Altered mental status and coma. Diagnosis and treatment
Altered mental status is a non-specific term referring to a status of impaired responsiveness to external stimuli, or to patients who are less responsive or unresponsive to external stimuli. In other words, altered mental status is an alteration of a patient’s level of cognitive(knowledge-related) or conscious functions (functions related to conscious response to external stimuli, emotions, thought, speech).The term of consciousness refers to one’s level of awareness and responsiveness to his or her surroundings and contains two cerebral functions: wakefulness (i.e. arousal, vigilance, alertness) and awareness of self or of the environment (this second part is the “content” of consciousness).
Definitions: lethargy, stupor, delirium, coma
Lethargy is mild to moderate depression in the level of consciousness, i.e. an abnormal condition of drowsiness or sleepiness in which it can be difficult to arouse the patient.
Stupor is a more profound depression of a patient's level of consciousness than lethargy, requiring a greater stimulus for a lesser degree of arousal.
Delirium is an acute confusional state characterized by an impairment of both the level and the content of consciousness with an organic etiology (meaning an etiology related to a recognizable functional or anatomic impairment). Delirium, if it is unrecognized and untreated, can result in significant morbidity and mortality, but if it is treated, then it is reversible in the majority of cases.
Definitions: lethargy, stupor, delirium, coma
The Central Nervous System ( a consise reminder of some basic facts)
The central nervous system (CNS) consists of the brain (which is the central organ of the nervous system) and the spinal cord.
The brain consists of the cerebrum, the brainstem, and the cerebellum. It processes and integrates information received from the sense organs and controls most of the activities of the body, by sending "instructions" in the form of nerve impulses.
The cerebrum is the largest part of the human brain and consists of the cerebral cortex, which is an outer layer of gray matter and the white matter which is the inner core.
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| The brain bisected in the sagittal plane |
The cerebrum is divided into two cerebral hemispheres, each of which is divided into four lobes – the frontal, temporal, parietal, and occipital lobes. The frontal lobe, situated toward the front of the cerebrum, just behind the forehead and under the frontal skull bones is associated with the higher and more complex brain functions. These functions include self-control, planning, reasoning, and abstract thought.
The parietal lobe rests near the top and center of the cerebrum, just behind the frontal lobe and above the occipital and temporal lobes. The lateral sulcus (or Sylvian fissure) separates the parietal from the temporal lobe. The parietal lobe's two hemispheres are divided by the medial longitudinal fissure.
The parietal lobe's main function is sensory perception and integration, including the perception and processing inputs of touch, taste, hearing, sight, and smell. The brain's primary sensory area, a region interpreting input from other areas of the body, is located in the parietal lobe. The more sensory input a region of the body provides, the more surface area of the parietal lobe is dedicated to receive and process the input from this region. The temporal lobe is positioned toward the base of the center of the brain. It plays a key role in processing auditory signals ( e.g. perceiving sounds, assigning meaning to sounds, and remembering sounds. Much of the auditory work of the temporal lobe is processed through the superior temporal gyrus, that receives sound input directly from the acoustic nerve.
The occipital lobe is located underneath the occipital bone and rests upon the tentorium cerebelli, a thick membrane separating the cerebrum from the evolutionarily older cerebellum. The occipital lobe mainly controls visual functions (functions of processing and understanding visual stimuli, mapping the visual world, spatial reasoning, visual memory, etc). Note that the lobes of the brain have complex connections and interactions between them and despite this simplified approach, each lobe has also additional functions and its function is not independent of the functions of the other brain lobes. Within each lobe, cortical areas are associated with specific functions, such as the sensory, motor and association regions.
Although the left and right hemispheres of the brain are similar in shape and function, some functions are associated with one side, such as language in the left hemisphere and spatial understanding in the right. The hemispheres are connected by nerve tracts, the largest of which is the corpus callosum.
