The patient with acute mental status change is a common visitor to the emergency department. But, regardless if the specialty a physician practices, it is almost certain that encounter with such a patient will occur. All physicians, including radiologists and ophthalmologists, and certainly primary care physicians, should develop a rapid and efficient strategy to effectively manage this medical or surgical emergency. Acute altered mental status or state (abbreviated AMS) is a term given to an abrupt or acute change in behavior. This change may be psychiatric, with no demonstrable primary causative physiologic cause. In this case, the emergency assessment of psychiatric patients often simply involves using interviewing skills during history-taking. Management is often straight forward, consisting of reassurance and modest sedation. However, the patient who abruptly becomes agitated and combative may have occult hypoxia. ?, all may exhibit an acute aggressive confused state in the pre-collapse phase of their illness. It is always best to assume an acute medical emergency exists when managing acute AMS, and leaving psychiatric diagnoses to the realm of exclusion. In fact, if one excludes ? from the differential diagnosis in any patient with an abrupt and marked AMS, the likelihood of a life-threatening illness being present is very high. One of the most dramatic examples of acute AMS occurs in the patient experiencing an acute large subarachnoid hemorrhage. In a patient who presents rapid unexplainable unconsciousness should be rapidly stabilized and a CAT scan of the brain should be obtained as soon as possible to ensure the greatest chance for survival. Please note that the sense of urgency with which the clinician should proceed in managing any patient with AMS cannot be over-emphasized. The family of the patient with AMS, most often the first people to detect that something was wrong, are very stressed in these situations. Family members should be placed in a quiet area, and be provided with a means to contact various family members. The physician should attempt to have a sit-down talk with the family as soon as possible, for often they will have historical information which will help you in the care of the patient when the diagnosis remains elusive. The goal of this section is to assist the student to develop the basic clinical skills required to manage a patient with acute AMS. For this reason, the content of the chapter has been left to brevity. This chapter should be mastered, as this will serve as the basis for further study and medical practice.
Basic Neurological Pathophysiology
Altered mental status is the behavioral result of disruption of normal central nervous system function. Billions of neurons course from cortex to cord to provide the human organism the privilege to interact rather impressively with its environment. Disruption of this integrity can lead to profound vulnerability. Neuronal tissue is highly energetic. A constant supply of large amounts of substrate (mainly oxygen and glucose) is necessary for normal neurologic function. The brain gets nearly 20% of the cardiac output and consumes roughly 25% of the total available oxygen. The total unavailability of either oxygen or glucose (and certainly both) results in unconsciousness in seconds, and irreversible neuronal injury will invariably occur if the supply of substrate is not restored. A progressive decline in available substrate will produce a predictable decline of global, symmetric central nervous system function. Hypoglycemia (glucose < ? mg % ) is a common causes of acute AMS seen in the emergency department. This can produce dramatic changes in behavior consisting of confusion and eventually coma if the sugar continues to fall. On rare occasion, a patient with hypoglycemia may present with focal neurologic findings which is probably related to hemispheric energy demands. Hypoxemia (02 saturation < ?%) will produce global, non-focal symptoms, especially if acute. Normal neuronal function requires intact neuronal membranes, precise trans-membrane electrical potentials (the result of electrolyte gradients), and optimum function of integral cell membrane enzymes (ATPase) to maintain these gradients. Recall from biochemistry that enzymes operate within a certain range of ?. ?, will produce cellular enzyme dysfunction resulting in impairment of thinking and AMS. Deep coma is rarely caused by lesions in the cerebral cortex, with the exceptions of ?. Abrupt and severe unilateral hemispheric cerebral insult (?) results in confusion and contra lateral paresis, but generally not unconsciousness. Simultaneous bi-hemisphere involvement is necessary to produce coma. Injury to the ascending tracts of the reticular activating system of the brainstem will produce coma, even if the hemispheres are spared. Understanding contra-lateral motor control and hemispheric dominance will assist in localizing CNS dysfunction. A patient experiencing a focal seizure is generally awake, possessing some degree of confusion, and if the motor strip is involved, exhibiting contralateral involuntary muscular activity. Todd's paralysis is a post-generalized seizure phenomenon characterized by transient residual hemiparesis. Persons presenting with acute confusion and expressive dysphasia have localized lesion in the ? with a high degree of accuracy. Be aware that most left handers are still left hemisphere dominant.
