Delirium is a frequent complication among older hospitalized patients. It not only increases length of hospital stays and Medicare expenditures, but is also associated with a significant increase in patient morbidity and mortality.

Intervention
In this study, 852 elderly patients admitted to the general-medicine service at a teaching hospital were prospectively assigned to either the intervention group or the control group. The intervention consisted of standardized protocols for the management of six risk factors for delirium: cognitive impairment, sleep deprivation, immobility, visual impairment, hearing impairment, and dehydration.

Quality of evidence
Level II-1

Outcome/effect
The incidence of delirium was significantly lower in the intervention group than in the control group (10% vs. 15%). There was also a reduction in the total number of hospital days in patients with delirium (105 vs. 161) and the total number of episodes (62 vs. 90) in the intervention group. However, the severity of delirium was not significantly different.

Historical significance/comments
This study shows that delirium is preventable, most effectively in patients with intermediate risk for delirium at baseline. The intervention, however, is labor intensive, involving multiple specialties, and further studies are needed to determine its effect on outcome such as mortality, repeat hospitalization, institutionalization, or need for home care.

Interpersonal and Communication Skills

Talk with Family When an Advance Directive Is Not Available

When an advance directive is not available, it is necessary to talk to a patient’s family in order to elicit information about a patient’s wishes. Be sure to ask family members what the patient would have wanted in this situation, not what the family members want for the patient. Family members will frequently confuse their own wishes to keep the patient alive with what the patient might have actually wanted. Determine whether the patient ever had any conversations with a family member about what he or she would or would not want toward the end of life. If they have not had direct conversations, ask if the patient ever expressed any opinions about a friend, family member, or anyone else who was in a similar situation. A family member’s recollection of such a conversation can be enlightening. At the conclusion of a family meeting, present all of the appropriate treatment options. Be sure to give the family members adequate time for thought and discussion before they are asked to come to a decision. Make a plan to check in with them at a specified interval. If there is no health-care proxy, it is imperative for the family to designate a point person with whom you will communicate primarily to prevent misunderstandings and repetitive discussions with different people. Be aware that some family members may react with anger, which is often a reflection of personal guilt. Remain calm and empathetic, and remember that you are there to provide your medical perspective. Thoughtful, honest, and clear communication goes a long way in guiding your care and preventing major missteps.

Professionalism

Assess Capacity and Respect Autonomy

Any physician is qualified to assess patient capacity, which is often at the crux of respecting the patient’s decision making. In general, it is important to remember that capacity is situation-specific and that patients may have capacity to make some decisions but not others. The patient must have insight into his or her disease and be able to understand the risks and benefits of treatment options. It is perfectly acceptable to obtain consent or have conversations about treatment when the patient is lucid. Keep in mind that a person who has capacity will be consistent in his or her decision, so if you ask the patient about the same issue multiple times, the decision should remain the same. In some instances, however, such as cases of coma or stupor, it is very clear that patients lack capacity; therefore, it is always important to check whether patients have advance directives or a health-care proxy in place, as these are meant to be extensions of patient autonomy.

Systems-Based Practice

Stroke Protocol Is an Example of System-Based Coordination for Best Patient Care

The assessment of patients with suspected stroke is an emergency because of the limited therapeutic window for thrombolytic treatment; the stroke patient must be examined, evaluated, and then optimally treated with tissue plasminogen activator (t-PA) within 3 hours of onset. Although many patients are not candidates for TPA, it is of the utmost importance to evaluate them quickly and decide on appropriate management. To this end, the hospital-wide “code stroke” was developed to ensure that a patient is seen by a neurologist, has appropriate lab tests, and has a CT scan interpretation within 60 minutes of arriving at the hospital. Once a code stroke is called, the staff understands that this patient’s workup becomes top priority. The code stroke has established a more efficient protocol for evaluating suspected stroke patients; previously, precious time was often wasted in the challenge to coordinate the required consultations, lab workup, and head imaging.