Monday, May 3, 2021

Altered Mental Status Case File

Posted By: Medical Group - 5/03/2021 Post Author : Medical Group Post Date : Monday, May 3, 2021 Post Time : 5/03/2021
Altered Mental Status Case File
Eugene C. Toy, MD, Manuel Suarez, MD, FACCP, Terrence H. Liu, MD, MPH

Case 30
A  60-year-old man was admitted to the ICU because of changes in his mental status after 2 short tonic-clonic seizures lasting <1 minute each. He had suffered a bout of seizures 5 years previously,  and none since that time. The patient has a heavy alcohol history, averaging a 6-pack of beer a day for the past 20  years. He presented  with confusion and dehydration, and it has been 4 days since his last drink. He is unable to respond coherently to questions and rambles with an unclear flow of ideas. His family members admitted that his mental status has deteriorated quickly over several weeks, at first with inattention and slight for getfulness, and then later progressing to confusion and lethargy. He was given thiamine in the ED.  IV fluids are being aggressively administered in the ICU. His vitals include a temperature of 101°F, a BP of 170/90 mm Hg, a regular heart rate of 135 beats/minute,  and an oxygen saturation of 95% on room air. ACT of the brain without contrast revealed no acute changes, only slight brain atrophy compatible with his  age. On physical examination, the pupils demonstrate equal size and reactivity and react to light and accommodation. The rest of the neurological examination was within normal limits.

What is the most likely diagnosis?
What are the initial steps in the management of this patient?


Altered Mental Status

Summary: A 60-year-old man is admitted to the ICU for an altered mental status. The patient has a long history of alcohol use and is confused. His BP is elevated, and he is febrile. 
  • Most likely diagnosis: Alcohol withdrawal with delirium tremens. 
  • Initial management steps: Secure the patient safety by stabilizing his clinical status with a rapid evaluation for the most common treatable and reversible causes of altered mental status (AMS).

  1. To list the common causes of alterations in mental status.
  2. To understand the methods used to evaluate alterations in mental status.
  3. To understand the possible choices in the treatment of patients in delirium.
This 60-year-old man has a long history of alcohol use and has been noted by his family members to have a deterioration of his mental capabilities over several weeks. The patient's last drink was 4 days previously, and he is having alcohol withdrawal, that has progressed to delirium tremens (DT). The first priority is to stabilize the patient by controlling the seizures and withdrawal symptoms with benzodiazepines. Thiamine, folic acid, vitamin B12, and other vitamins should be administered and aggressive hydration should be initiated. Glucose should be avoided until thiamine is given. Although this patient's findings are likely to be due to alcoholism and the complications of alcohol, a careful differential diagnosis for neurological problems should be undertaken to assess for conditions such as meningitis, drug toxicity, electrolyte abnormalities, and stroke.

Approach To:
Altered Mental Status


DELIRIUM: It is an acute state of confusion.
COMA: It is a sleeplike state in which the eyes are closed and the patient is unarousable even when vigorously stimulated.


In the ICU, evaluating and monitoring the mental status of patients with multiple serious disease processes is a daunting task. It is estimated that half the patients admitted to a hospital in an acute condition will undergo some form of delirium during their admission. Half of these cases of delirium go undiagnosed. In normal consciousness, there is a state of awareness of self and the environment and the ability of the patient to interact with the activities of daily living (ADL); an intact and functioning brain stem and reticular activating system and its cortical projections are required for normal consciousness. Alterations in mental status (AMS) may range from an agitated, confused state (delirium) to an unarousable, unresponsive state (coma). Whether it is delirium, coma, or some state in between, each category represents a stage of the same disease process and is investigated in the same manner. The potential causes are broad and diverse; major causes include metabolic derangement, exposure to toxins, structural lesions, vascular insult, seizure, infection, and substance abuse.