Within the cerebrum is the ventricular system, consisting of four interconnected ventricles in which cerebrospinal fluid is produced and circulated. The cerebrospinal fluid (CSF) produced in the choroid plexus (present in all four ventricles) is a clear, colorless fluid that circulates around the brain in the subarachnoid space, in the ventricular system of the brain, and in the central canal of the spinal cord. There are several important structures, lying underneath the cerebral cortex, such as the thalamus, the epithalamus, the hypothalamus, the pineal gland, the pituitary gland, the limbic structures, including the amygdala and the hippocampus, the claustrum, and the various nuclei of the basal ganglia.
The thalamus (from the Greek word "thalamos", meaning"chamber") is a large mass of gray matter in the dorsal part of the diencephalon of the brain with several functions such as relaying and transmitting of sensory signals to the cerebral cortex, and the regulation of consciousness, alertness, and sleep. The thalamus is superior to the midbrain, near the center of the brain, with nerve fibers projecting out to the cerebral cortex in all directions. The medial surface of the thalamus constitutes the upper part of the lateral wall of the third ventricle.
The basal ganglia are structures deep within the hemispheres involved in behavior and movement regulation.
The brainstem is the posterior part of the brain, a region that connects the cerebrum to the spinal cord. The brainstem consists of the midbrain, the pons, and the medulla oblongata.
The brainstem provides the main motor and sensory innervation to the face and neck via cranial nerves. Of the twelve pairs of cranial nerves, ten pairs arise from the brainstem. The nerve connections of the motor and sensory areas of the cerebrum to the spinal cord and then to the rest of the body pass through the brainstem.
The brainstem also plays a very important role in the regulation of cardiac and respiratory function (heart rate, respiratory rate, and depth of respiration) and it also has the function of maintaining consciousness and regulating the sleep cycle.
The cerebellum (Latin for "little brain"), much smaller than the cerebrum, plays an important role in motor control (control of movements) and in several types of motor learning. The cerebellum forms a separate structure attached to the posterior and inferior part of the brain. The cerebellum is connected to the brainstem by pairs of tracts. The cerebellum does not initiate movement but contributes to the coordination and precision of movements, by receiving input from sensory systems of the spinal cord and from other parts of the brain and processing these inputs to coordinate and improve motor activity.
The cerebrum, brainstem, cerebellum, and spinal cord are covered by three membranes called meninges. The meninges are, from the outside to the inside, the tough dura mater; the middle arachnoid mater and the inner pia mater. Between the arachnoid mater and the pia mater is the subarachnoid space, which contains cerebrospinal fluid.
The cells of the brain include neurons and supportive glial cells. The brain contains more than 86 billion neurons and a similar number of other cells. Brain activity is performed by the interconnections of neurons, which form neural pathways, networks, and circuits. and the release of neurotransmitters from neurons in response to nerve impulses. Each neuron consists of the dendrites which receive input (neural stimuli from other neurons), a cell body, and the axon which sends output to other neurons or cells.
Allow me to recommend this video (by Associate Professor Dr. Kia Shahlaie You tube channel: World Federation of Neuroscience Nurses)
LINK Neuroanatomy made ridiculously simple
Etiology and pathophysiology of impaired consciousness
The etiology of altered mental status may be chronic or acute (but emergency medicine deals primarily with the acute etiologies), life-threatening or benign, reversible or irreversible.
The mechanism responsible for coma or impaired consciousness involves dysfunction of either both cerebral hemispheres or of the reticular activating system.
The reticular activating system is an extensive network of neurons in the upper pons, midbrain, and posterior diencephalon. These structures that play a major role in the level of consciousness (the cortex of both cerebral hemispheres or the reticular activating system) can be compromised by chemical, metabolic, structural, or infectious disease processes.
Unilateral impairment of the cerebral cortex will not result in unconsciousness unless the brain stem is also affected as a result of an increased intracranial pressure. Bilateral and extensive impairment of the function of the cerebral cortex can result in unconsciousness.