-Asthmatics, hemorrhage victims, patients experiencing cardiogenic shock
-alcohol, drugs, and hypoglycemia
-temperature and pH
-Hyperthermia and hypothermia, as well as acidosis and alkalosis
-profound and prolonged hypoxia, intracerebral hemorrhage, and large lesions which produce mass effect
-ischemia, blood, tumor, injury
-left parietotemporal region
Management of the Patient with AMS
The management of the patient with acute AMS must be undertaken with a high degree of urgency. The physician must rapidly attempt to obtain data while simultaneously addressing any immediate life threatening concerns. For this reason, the evaluation of the patient with acute AMS should be undertaken in the following order:
1. Rapid assessment of mental status using either the AVPU Scale and/or the Glasgow Coma Scale.
2. Immediate attention to the patient's airway, breathing, oxygenation, circulation, and cervical spine integrity.
3. Administration of oxygen, intravenous fluids, thiamine, glucose, naloxone, or other specific antidotes wherever indicated.
4. Simultaneously obtain a history on the patient, including events preceding AMS, important medical and surgical history, and medications and habits.
5. Complete multi-system physical examination, looking for signs of trauma or other stigmata.
6. Compile a reasonable differential diagnosis based upon historical and examination findings.
7. Order appropriate radiological and laboratory testing in order to narrow diagnosis.
8. Prompt consultation with the appropriate medical and/or surgical specialists and disposition.
Assessment of Mental Status
Recognize that assessment of mental state should take no more than half of a minute to complete. First observe the patient for spontaneous movements and reaction to your presence. Talk to the patient and note their response. If the patient does not follow commands, note their response to tactile or painful stimulation. The AVPU Scale is the easiest way to determine the patient's responsiveness:
A similarly simple but more detailed and widely-used method of documenting a patient's level of consciousness is with the Glasgow :::oma Scale (GCS): page 28
The usefulness of the GCS is increased by relating the total score, as well as in describing all three categories accurately. A GCS of 13 to 15 is not considered to be immediately life-threatening. A GCS of< ? implies a life-threatening condition and requires aggressive treatment. Prognostic power of the GCS is limited in patients with ?. A patient with a GCS between 8 and 9, unless rapidly reversible with antidotes and/or specific therapy, the condition is serious to critical and resuscitative measures and/or surgery must be undertaken or the prognosis is poor.
The change in mental status in many cases may not be dramatic and obvious as coma. The seemingly alert patient who is "not quite right" is a significant challenge for the evaluating physician. If the patient is conversant and following commands, the modified Folstein Mini-Mental Status Examination is a useful tool to assess frontal lobe function: page 29
An abnormal Folstein score simply lets you know that something is wrong. Your differential diagnosis remains the same as with coma. Remember that in many cases early detection of mental deterioration may thwart progression to coma and maximize outcome. Other common terms used to describe a patient's behavior and levels of consciousness include:
Confusion is the loss of a patient's orientation or conscious ability to appreciate time, place, or person. This may occur in ?.
Delirium, a mental disturbance of relatively short duration, is usually the result of a ? state, characterized by illusions, delusions, hallucinations, excitement, restlessness, and incoherence.
Dementia is used to describe subacute or chronic organic cerebral deterioration.
Coma is a state of profound unresponsiveness, patient is unarousable, even by powerful stimuli.
Amnesia is a pathologic failure of recall of memory.
Catatonia is a psychiatric condition characterized by excessive and sometimes violent motor activity and excitement, or generalized inhibition.
Sleep, on the other hand, is a normal physiologic condition from which even the most exhausted medical student can be aroused with sufficient stimuli. It is extremely important and useful to address the patient's mental change in conversation with the family as well as with the primary physician in order to appreciate a change from baseline mental function .
In managing the patient with acute mental status, your first obligation is to safely get the patient to a stretcher, undressed, and covered in a gown and sheet ready for examination. This may require the temporary use of physical restraints if the patient's safety or the safety of others is in question. The emergency management of the patient with acute mental status change should always begin with rapid assessment of consciousness and attention to life-preserving measures. If the patient presents with coma, follow i.he ABC's: page 30
In many patients with AMS, the ABCD's can be quickly affirmed, especially if the patient is ambulatory and conversant. However, if a problem exists, critical resuscitative actions must be performed immediately. Consideration should then be given to those diagnoses which are rapidly reversible using specific antidotes, such as ?. Further critical actions include (the so-called "coma cocktail"):
F. Obtain vital signs and treat hypotension with fluids.
G. Monitor the patient (ECG and pulse oximetry). , H. Determine blood glucose and/or administer one or two ampoules of glucose
IV. Blood glucose > 70 mg% does not require glucose administration.
Adults: ?, 50 cm3
IV Children: ? Dextrose solution, 2 - 4 cm3/kg IV Administer ? 100 mg IV to suspected ?.
I. After evaluating pupil size and reactivity, administer naloxone 0.2 to 2 mg IV if suspicion of opiate overdose. Gastric lavage should be performed if indicated .
• The patient should then be re-evaluated to determine the patient's response to the above initial measures. Should prompt clinical improvement occur, obtain a history from the patient and anticipate further management if warranted.