Differential Diagnosis of AMS
Metabolic derangements may include disorders of temperature control, electrolyte balance, glucose or hormone levels, or vitamin insufficiency. Both hyperthermia and hypothermia can cause alterations in mental status. Electrolyte disorders include hypematremia, hyponatremia, hyper and hypoglycemia, and hypercalcemia. Hypoglycemia occurs commonly in the treatment of diabetes mellitus and is life-threatening. Severe untreated hypothyroidism can result in a myxedema-derived coma. Thyrotoxic crisis, or "thyroid storm," is a life-threatening complication of hyperthyroidism characterized by marked agitation, restlessness, delirium, or coma. AMS is a broad term that can encompass anything from sudden confusion and agitation to impaired awareness and profound unresponsiveness, even coma. A patient's mental status is assessed by the level of consciousness (ie, attentiveness) via the reticular system, while cognition (ie, thought process) happens via the cortical projections. Delirium is an acute altered level of consciousness described as waxing and waning with fluctuating inattentiveness and perceptual disturbances. A patient in delirium will present in a confused and agitated state, unaware of his/her surroundings. It is common to see delirium superimposed on dementia in the elderly in up to 80% of cases.

A patient in a comatose state is considered a medical emergency and must be assessed immediately for underlying, reversible causes. The most common causes of coma are cerebrovascular disease or hypoxic injury, electrolyte disorders, encephalopathies, and drug toxicity. The longer the coma state lasts, the less likelihood there is of recovery. Hepatic encephalopathy needs to be investigated immediately as a possible cause of coma. The administration of D50W is standard in patients found in a comatose state since reversing hypoglycemia, if present, can be lifesaving. Coma without focal signs but with meningismus, with or without fever, suggests meningitis, meningoencephalitis, or subarachnoid hemorrhage. Coma with focal signs implies a structural lesion such as stroke, hemorrhage, tumor, or abscess formation.

Acute pituitary gland hemorrhage or infarction can lead to pituitary apoplexy. Lastly, thiamine deficiency in alcoholics or the malnourished may lead to Wernicke encephalopathy when glucose-containing fluids are administered. Toxins can arise from exogenous or endogenous sources. Exogenous sources include illicit and prescription drugs, alcohol, and noxious fumes. Endogenous sources can arise from organ system failure. Examples include liver failure (hepatic encephalopathy), kidney failure (uremic encephalopathy), and cardiopulmonary insufficiency (hypoxia and/or hypercapnia). Structural lesions can cause coma through diffuse insult to the cerebral hemispheres, damage to the reticular activating system in the brainstem, or interruption of the connections between the two. Massive hemispheric lesions result in coma either by expanding across the midline laterally to compromise both cerebral hemispheres (lateral herniation) or by impinging on the brain stem to compress the rostral reticular formation (transtentorial herniation). Mass lesions of the brain stem produce coma by directly affecting reticular formation. Because the pathways for lateral eye movements traverse the reticular activating system, impaired eye movements (doll's eye) are often an element of diagnosis.

Space-occupying lesions include neoplasms (primary or metastatic), intracranial hemorrhage, and infection. Vascular insults include hemorrhagic or ischemic phenomena, inflammation, and hypertension. Subarachnoid hemorrhage and hemorrhagic stroke cause intracerebral hemorrhage, and cerebral ischemia can result from thrombotic or embolic occlusion of a major vessel. Unilateral hemispheric lesions from stroke can blunt awareness, but do not result in coma unless edema and mass effect cause compression of the other hemisphere. Global cerebral ischemia, usually resulting from cardiac arrest or ventricular fibrillation, may cause anoxic encephalopathy and coma. Vasculitis of the central nervous system may also cause AMS, as well as other systemic signs and symptoms.

Malignant hypertension can lead to a stroke or hypertensive encephalopathy. Central nervous system infections also adversely affect mental status. Examples of these include meningitis, encephalitis, and subdural empyema. Infection may also travel from a distant site to cause AMS, such as the development of septic emboli from endocarditis. Infection or fever from any source can cause delirium in the elderly. Delirium tremens is characterized by hallucinations, disorientation, tachycardia, hypertension, low-grade fever, agitation, and diaphoresis. Most commonly, altered mental status is caused by metabolic derangements, toxin exposure, structural lesions, vascular insults, seizures, infections, and withdrawal syndromes. A mnemonic used to remember the most common causes of altered mental status is: WITCH HAT-withdrawal, infection, toxins/drugs, CNS pathology, hypoxia, heavy metals, acute vascular insult, and trauma.