Altered mental status or coma is caused by one of two broad groups of problems:
-The first is morphologic (discrete anatomic lesions that can be identified on imaging studies such as brain computerized tomography-CT scan or magnetic resonance imaging-MRI). These causes can be
1)Either discrete lesions in the upper brainstem and lower diencephalon (which may be primary, located in these structures, or secondary due to their compression from another lesion) or
2) Widespread systemic disorders affecting both hemispheres. This second group of causes consists of metabolic (e.g. hypoglycemia, hyperglycemia, hyponatremia), toxic (e.g. drug overdose), infectious causes (e.g meningitis, encephalitis), hypoperfusion (shock), or organ failure (e.g. uremia, severe hepatic failure) that may result in a generalized suppression of neuronal activity.
Causes of coma or altered mental status
-A traumatic head injury which can be supratentorial causing herniation (such as a traumatic intracranial hematoma) or infratentorial (such as traumatic hemorrhage in the region of the posterior cranial fossa compressing brainstem structures). In general, traumatic causes can result in extensive edema or pressure to both hemispheres or to the brainstem and may include subdural
and epidural hematomas, intraparenchymal or subarachnoid
hemorrhage, concussion or contusion.
and epidural hematomas, intraparenchymal or subarachnoid
hemorrhage, concussion or contusion.
-Vascular causes such as
a) An ischemic stroke at the territory of the basilar artery, causing damage to brainstem structures and thus an insult to the reticular activating system.An ischemic (non-hemorrhagic) stroke of the anterior cerebral circulation very unusually causes a depressed level of consciousness (only if it is a massive stroke causing compression and damage to the contralateral side due to extensive edema). Generally, a lesion of the cerebral cortex must affect a large area of both hemispheres to cause a depressed level of consciousness. A unilateral lesion causing damage only to areas of one brain hemisphere does not result in uncosciousness,
or
b) A hemorrhagic stroke (due to vessel rupture) resulting subarachnoid hemorrhage (SAH), or intracerebral, pontine, or cerebellar hemorrhage.
or
c) Another vascular cause of depressed consciousness can be severe hypertensive encephalopathy ( a rare cause).
c) Another vascular cause of depressed consciousness can be severe hypertensive encephalopathy ( a rare cause).
-A mass, such as a brain tumor or a brain abscess which, as any space occupying lesion, can raise the intracranial pressure (ICP) and compress the brain. In this way, a supratentorial tumor can cause coma. An infratentorial tumor such as a brain stem tumor can cause coma by direct compression and damage of the reticular activating system of the brainstem, which is crucial for the mechanism of consciousness. In general, a brain tumor can be primary or metastatic.
-Infectious causes such as meningitis, encephalitis, brain abscess, cerebral malaria, or generalized severe infection (sepsis), or a severe infection in an elderly individual.
-Epilepsy and postictal states (Postictal state is the state of a patient after generalized seizures)
-Metabolic causes
Hypoglycemia, hyperglycemia (diabetic ketoacidosis or hyperosmolar hyperglycemic coma)
Hypernatraemia, hyponatremia
Hyperthermia, hypothermia
Hypercalcemia,
Acute severe thyroid disorders (either acute severe thyrotoxicosis or severe hypothyroidism)
-Organ failure: respiratory coma (from acute severe respiratory failure causing brain dysfunction as a result of the hypoxia and the elevated carbon dioxide) hepatic coma, uraemic coma (due to severe renal failure)
-Intoxication: drugs such as opioids (morphine, heroin, pethidine) sedatives, psychotropic medications etc. Drug intoxication or drug overdose is a common cause of altered mental status or coma.
Alcohol intoxication or alcohol withdrawal
Carbon monoxide (CO) intoxication (This causes coma due to hypoxia).
Carbon monoxide (CO) intoxication (This causes coma due to hypoxia).
