328 Coma Flashcards
Deep sleeplike state from which the patient cannot be aroused
Coma
Higher degree of arousability in which the patient can be transiently awakened by vigorous stimuli, accompanied by motor behavior that leads to avoidance of uncomfortable or aggravating stimuli
Stupor
Simulates light sleep characterized by easy arousal and the persistence of alertness for brief periods
Drowsiness
Signifies an awake-appearing but nonresponsive state in a patient who has emerged from coma
Vegetative state / “awake coma”
T or F: Respiratory and autonomic functions are retained in vegetative state
True
Term used once vegetative had supervened after a year, wherein the prognosis for regaining mental faculties are almost nil
Persistent vegetative state
A partially or fully awake state in which the patient is able to form impressions and think, but remains virtually immobile and mute
Akinetic mutism
A milder form of akinetic mutism characterized by mental and physical slowness and diminished ability to initiate activity; usually a damage to the frontal lobes
Abulia
Curious hypomobile and mute syndrome that occurs as part of a major psychosis, usually schizophrenia or major depression
Catatonia
Type of pseudocoma in which an awake patient has no means of producing speech or volitional movement but retains voluntary vertical eye movements and lid elevation, thus allowing the patient to signal with a clear mind
Locked-in state
Common cause: infarction or hemorrhage of ventral pons
Eyelid elevation is actively resisted, blinking occurs in response to visual threat, eyes move concomitantly with head rotation, limbs to retain postures in which they have been placed by the examiner (catalepsy or “waxy flexibility”)
Catatonia
Principal causes of coma
- Lesions that damage the reticular activating system (RAS) in the upper midbrain or its projections
- Destruction of large portions of both cerebral hemispheres
- Suppression of reticulocerebral function by drugs, toxins, or metabolic derangements (hypoglycemia, anoxia, uremia, hepatic failure)
Displacement of brain tissue by an overlying or adjacent mass into a contiguous compartment that it normally does not occupy
Herniation
T or F: “False localizing” signs can be seen in herniation since they are derived from compression of brain structures at a distance from the mass
True
Brain tissue is displaced from the supratentorial to the infratentorial compartment through the tentorial opening
Transtentorial herniation
Impaction of the anterior medial temporal gyrus (uncus) into the tentorial opening just anterior to and adjacent to the midbrain
Uncal transtentorial herniation
Figure 328-1, p. 1772
The nerve that traverses the subarachnoid space and when compressed by the uncus, causes enlargment of the ipsilateral pupil
Third nerve
Hemiparesis contralateral to the hemiparesis that resulted from the mass (in short, ipsilateral to the mass)
Kernohan-Woltman sign
Symmetric downward movement of the thalamic structures through the tentorial opening with compression of the upper midbrain
Central transtentorial herniation
Figure 328-1, p.1772
Displacement of cingulate gyrus under falx and across the midline
Transfalcial herniation
Figure 328-1, p. 1772
Downward forcing of the cerebellar tonsils into the foramen magnum
Foraminal herniation
Figure 328-1 p. 1772
Level of arousal based on horizontal displacement of pineal calcification in cases of acutely enlarging masses
3-5mm : drowsiness
6-8mm : stupor
>9mm : coma
Cerebral blood flow (CBF) in gray matter and white matter
Gray matter: ~75ml per 100 g/min
White matter: ~55ml per 100g/min
Oxygen consumption of cerebral neurons
3.5ml per 100g/min
Glucose utilization of cerebral neurons
5mg per 100g/min
How long will brain stores of glucose last after blood flow is interrupted?
~2 minutes
How long will oxygen stores in the brain last after cessation of blood flow?
8-10 seconds
Unlike hypoxia-ischemia which cause neuronal destruction, what metabolic disorders cause minor neuropathologic changes and are thus reversible
- Hypoglycemia
- Hyponatremia
- Hyperosmolarity
- Hypercapnia
- Hypercalcemia
- Hepatic failure
- Renal failure
Sodium levels that induce confusion
<125 mmol/L
Sodium levels associated with coma and convulsions
<115 mmol/L
Serum osmolarity in hyperosmolar coma
> 350 mosmol/L
T or F: In the approach to a coma patient, most instances, complete medical evaluation, except VITAL SIGNS, FUNDOSCOPY, EXAM FOR NUCHAL RIGIDITY, may be deferred until the neurologic evaluation has established severity and nature of coma
True
Useful points in the history of a patient in coma
- Circumstances and rapidity with which neurologic symptoms developed
- Antecedent symptoms (confusion, weakness, headache, fever, seizures, dizziniess, double vision, vomiting)
- use of medications, drugs, alcohol
- chronic liver, kidney, lung, heart of medical disease
At what temperature does hypothermia cause coma?
<31 C (87.8 F)
What can fundoscopy reveal in a coma patient?