Rapid identification of the cause of AMS is required to treat the patient effectively. The etiologies of AMS are various and multifactorial in most instances. Patient safety is foremost, and the ABCs of resuscitation and adequate hydration must be prioritized. Vital signs, O2 sat levels, glucose, electrolytes, CBC, and urine analysis should be evaluated. The patient should be screened for illicit drugs and possible toxic levels of prescribed medications. Potential interactions of medications should not be ignored. When possible, a history obtained from family members can help pinpoint the cause of AMS. Pertinent details of the patient's history, including the use of prescribed or over-the-counter medications, vitamin supplements, and drug abuse will aid the correct diagnosis and treatment.

The laboratory evaluation should include an arterial blood gas, complete metabolic panel, CBC with differential, ammonia, and liver enzyme level. Focused testing for ASA, acetaminophen, and tricyclic antidepressants depends upon the history and clinical suspicion. The physical examination should address 3 main questions: (1) does the patient have meningitis? (2) are signs of a mass lesion present? and (3) is this a diffuse syndrome of exogenous or endogenous metabolic origin?

The neurological examination should focus on whether there are lateralizing signs suggesting a focal lesion or signs of meningismus and fever that would suggest an infection. The key features to be noted during the physical examination are pupil size and reactivity, ocular motility, motor activity (including posturing), and certain respiratory patterns. Coma without focal signs, fever, or meningismus suggests a dif­fuse insult such as hypoxia or a metabolic, drug-induced toxicity, an infectious or postictal state. In the case of coma after cardiac arrest, patients who lack pupillary and corneal reflexes at 24 hours and lack motor responses at 72 hours have a poor chance of meaningful recovery.

Patients with focal findings on examination or who exhibit unexplained coma should undergo emergent imaging to exclude hemorrhage or mass lesion. Lumbar puncture is indicated when meningitis or subarachnoid hemorrhage is suspected and when neuroimaging is normal. The possibility of nonconvulsive status epilepticus should be evaluated by emergent electroencephalogram. Delirium may predispose patients to prolonged hospitalization, frequent impairment of physical function, and increased rates of institutionalization. Therefore, rapid detection, evaluation, and intervention are essential. Diagnosis of delirium is based upon clinical information. The confusion assessment method (CAM) algorithm is a useful tool in diagnosing delirium. Physical examination is useful in determining the etiology of AMS. Assessing for neurologic causes may help determine the severity of damage to the CNS. Focal neurologic signs should be assessed, and a CT scan should be performed to evaluate intracranial pathology. It is important to remember that before performing a lumbar puncture in the case of suspected meningitis, CT imaging of the brain should be performed first. This will detect any structural abnormalities and possibly avoid herniation from a lumbar puncture.

Diagnosis of Delirium
It is critical to diagnose and determine the cause of delirium. To diagnose delirium, a patient must have an acute change in mental status that is fluctuating between altered levels of consciousness. Laboratory testing and physical examination can shed light on the source of the delirium. The confusion assessment method (CAM) is the most accurate tool available to diagnose delirium. Table 30-1 outlines the CAM method allowing clinicians to evaluate delirium and to present focused questions that expedite the correct diagnosis of the delirium.

There are no laboratory tests, imaging studies, or other tests that can provide greater accuracy than the CAM algorithm (sensitivity 94%-100%; specificity, 90%-95 %). Some clues that can help in identifying the etiology of the AMS include: the time course of mental status changes, the association of those changes with other events (eg, medication changes or development of physical symptoms), the presence of sensory deprivation (absence of glasses or hearing aids), and the

diagnosis of delirium

presence of uncontrolled pain. A medication history with particular attention to sedative hypnotics, barbiturates, alcohol, antidepressants, anticholinergics, opioid analgesics, antipsychotics, anticonvulsants, antihistamines, and medications for Parkinson disease is very useful in including or excluding these in the list of possible etiologies of the patient's AMS. The more medications the patient is taking, the greater the likelihood that a medication is causing or contributing to the delirium. Patients and caretakers must be aware that medications include any over-the counter medications, vitamins, supplements, elixirs, and creams.