Some psychiatric problems (hysteria, depression, catatonia ) can cause a clinical picture that can mimic a depressed level of consciousness, and this should be distinguished from a true impairment of the level of consciousness
Diagnostic approach to the patient with altered mental status or coma
In patients with altered mental status, consciousness is decreased to varying degrees. Repeated stimuli arouse the patient only briefly or not at all. Diagnostic workup and treatment should be performed concomitantly. First steps include the evaluation of the ABC's (airway, breathing, circulation)/ vital signs (pulse, respiratory rate, blood pressure, body temperature), assessment for signs of meningismus, efforts to obtain a relevant history (e.g from family members, friends, bystanders: ask if they know any facts about the patient's previous medical history, drug treatment and about the circumstances of the present illness, e.g. any preceding symptoms or events). Identification cards or drugs that the patient has, may provide important clues.
Important clues from the history and physical examination:
Medications: Some medications can cause alterations in mental status especially in the elderly.
Try to find quick information about the patient's past medical history (from relatives, identification cards, from the patient's physician, from the patient's file or chart in case of an inpatient. A history of diabetes can raise suspicion of altered mental status due to hyper- or hypo-glycemia. The latter can result from treatment (oral hypoglycemic medications, or insulin).It is important to know if there is a history of severe renal or liver disease, hypothyroidism, epilepsy, severe disease of the respiratory system (since respiratory failure can depress the level of consciousness). All the above diseases can cause a depressed level of consciousness.
Fever: In a patient with altered mental status and fever suspect meningitis, or another infection especially in the elderly (e.g. pneumonia, pyelonephritis).
Hypotension: Hypotension or shock can cause impairment of the mental status, due to a diminished cerebral perfusion. In such cases, you should search for the underlying cause of hypotension or shock and treat accordingly (see the chapter on shock).
Try to find out if there is a history of recent head trauma. If so suspect a subdural or epidural hematoma. patients on oral anticoagulation, the elderly, and alcoholics are particularly susceptible.
Have a quick look at the patient, the general appearance (e.g skin color: cyanosis in hypoxemia, cherry- red color of the skin in carbon monoxide poisoning, a maculohemorrhagic rash in meningitis or sepsis, pallor in internal hemorrhage or other causes of hypotension and shock, evidence of trauma or head injury-see also chapter on brain trauma for signs of a cranial fracture- needle marks indicative of intravenous drug use, etc).
The neurologic examination can provide evidence of a focal lesion and where the lesion is located within the central nervous system (CNS). Discovery of a focal neurologic deficit suggests a structural etiology as the most probable cause (e.g. intracranial hemorrhage, a tumor, a stroke at a region of the brainstem,etc), with a systemic cause (e.g a metabolic, toxic cause, or organ failure) being less probable in this case.
The level of consciousness is evaluated by attempting to wake patients first with verbal commands, then with tactile non-painful stimuli, and finally with noxious stimuli ( stimuli causing pain such as pressure to the nail beds, supraorbital ridge, or sternum).
The Glasgow Coma Scale (GCS) is a relatively simple, objective measure of the severity of conscious impairment and can be used serially for monitoring. The GCS assigns points according to the patient's responses to stimuli (for the GCS see chapter about brain trauma). Eye opening, purposeful withdrawal of limbs from a noxious stimulus and facial grimacing, are indications that consciousness is not greatly impaired. The deep tendon reflexes should also be tested.
Important indications suggesting a focal lesion in a brain hemisphere are asymmetric motor responses to pain or asymmetry of deep tendon reflexes.
In more severe states of coma, noxious (painful) stimuli may trigger stereotypic reflex posturing such as
-Decorticate posturing is flexion of elbows and wrists, abduction and internal rotation of the shoulders. It is an indication of severe damage above the midbrain( in structural or metabolic disorders causing hemispheric damage or dysfunction with preservation of the motor centers in the upper portion of the brain stem).
