Coma Flashcards
What is a coma?
Coma reflects brain failure that may occur from a process originating in the central nervous system or may reflect a systemic metabolic process
Coma is defined as a state of deep unconsciousness, an eyes-closed unresponsive state.
Coma is usually a transitory state though it may last for an indefinite or even prolonged period.
Alerting and arousal functions of the brain are affected as well as awareness and the content of consciousness.
Brief loss of consciousness with full return to alertness defines syncope.
What is lethargy?
Lethargy indicates a defect in attention with only minimally reduced wakefulness
What is obtundation?
Obtundation refers to more blunted awareness and lessened response to the environment
What is stupor?
Stupor describes a deeper unresponsive state from which the patient can be only transiently aroused with vigorous stimulation
Outline the etiology of comas
Coma represents brain failure. It may be caused by neuronal dysfunction from many causes including structural or non-structural processes affecting the central nervous system.
Metabolic or infectious etiologies may diffusely affect the brain and lead to a coma.
Common toxic or metabolic causes of coma include hypoglycemia, hyperglycemia, excessive alcohol intake, and medication overdose or illicit drug use.
Of all the non-structural causes of coma, hypoglycemia and systemic infections likely account for the majority of patients presenting with coma
Other less common metabolic causes include hepatic encephalopathy, hyponatremia, hypernatremia, hypercalcemia, endocrine abnormalities, and many others.
Primary central nervous system infections such as meningitis or encephalitis may lead to coma but are relatively uncommon though vitally important to detect
Structural brain diseases
Generalized status epilepticus may evolve to a subtle or non-convulsive form, sometimes called transformed or end-stage status epilepticus, where unresponsiveness predominates the clinical picture and there is only minor or even no associated motor activity.
Additionally, with the increasing use of electroencephalogram (EEG) monitoring in intensive care units, patients are now being identified with highly abnormal electroencephalographic findings suggesting non-convulsive status epilepticus in patients who are clinically without generalized seizures
List the structural brain diseases associated with comas
Structural brain diseases such as subdural or epidural traumatic hematomas, spontaneous intracranial hemorrhages, venous thrombosis, tumors, acute hydrocephalus, raised intracranial pressure, anoxic brain injury, or brainstem strokes may all cause altered mental status or coma
List the common causes of comas
Common causes of coma include
1. Anoxic brain injury
2. Cerebral infarction
3. Cerebral hemorrhage
Spontaneous
Traumatic
4. Cerebral neoplasms
5. Hypertensive encephalopathy
6. Hypoglycemia
7. Metabolic encephalopathy
8. Myxedema
9. Status epilepticus
10. Toxic encephalopathy
Outline the epidemiology of a coma
Though coma is a common clinical presentation to the emergency department (ED), the actual frequency of coma at ED presentation is difficult to determine.
The number of published studies of patients presenting with coma is surprisingly small.
The use of many terms to describe patients with depressed mental states leads to multiple coding options, making retrospective reviews challenging.
Within a clinical record, there is often variation in assessments by different providers
The fact that a common cause of coma, hypoglycemia, is often treated by emergency medical service providers with resolution prior to emergency department arrival adds to coding confusion
A more recent single-center study of over 1000 consecutive patients with coma of unknown etiology that excluded traumatic brain injury and cardiac arrest survivors found that patients with coma of unknown etiology comprised 0.4% of all ED patients.
The main diagnoses were classified into acute primary brain lesions such as hemorrhage and tumors (39%), pathologies that affected the brain secondarily such as sepsis, intoxications, or metabolic conditions (36%) primary brain pathologies without acute lesions, largely epilepsy (25%).
One-third of subjects had more than one coma-explaining pathology
Explain the pathophysiology of a coma
The accepted pathophysiology of a coma involves neuronal dysfunction from a decrease in the supply of glucose or oxygen to the brain. A myriad
of etiologies may lead to essential substrate disruption with diffuse central nervous system (CNS) dysfunction and coma as the extreme clinical
condition.
For example, any clinical process that causes circulatory collapse or profound hypoxemia may manifest as a coma. As little as fifteen seconds of circulatory collapse will result in loss of consciousness.