Performance of a complete neurological and medical examination is critical in determining the patient's mental status. One should seek for signs of infection, heart failure, myocardial ischemia, dehydration, malnutrition, urinary retention, and fecal impaction. The laboratory evaluation should be tailored to the specific clinical situation. Cerebral imaging, although commonly used, is usually not helpful in the diagnosis of delirium unless there is a history of a fall or evidence of focal neurologic impairment. Targeting intervention to the individual's risk factors, such as cognitive impairment, sleep deprivation, immobility, visual and hearing impairment, and dehydration may reduce the incidence of delirium. Delirium often results from a combination of underlying vulnerability and acute precipitating factors (Table 3 0-2 ).

Amelioration of underlying vulnerability and prevention of acute precipitants will reduce the incidence of delirium. The use of physical restraints is generally avoided because they can increase agitation and the risk for patient injury. However, if other measures to control a patient's behavior are ineffective and it seems likely that the patient, if unrestrained, may cause personal injury or injury to others, restraints can be used with caution. The use of sedating agents may exacerbate or

common causes of delirium

prolong delirium. Antipsychotics or anxiolytics should only be used in life threatening circumstances such as in the ICU or when behavioral measures have been ineffective. Low-dose haloperidol, risperidone, and olanzapine are equally effective in treating agitation associated with delirium. These are associated with little respiratory depressive effect, a feature much desired in the respiratory compromised patient. One should attempt to use the lowest dose of the least toxic agent that successfully controls the agitation. Lorazepam used along with antipsychotics agents is complementary without adding undesirable side effects.

The treatment of AMS depends upon its etiology. A significant part of the treatment of delirium is to institute preventive measures. In prevention of relapses of DTs, precipitating factors such as lack of sleep and dehydration should be addressed. Vitamin B12 and folic acid should also be administered and patients be hydrated adequately. A quiet, lowly lit environment during the day and an even darker environment during the evening and sleeping hours should be maintained. The patient should be advised to avoid reversing the normal rest and sleeping pattern.

Neuroleptics should be used with caution to avoid possible undesirable side effects. Newer neuroleptics such as risperidone, olanzapine, and quetiapine have fewer adverse effects than haloperidol. The lowest effective dose should b e used, and therapy should be tapered downward ASAP, especially in the elderly. Low-dose haloperidol causes less sedation and is highly effective in treating delirium, especially when used in combination with lorazepam. The combination of 5 mg of haloperidol with 1 mg of lorazepam is effective in the treatment of delirium. The use of risperidone has fewer side effects than haloperidol and should be substituted for the latter when possible. Sedatives such as lorazepam are the drugs of choice when treating delirium due to alcohol withdrawal. These agents are also useful in decreasing anxiety. Respiratory depression can be minimized by careful monitoring, especially in the elderly.

Flumazenil can be used for benzodiazepine intoxication. This can lead to rapid withdrawal symptoms including seizures, which now may be untreatable with benzodiazepines since flumazenil will block its effect. Dexmedetomidine is also a sedative that does not cause respiratory depression. Naloxone and naltrexone should also be kept in mind with narcotic drug overdose, especially opioid intoxication where they competitively inhibit opioid-binding sites and are therefore useful in any opioid intoxication. Proper nutrition and removal of precipitating factors are essential in preventing a relapse. Weeks of treatment are needed to recover from delirium and the patient should be monitored continuously.

  • See also Case 3 (Scoring Systems and Patient Prognosis), Case 27 (Traumatic Brain Injury), Case 32 ( Stroke), and Case 37 (Poisoning).