-Decerebrate posturing (in even more severe cases, where the upper brain stem motor centers, which facilitate flexion, have been damaged and only the lower brain stem centers which facilitate extension, are responding to sensory stimuli).Decerebrate posturing is characterized by extension of the elbows and wrists, adduction and internal rotation of shoulders and pronation of the forearms
and is an indication of damage at the midbrain or diencephalon
Important clues from the history and physical examination:
Medications: Some medications can cause alterations in mental status especially in the elderly.
Try to find quick information about the patient's past medical history (from relatives, identification cards, from the patient's physician, from the patient's file or chart in case of an inpatient. A history of diabetes can raise suspicion of altered mental status due to hyper- or hypo-glycemia. The latter can result from treatment (oral hypoglycemic medications, or insulin).It is important to know if there is a history of severe renal or liver disease, hypothyroidism, epilepsy, severe disease of the respiratory system (since respiratory failure can depress the level of consciousness). All the above diseases can cause a depressed level of consciousness.
Fever: In a patient with altered mental status and fever suspect meningitis, or another infection especially in the elderly (e.g. pneumonia, pyelonephritis).
Hypotension: Hypotension or shock can cause impairment of the mental status, due to a diminished cerebral perfusion. In such cases, you should search for the underlying cause of hypotension or shock and treat accordingly (see the chapter on shock).
Try to find out if there is a history of recent head trauma. If so suspect a subdural or epidural hematoma. patients on oral anticoagulation, the elderly, and alcoholics are particularly susceptible.
Have a quick look at the patient, the general appearance (e.g skin color: cyanosis in hypoxemia, cherry- red color of the skin in carbon monoxide poisoning, a maculohemorrhagic rash in meningitis or sepsis, pallor in internal hemorrhage or other causes of hypotension and shock, evidence of trauma or head injury-see also chapter on brain trauma for signs of a cranial fracture- needle marks indicative of intravenous drug use, etc).
The neurologic examination can provide evidence of a focal lesion and where the lesion is located within the central nervous system (CNS). Discovery of a focal neurologic deficit suggests a structural etiology as the most probable cause (e.g. intracranial hemorrhage, a tumor, a stroke at a region of the brainstem,etc), with a systemic cause (e.g a metabolic, toxic cause, or organ failure) being less probable in this case.
The level of consciousness is evaluated by attempting to wake patients first with verbal commands, then with tactile non-painful stimuli, and finally with noxious stimuli ( stimuli causing pain such as pressure to the nail beds, supraorbital ridge, or sternum).
The Glasgow Coma Scale (GCS) is a relatively simple, objective measure of the severity of conscious impairment and can be used serially for monitoring. The GCS assigns points according to the patient's responses to stimuli (for the GCS see chapter about brain trauma). Eye opening, purposeful withdrawal of limbs from a noxious stimulus and facial grimacing, are indications that consciousness is not greatly impaired. The deep tendon reflexes should also be tested.
Important indications suggesting a focal lesion in a brain hemisphere are asymmetric motor responses to pain or asymmetry of deep tendon reflexes.
In more severe states of coma, noxious (painful) stimuli may trigger stereotypic reflex posturing such as
-Decorticate posturing is flexion of elbows and wrists, abduction and internal rotation of the shoulders. It is an indication of severe damage above the midbrain( in structural or metabolic disorders causing hemispheric damage or dysfunction with preservation of the motor centers in the upper portion of the brain stem).
-Decerebrate posturing (in even more severe cases, where the upper brain stem motor centers, which facilitate flexion, have been damaged and only the lower brain stem centers which facilitate extension, are responding to sensory stimuli).Decerebrate posturing is characterized by extension of the elbows and wrists, adduction and internal rotation of shoulders and pronation of the forearms
and is an indication of damage at the midbrain or diencephalon
 |
| Decorticate posture |
 |
| Decerebrate posture |
Pupillary responses to light:
In coma due to structural (localized) lesions such as space- occupying brain lesions, one or both pupils usually become fixed early (i.e. one or both pupils do not respond to light).