The medical history should be immediately obtained. If the patient is non-verbal, obtain history from friends and acquaintances, family, and EMS or other personnel. The history should include:
l. Condition and vital signs
2. Environment where victim was found and transportation time
3. Observation of the scene (blood, Rx bottles, evidence or drug use, etc.)
4. Time course of events (acute, sub acute, chronic, lucid intervals)
5. Previous mental status
6. Preceding events (activity, trauma, social situation) 7. Predrome (headache, syncope, seizure)
8. Medical illness (DM, HTN, renal/hepatic disease, psychiatric, etc)
9. Recent surgical or orthopedic procedures
10. Current medications, habits (drug/alcohol use)
The physical examination should be limited and expeditious. Assessment of the five following areas will assist in determining whether the problem is structural or metabolic and/or drug-related:
1. Level of consciousness
a. AVPU b. Glasgow Coma Score c. Toxidromes
-Small reactive pupils occur with ?
-Midpoint-fixed pupils indicate a lesion in the ?
-Pinpoint-fixed pupils indicate a lesion in the ?
-A single dilated pupil indicates ?
3. Oculocephalic and oculovestibular reflexes
a. Doll's eyes: after clearing the cervical spine with the patient supine, turn the head to one side and the other observing for movement of the eyes (which should remain ?). Lack of movement (eyes "painted on") indicates a structural lesion below the ?.
b. Cold water caloric: after examining the external auditory canal, with the head at 30 degrees (low Fowler's position) 30 mL of ice water is injected into the EAC for 30 seconds, and the eyes are observed for movement. An intact brainstem will produce ?. If the cortex is intact, the eyes will ?.
4. Tone position and abnormal reflexes
a. Increased tone is found with ?
b. Flaccidity is observed with ?
c. Decorticate posturing is seem with ?
d. Decerebrate posturing is seen with ?
a. Hypoventilation is seen with ?
b. Cheyne-stokes breathing is seen with ?
c. Hyperventilation is seen with ?
d. Apneustic/ataxic breathing is seen with ?
An HEENT exam should be undertaken. The head should be inspected for signs of trauma, including bruising, hematomas, lacerations, and abrasions. The examiner is encouraged to look for clinical signs of a basilar skull fracture: ?
The eye grounds should be inspected for ?. The naso- and oropharynx should be inspected signs of trauma, odors, and moisture. The neck and cervical spine should be inspected and palpated, looking for ?. Always place cervical collar if trauma cannot be ruled out by history. Cervical spine films should be obtained if ?. The chest wall should be inspected and palpated for bruising, crepitus (indicating subcutaneous emphysema), rib fractures, and tenderness. Breath sounds should re auscultated for wheezing, rales, and asymmetry (pneumothorax, consolidation, or effusion). A cardiac examination should consist of listening for heart tones, murmurs, and ?.
The abdomen should be inspected for external signs of trauma or other findings (Cullen's sign and GreyTurner's sign, indicating ?). Palpation for masses and/or tenderness, as well as a rectal examination should be performed checking for tone and/or bleeding.
Extremities should be examined, noting the strength and symmetry of pulses, presence of signs of injury, and condition of the skin (pallor, diaphoresis, cyanosis). The neurological examination should be competed, consisting of cranial nerve testing, observing for symmetry of movement, strength, weakness, and sensory deficits, as well as the presence of abnormal reflexes (Babinski). A positive Babinski sign indicates a lesion of the ? tract.
-thalamic lesions or organophosphate poisoning
-midbrain or medulla
-pons or with opiate poisoning
-third CN nerve pressure or ocular injury or Adie's tonic pupil, a normal variant.
-conjugate and "looking" toward the ceiling
-slow tonic deviation of the eyes toward a cold stimulus
-jerk quickly (fast component) to the opposite direction of the cold stimulu
-midbrain and less often with pontine lesions
-midbrain and upper pontine lesions
-hypoglycemia, sedative drugs, and hypercapnia
-metabolic lesions or pre-herniation
-midbrain or upper pons lesions
-lower pons or medullary lesions
-racoon's eyes (periorbital ecchymosis), CSF rhinorrhea, hemotympanum, CSF otorrhea, and Battle's sign (perimastoid ecchymosis).
-retinal hemorrhages or papilledema
-jugular distention, tracheal shift, thyromegaly, masses, and any abnormalities
-unable to evaluate (intoxication, coma)
-Hamman's crunch (indicating mediastinal emphysema)
Differential Diagnosis An appropriate differential diagnosis can be developed by using the four distinct categories:
Differential Diagnosis (continued) The simplest way to remember a differential diagnosis for acute mental status change is to use the mnemonic AEIOU TIPS: page 33
Head injury resulting in AMS or coma should be considered life-threatening. Severe diffuse ? can produce herniation of brain parenchyma through either the ?. This may occur fairly acutely. It is imperative the physician recognize the clinical signs of cerebral herniation syndromes and rapidly implement the appropriate resuscitative measures if the patient is to survive. The types of herniation and their presentation are as follows:
Headache and vomiting
Rapid progression to stupor and coma
Headache with progressive drowsiness
Periodic respirations (?)