- Subarachnoid hemorrhage (subhyaloid hemorrhages)
- Hypertensive encephalopathy (exudates, hemorrhages, vessel-crossing changes, papilledema)
- Increased intracranial pressure (papilledema)
In a drowsy or confused patient, what is a certain sign of metabolic encephalopathy or drug intoxication
Bilateral asterixis
Flexion of elbows and wrists and supination of arm suggesting bilateral damage rostral to midbrain
Decorticate posturing
Extension of elbows and wrists with pronation indicating damage to motor tracts in midbrain or caudal diencephalon
Decerebrate posturing
Pupillary signs and probable causes
> 6mm, unilateral, poorly reactive pupils : compression of Third nerve from cerebral mass
1-2.5mm, bilaterally small, reactive pupils but not pinpoint: metabolic enceph, hydrocephalus, thalamic hemorrhage
<1mm, smaller reactive pupils : narcotic or barbiturate overdose, extensive pontine hemorrhage
This phenomenon is summarized as: The eyes look toward a hemispheral lesion and away from a brainstem lesion
Conjugate horizontal roving
Brisk downward and slow upward movements of eyes associated with loss of horizontal eye movements and is diagnostic of bilateral pontine damage
“Ocular bobbing”
Slower arrhythmic downward movement followed by a faster upward movement in patients with normal reflex horizontal gaze; indicates diffuse cortical anoxic damage
“Ocular dipping”
Reflex elevation of eyelids with flexion of neck, normally suppressed in the awake patient
“doll’s eyes”
Eliciting this response reflects both reduced cortical influence on brainstem and intact brainstem pathways; coma is caused by lesion or dysfunction in cerebral hemispheres
Positive “doll’s eyes”
Useful test of pontine function
Corneal reflex
Breathing pattern described as typical cyclic form, ending with a brief apneic period, signifying bihemispheral damage or metabolic suppression
Cheyne-Stokes respiration
Breathing pattern that is rapid and deep, usually implies metabolic acidosis
Kussmaul breathing
Result of lower brainstem (medullary) damage recognized as terminal respiratory pattern of severe brain damage
Agonal gasps
Studies most useful in diagnosis of coma
- Chemical-toxicologic analysis of blood and urine
- Cranial CT or MRI
- EEG
- CSF examination
Ethanol levels in nonhabituated patients that causes impaired mental activity and stupor
Impaired mental activity: 43 mmol/L (0.2g/dL)
Stupor : >65 mmol/L (0.3g/dL)
Chronic alcoholics develop tolerance which makes them awake at what ethanol levels?
> 87 mmol/L (0.4g/dL)
T or F:
CT or MRI in coma patients is prudent
False.
Imprudent because most cases of coma are metabolic or toxic in origin.
If source of coma remains unknown, a scan should be obtained
EEG findings in metabolic coma (e.g. hepatic failure)
Predominant high-voltage slowing delta or triphasic waves in frontal regions
EEG findings implicating sedative drugs (e.g. BDZ)
Widespread fast beta activity
T or F:
For patients with altered level of consciousness, imaging study should be performed prior to lumbar puncture
True.
To exclude a large intracranial mass lesion.
3 broad categories on causes of coma
- Cases without focal neurologic signs (metabolic and toxic enceph)
- Meningitis syndromes (fever, stiff neck, excess of cells in spinal fluid)
- Diseases associated with prominent focal signs (stroke, cerebral hemorrhage)
Conditions that cause sudden coma
- Drug ingestion
- Cerebral hemorrhage
- Trauma
- Cardiac Arrest
- Epilepsy
- Basilar artery occlusion (due to embolism)
Coma in cerebrovascular disease is associated with
- basal ganglia and thalamic hemorrhage
- pontine hemorrhage
- cerebellar hemorrhage
- basilar artery thrombosis
- subarachnoid hemorrhage
T or F:
Infarction in territory of MCA can cause coma
False.
Edema surrounding the large infarctions can cause coma from mass effect.
Characterized by headache and sometimes vomiting that may progress quickly to coma with extensor posturing of the limbs, bilateral Babinski signs, small unreactive pupils, impared oculocephalic movements in vertical direction
Syndrome of acute hydrocephalus (particulary subarachnoid hemorrhage)
State of irreversible cessation of all cerebral function with preservation of cardiac activity and maintenance of respiratory and somatic function by artificial means
Brain death
Three essential elements of brain death
- widespread cortical destruction reflected by deep coma and unresponsiveness to all forms of stimulation
- global brainstem damage (absent pupillary light reaction and loss of oculovestibular and corneal reflexes)
- destruction of medulla (complete and irreversible apnea)
Apnea testing procedure
- Preoxygenation with 100% oxygen thru tracheal cannula
- CO2 tension increases ~0.3-0.4 kPa/min (2-3 mmHg/min ) during apnea
- arterial PCO2 should be atleast >6.6 - 8.0 kPa (50-60mmHg)
Apnea confirmed if no respiratory effort has been observed in presence of sufficiently elevated PC02
Immediate goal in comatose patient
Prevention of further nervous system damage
Indications for tracheal intubation in comatose patients
- Apnea
- Upper airway obstruction
- Hypoventilation