In coma resulting from diffuse metabolic or toxic disorders, pupillary responses are often preserved until very late, although responses may be sluggish. In general, loss of pupillary reflexes or unequal pupils suggests a structural lesion of the brain, which should be evaluated with a prompt CT scan and also keep in mind that consultation from a neurologist or a neurosurgeon may be needed.
Miosis (excessive constriction of the pupils) can be the result of opioid narcotics, anticholinergics, or a pontine lesion of the brain.
Miosis (excessive constriction of the pupils) can be the result of opioid narcotics, anticholinergics, or a pontine lesion of the brain.
Mydriasis (dilated pupils) can be due to organophosphate poisoning.
Another element of the physical examination is the search for signs of meningeal irritation. These signs can occur in either bacterial meningitis or subarachnoid hemorrhage. In all but the deepest stages of coma, meningeal irritation may become manifest with resistance to the initial excursion of passive flexion of the neck. However, there is no resistance to the extension, turning, or tilting of the head. This is a fairly specific but relatively insensitive sign of meningeal irritation.
The motor examination includes assessment of the muscle tone, spontaneous and elicited movements and motor reflexes Asymmetries of these aspects of motor function between the two sides of the body should lead to the suspicion of hemiplegia of the non-moving side. This is caused by a lesion affecting the opposite cerebral hemisphere or upper brainstem.
A general approach to the clinical evaluation of coma is to classify the patient into one of a few broad etiologic categories:
-Coma without focal signs or meningism.
This is the most common form. Causes include those that result in a diffuse and generalized brain dysfunction or damage, i.e, not focal causes, such as generalized anoxia or ischemia of the brain (e.g in severe shock, or encephalopathy after resuscitation from cardiac arrest), toxic (drug overdose, alcohol, carbon monoxide, etc) ,metabolic causes (e.g. hypoglycemia, hyperglycemia, hypo- or hypernatremia, hypoxia, hypercapnia, hypo- or hyperthermia, thiamine deficiency, etc), coma due to organ failure (Uremic encephalopathy, hepatic encephalopathy), infections (sepsis), seizures and post-ictal states (states after generalized seizures). However in some cases patients with the above causes of coma may also have focal neurologic signs, but this is the exception, not the general rule.
This is the most common form. Causes include those that result in a diffuse and generalized brain dysfunction or damage, i.e, not focal causes, such as generalized anoxia or ischemia of the brain (e.g in severe shock, or encephalopathy after resuscitation from cardiac arrest), toxic (drug overdose, alcohol, carbon monoxide, etc) ,metabolic causes (e.g. hypoglycemia, hyperglycemia, hypo- or hypernatremia, hypoxia, hypercapnia, hypo- or hyperthermia, thiamine deficiency, etc), coma due to organ failure (Uremic encephalopathy, hepatic encephalopathy), infections (sepsis), seizures and post-ictal states (states after generalized seizures). However in some cases patients with the above causes of coma may also have focal neurologic signs, but this is the exception, not the general rule.
-Coma without focal signs, but with meningism.
It is caused by subarachnoid hemorrhage, meningitis, or meningoencephalitis.
It is caused by subarachnoid hemorrhage, meningitis, or meningoencephalitis.
-Coma with focal signs.
Testing of the patient with coma or altered mental status
Initial tests include pulse oximetry, fingerstick plasma glucose measurement, cardiac monitoring, a 12-lead ECG and blood tests consisting of complete blood count (CBC), a comprehensive metabolic panel (serum electrolytes, BUN, creatinine, and calcium levels), liver function tests, ammonia level and TSH (thyroid stimulating hormone).
Arterial blood gasses (ABGs) are also a necessary test. Carboxyhemoglobin level is measured if there is a suspicion of carbon monoxide toxicity.
Blood and urine should be obtained for culture and usually also for routine toxicology screening e.g ethanol level, serum drug levels, according to the clinical suspicion)
If the cause of altered mental status (impaired consciousness) is not apparent, non-contrast brain CT should be undertaken as soon as possible (to assess for tumors, hemorrhage, edema, evidence of bone trauma, etc). Contrast CT or MRI can be performed later if the results of non-contrast CT are not diagnostic. These tests may detect lesions and pathologic findings missed by non-contrast CT. A chest x-ray should also be obtained.