Paucity of focal motor signs
-Tonsillar (Foramen magnum) Herniation
Headache, vomiting, and ?
Rapid progression to ?
? of the eyes
Evidence of increasing intracranial pressure necessitates obtaining a CT of the head and neurosurgical consultation as quickly as possible. By rapidly identifying a surgically-correctable lesion (subdural or epidural hematoma with mass-effect), herniation can be avoided with a timely emergency craniotomy. The medical management of increased intracranial pressure involves avoiding ?, avoiding ?through intubation and ventilation, maintaining the neck in a ?, maintaining ?, and by using ? as needed.
Laboratory and Radiographic Diagnosis
Laboratory testing may include a complete blood count, electrolytes, calcium, urea nitrogen, serum glucose, acetone, osmolality, arterial blood gases, serum lactate, anion and osmolar gaps, toxicology screens - ethanol, acetaminophen, and aspirin levels. The rapid urine drug screen, is qualitative and not quantitative, and takes time and this is not usually helpful initially. Thyroid studies (which also are not usually immediately available) may help in diagnosis of severe thyroid dysfunction, but the diagnosis should be entertained based upon clinical criteria, especially thyrotoxicosis or thyroid storm. Also, a carboxyhemaglobin level should be obtained if AMS is unexplained and the history is suggestive. Any patient presenting from a house fire, with or without burns or AMS, should be assumed to have carbon monoxide poisoning. During the winter months, the use of in-door kerosene heaters, fire places, and faulty furnaces are common causes of carbon monoxide poisoning. The history of riding in an auto with a faulty muffler, and especially rotting floor board, also is a classic presentation for those suffering from CO poisoning. The serum electrolytes osmolarity can provide clues to the diagnosis when metabolic causes are suspected. When metabolic acidosis is suspected based upon the finding of a CO2 combing power, (HCO3) < 20 or a pH< 7.35, the anion gap should be calculated: AG= Na- (Cl+ HCO3). The presence of an anion gap> 15 is abnormal and should prompt a search for one of the following clinical entities: (MUD PILES) methanol or ethylene glycol consumption, uremia, diabetic ketoacidosis, paraldehyde, isoniazid, lactic acidosis (indicating anaerobic glycolysis), ethylene glycol, and salicylate poisoning. If the consumption of methanol or ethylene glycol is suspected, calculation of the Osmolar gap can assist in · diagnosis. Osm. measured = ?. Please recall that the serum osmolarity can be calculated using the following equation: Osm = ?. The presence of a 10+ gap, especially if metabolic acidosis-exists, should strongly suggest ingestion of one of these alcohols and treatment should be started and nephrology consultation obtained when necessary.
Appropriate radiological studies may include cervical spine films, chest and /or abdominal films, computerized axial tomography of the head, and magnetic resonance imaging of the brain and/or spinal cord. An electrocardiogram should also be obtained. ECG changes indicating global ischemia (?) can be seen in a patient who had suffered prolonged ·hypoxemia. The presence of tall, peaked T-waves seen in hyperkalemia may indicate ?. Shortened or prolonged Q-T intervals may indicate the presence of ?, respectively. Also recalling that intracranial pathology will often produce repolarization abnormalities which can mimic ?
A-- alcohols, acidosis, accidents (cerebral hemorrhage, embolic stroke)
E-- encephalopathy, endocrine (thyrotoxicosis, addisonion crisis, myxedema), electrolytes
I -- Insulin (hypoglycemia, hyperglycemia)
O -- opiates/narcotics
T-trauma (cerebral, cardiac, pulmonary)
I- Infection, Intracranial pressure
P- poisoning, psychiatric (catatonia, malignant hyperthermia)
S- Shock, sepsis
-brain edema or intracranial hematomas
-tentorium cerebrii, or through the foramen magnum
-Decorticate and decerebrate
-extensor plantar responses
-stupor and coma
-secondary brain injury (hypoxia and hypotension)
-straight position at 30 degrees elevation
-deep sedation (benzodiazepines, barbiturates) and neuromuscular paralysis
-mannitol (an osmotic agent) or furosemide
-Osm. calculated + 10
-2[Na] + BUN/2.8 + Glucose/18 + Ethanol
-anterior, inferior, and lateral ischemic T-wave changes or ST-segment depression
-uremia and acute renal failure
-hypocalcemia or hypercalcemia