30.1  A 78-year-old woman who has acute respiratory distress syndrome and was admitted to the ICU for mechanical ventilation (MV) 2 days ago is being evaluated for disorientation. Prior to hospitalization, she lived alone and functioned well independently. The patient is receiving MV. She received lorazepam over the past 48 hours for periods of agitation. The nurse indicates that the patient recently became disoriented and is not interacting as clearly with her family as she had done previously. Her mental status has fluctuated over the past 24 hours. On physical examination, her vital signs were normal except for a sinus tachycardia of 110 beats/minute. She is awake but does not follow directions. Neurologic examination shows no focal abnormalities and the cranial nerve examination is normal. Which of the following is the most likely cause of her current symptoms?
A. Cerebrovascular accident
B. Delirium
C. Dementia
D. Paranoid psychosis
E. Transient ischemic attack

30.2  A 19-year-old man is admitted to the ICU after presenting to the ED 6 hours ago with a drug overdose. His friends brought him to the ED after he collapsed at a party. They admitted to mixing codeine and oxycodone with alcohol and ingesting multiple drinks throughout the night. The patient is intubated for airway control and MV. His vital signs are stable. Upon physical examination, the patient's pupils are constricted and the mucous membranes appear dry. The patient is unresponsive except to deep stimuli. What is the next best step in the management of this patient?
A. Benzodiazepines intravenously
B. Haloperidol and psychiatry consult
C. Flumazenil intravenously
D. Nalaxone or naltrexone intravenously
E. Thiamine intravenous infusion


30.1  B. This patient has several causes for delirium: advanced age, intubation, and mechanical ventilation, unfamiliar surroundings, and underlying significant medical problems like ARDS. Protection of the patient to avoid self-harm and self-removal of the ventilation tubing and lines is the first consideration. The early treatment should involve the use of haloperidol and lorazepam to control the agitation and delirium. Propofol may be also used here to control agitation and to improve the coordination between the patient and the MV. Avoid the "sundown syndrome" by increasing the patient's awareness of her surroundings. The TV should be on. Frequent communication with the patient explaining her condition, intended therapy, and why low level lighting and control of sunlight entering the room are the key first steps in easing the patient's anxiety. Controlling the ambient lighting will assist the patient to discern the difference between day and night. Close attention to hydration and potential electrolyte disorders and the immediate correction of any such abnormalities is important in improving the underlying medical conditions.

30.2  D . Reversal of the narcotic overdose, which is the source of the respiratory depression and coma, is accomplished by giving nalxoxone expeditiously. This reversal is usually rapid but may be blunted since it was accompanied by alcohol. By reversing the narcotic quickly, the patient may awaken in an aggressive state. Ethanol and acetaminophen levels should be evaluated. Oxycodone and codeine are frequently available in combination with acetaminophen. Acetaminophen overdose should also be considered. If acetaminophen levels are elevated, acetyl cysteine should be administered to avoid irreversible hepatic damage. Codeine and oxycodone are not water soluble but acetaminophen is, so abusers frequently dissolve the combined medications in water and filter out the acetaminophen leaving the narcotic compound free of acetaminophen. The patient's airway should be controlled via ETI. MV is advised to control hypoventilation and hypercapnia induced by the narcotic overdose. Elevating the head of the bed to 45 degrees should be done to avoid aspiration. Narcotic overdose can cause ARDS and a chest x-ray and blood gases should be evaluated. If an osmolal gap between measured and calculated osmolality of >10 mOm/kg water exists in the presence of a positive gap metabolic acidosis, ethylene glycol and methyl alcohol should be considered as the cause of the coma. Isopropyl alcohol causes an osmolal gap but not acidosis.


 AMS is an acute change in consciousness and cognition and considered a medical emergency that must be diagnosed early and treated immediately to reach the best outcome. 
 The most common causes for AMS are (WITCH HAT); Withdrawal, Infection, Toxins/drugs, CNS pathology,  Hypoxia, Heavy metal, Acute vascular insult, Trauma. 
 CAM assessment of delirium is the most accurate test available for diagnosing delirium. 
 Differentiate dementia from delirium in the elderly as the 2 may superim­pose each other. 
 Haloperidol, risperidone, and olanzapine are all effective in treating agita­tion with delirium. 
 Delirium is a disturbance of consciousness and cognition over a short period of time, and is associated with increased morbidity and mortality no matter the cause. 


Clifford S, Deutschman MS. Evidence Based Practice of Critical Care. Saunders; 2010. 

Loscalzo J. Harrison's Pulmonary and Critical Care Medicine. McGraw-Hill; 2010. 

Toy E, Simon B, Takenaka K, Liu T, Rosh A. Case Files Emergency Medicine, 2nd ed McGraw-Hill, Lange, 2009.


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