If after MRI or CT and the other tests the diagnosis of the cause of coma cannot be established, then lumbar puncture (spinal tap) is done, in order to detect infection, subarachnoid hemorrhage, and other abnormalities. Before deciding to proceed with a lumbar puncture, CT images should be reviewed for intracranial masses, obstructive hydrocephalus, and other abnormalities that could obstruct the flow of the cerebrospinal fluid (CSF) or the ventricular system and thus result in a significantly elevated intracranial pressure (ICP). Such conditions present a contraindication to lumbar puncture. The reason is that in such cases there is a risk (although rare) that lumbar puncture may precipitate herniation of the brain.
CSF analysis includes cells (number and differential counts), glucose, protein, Gram stain, cultures, and occasionally some other specific tests if there are certain clinical suspicions (eg, PCR for herpes simplex virus, cryptococcal antigen test, cytology, measurement of tumor markers, VDRL for syphilis).
Management (treatment) of altered mental status or coma
Coma is a medical emergency and often constitutes a diagnostic and therapeutic challenge.
As in every emergency situation assessment and treatment begins with the ABCs (airway, breathing, circulation). Ensure that the airway is patent and clear (see the chapter on airway management).
A patient’s inability to protect against aspiration (e.g a patient with stupor or coma and recent vomiting, or Glasgow Coma Scale-GCS ≤ 8, or poor cough and gag reflex) or the presence of either severe hypoxia (oxygen saturation < 90% which cannot be corrected by the administration of oxygen) or hypoventilation are indications for endotracheal intubation and positive-pressure ventilation. This is initially performed with an Ambu bag connected to an oxygen source and to the endotracheal tube until the endotracheal tube is promptly connected to a mechanical respirator (ventilator). (Ventilation through an endotracheal tube can be maintained for up to 1 week if necessary. If mechanical ventilation is needed after 1 week then this is done through a tracheostomy).
In case of a patient with altered mental status or coma, an intravenous (IV) line is promptly established and blood samples are drawn for determination of glucose, complete blood count (CBC), electrolytes and for tests of liver and kidney function, intoxicating drugs.
As mentioned above, the initial management of a patient with altered mental status or coma consists of immediate assessment and support (if needed) of the airway, breathing, and circulation. These general measures should be undertaken before diagnosing or treating specific causes of coma. Regarding endotracheal intubation, the physician may consider to postpone it until the administration of empiric therapy for coma.
Circulation is an important issue since severe hypotension and/or shock can cause a severe impairment of mental status or consciousness. Management of shock must begin immediately with IV fluids (crystalloids) and further treatment depending on the suspected cause of shock (see the chapter about circulatory shock).
Empiric therapy for coma, abbreviated by the acronym “D.O.N.T.” consists of intravenous (IV) dextrose, administration of oxygen, IV naloxone, and thiamine. Dextrose (50 mL of 50% solution in adults) is administered IV if the rapid testing of blood glucose shows hypoglycemia, or if this rapid glucose test is not available. Ιn children 4 ml/kg of 25% dextrose (0.5-1.0 g/kg) is given IV and in neonates 5 ml/kg of 10% dextrose (0.5 g/kg) IV.
Oxygen levels should be checked on all patients with altered mental status. This can be checked in most patients by pulse oximetry. Oxygen therapy (administration of supplemental oxygen via nasal cannula or face mask) should be initiated especially in patients with a hemoglobin oxygen saturation < 95%, to immediately correct possible hypoxemia. Hypoxemia if present, can induce coma or contribute to the worsening of brain function, even if there is another initial cause.
Naloxone (0.4-2.0 mg IV) is administered if there is a suspicion that the cause could be a narcotic (opioid) overdose. Narcotic overdose can induce coma or respiratory depression, which both can be rapidly reversed by IV naloxone. This antidote has a short half-life, therefore multiple doses may be required.
Thiamine 100 mg IV is commonly administered along with dextrose to avoid the precipitation of Wernicke encephalopathy in predisposed patients (see below).
Thiamine 100 mg IV is commonly administered along with dextrose to avoid the precipitation of Wernicke encephalopathy in predisposed patients (see below).
Apart from naloxone, another antidote which is useful in some cases is flumazenil (0.2 mg/min IV), which is an antidote to benzodiazepines. Flumazenil is not routinely given empirically in cases of coma because in some cases it may precipitate seizures
that are refractory to benzodiazepines. It is indicated for the management of coma secondary to excess benzodiazepine administration.
Thiamine administration should be considered in all patients with an impaired level of consciousness unless the cause is known. Thiamine is an effective treatment for Wernicke’s encephalopathy, which is caused by thiamine depletion. Wernicke's encephalopathy is characterized by the abrupt onset of oculomotor disturbances, ataxia, and confusion.
Alcoholism is the main cause of thiamine deficiency, but not the only cause. Patients at risk for thiamine deficiency and Wernicke’s encephalopathy are those who have a condition causing malnutrition or vitamin deficiency, such as malignancy. anorexia, AIDS, bulimia, and pregnancy. The dosage of thiamine is 100 mg IV in adults and 10-25 mg IV in children.
In case of an elevated intracranial pressure from a mass lesion, IV mannitol should be given (see also chapter on brain trauma) and a neurosurgeon should be emergently consulted.
In patients with a suspected infectious cause for their altered mental status, broad spectrum intravenous antibiotics should be started early. If there is a suspected source or focus of infection (e.g. meninges, lungs, urinary tract) then this should direct the choice of antibiotics. The choice depends on the microorganisms commonly responsible for the infection that is suspected.
In patients with altered mental status do not forget to identify and correct hypothermia(<35 C) or hyperthermia >38.5 C). In severe hyperthermia, evaporative- cooling measures are indicated in addition to the administration of antipyretics.
Both diabetic ketoacidosis and the hyperosmolar nonketotic state can manifest with lethargy or coma. In such cases, keep in mind to search for an underlying precipitating cause or factor, especially infection, while administering treatment with IV fluids and insulin.
Both diabetic ketoacidosis and the hyperosmolar nonketotic state can manifest with lethargy or coma. In such cases, keep in mind to search for an underlying precipitating cause or factor, especially infection, while administering treatment with IV fluids and insulin.
I STRONGLY RECOMMEND THIS VIDEO : A review of coma and altered state of consciousness (you tube channel World neurology foundation Speaker: Rafael H. Llinas, M.D., Associate Professor of Neurology
LINK https://www.youtube.com/watch?v=il6UKOuUaVs
GO BACK TO THE TABLE OF CONTENTS
LINK: Emergency medicine book-Table of contents
BIBLIOGRAPHY AND LINKS
Kanich W, Brady WJ, Huff SJ, et al. Altered mental status: evaluation and etiology in the
ED.Am J Emerg Med 2002;20.
ED.Am J Emerg Med 2002;20.
Clinical policy for the initial approach to patients presenting with AMS. Ann Emerg
Med1999;33:2
Med1999;33:2
A powerpoint presentation from slide-share LINKComa
Another powerpoint presentation from slide share :
Mehakinder Singh, MD Approach to the comatose patient LINK https://www.slideshare.net/keepsmilingdoc/approach-to-the-comatose-patient
Traub SJ, Wijdicks EF.Initial Diagnosis and Management of Coma.Emerg Med Clin North Am. 2016 Nov;34(4):777-793. doi: 10.1016/j.emc.2016.06.017. Epub 2016 Sep 3.
Huff JS, Stevens RD, et al.Emergency neurological life support: approach to the patient with coma. Neurocrit Care. 2012 Sep;17 Suppl 1: S54-9.
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