If the cause of the circulatory collapse is brief and promptly restored, such as
from a simple faint, consciousness is regained. If hypotension or hypoxemia continues, the altered mental state continues, and secondary CNS
damage may occur
Hypoglycemia is encountered frequently in clinical practice most often in the association of treatment for diabetes mellitus or as a complication of alcoholism.
Electrolyte abnormalities such as hyponatremia or hypercalcemia may disrupt normal neuronal metabolism.
The pathophysiology of other causes of metabolic coma is not clear but may involve false neurotransmitters as is suggested in hepatic encephalopathy.
Global depression of neuronal functioning is the most common mechanism of coma in toxins and poisonings.
Structural lesions of the CNS, such as intracerebral hemorrhage, may lead to coma from direct destruction of arousal areas of the brain or from secondary damage from shifting of intracranial structures, vascular compression, or increased intracranial pressure
Describe the pathophysiology of herniation syndromes in a coma
Herniation syndromes describe clinically recognizable physical examination features that may suggest the anatomic location of the CNS lesion.
The most discussed of the herniation syndromes is uncal herniation, where the medial portion of the temporal lobes shifts with resulting loss of consciousness from brainstem compression.
The pathophysiologic findings are often compression of the brainstem and cranial nerve III as it exits the brainstem and crosses the tentorium cerebelli.
This results in impairment of the parasympathetic fibers (pupillo-constrictors) that travel with the third nerve, and in most cases pupillary dilatation on the same side (roughly 90%) of the mass lesion.
A) Uncal (lat transtentorial): Ipsi CI Ill palsy (“blown pupil) + contra hemiplegia/posturing (Kernohan notch phenomenon)
temporal lobe mass → medial temporal lobe under tent. cerebelli
B) Central transtentorial: Coma + b/l small pupils → decorticate → decerebrate posturing + rostral → caudal loss brainstem reflexes
diffuse cerebral edema → decrease displacement diencephalon
C) Subfalcine: Coma + contra. weakness
→ posturing esp leg ‡ ACA stroke
frontal/parietal mass → cingulate gyrus -
under falx
D) Cerebellar (increase or decrease ): Cerebellar Si/Sx + medullary dysfxn → coma + b/l posturing
Describe the pathophysiology of increased intracranial pressure in comas
Increased intracranial pressure is a frequent cause of coma.
Since the brain is enclosed in the closed skull, conditions that increase intracranial pressure may impair cerebral perfusion.
The equation that approximates this relationship is unforgiving.
CPP = MAP – ICP
CPP: cerebral perfusion pressure
MAP: mean arterial pressure estimated as 1/3 systolic BP [blood pressure]
+ 2/3 diastolic BP)
ICP: intracranial pressure
As ICP approaches MAP, cerebral perfusion diminishes. It is essential to maintain CPP by reducing increased intracranial pressure while avoiding hypotension
- Brain survival depends on cerebral blood flow meeting cerebral metabolic requirements
- Cerebral blood flow depends on Cerebral Perfusion Pressure
- CPP depends upon ICP
Normal CPP > 50 mm Hg
Outline the physical exam of a coma
Physical examination should be directed to detect any signs of trauma during the general physical examination.
Initial neurological examination should include the response to pain, a brief assessment of motor function, eye-opening, and verbalization.
Cranial nerve examination should include an evaluation of extraocular movements, pupillary, corneal, cough, and gag reflex.
Any abnormal posturing should be noted. The presence of ipsilateral dilation of the pupil suggests the uncal herniation syndrome with compression of the third cranial nerve from a mass.
Lack of focal findings on examination suggests a metabolic, infectious, or toxicologic cause of coma.
Recording of the neurologic examination and the depth of the coma can be roughly quantified by the Glasgow Coma Scale, the FOUR score, or other rating scales.
Brief rating scales are useful for sequential monitoring of the patient but do have limitations
What are the aspects of the Glasgow Coma scale
Eye response
4 = eyes open spontaneously
3 = eye-opening to verbal command
2 = eye-opening to pain
1 = no eye-opening
Motor response
6 = obey commands
5 = localizing pain
4 = withdrawal from pain
3 = flexion response to pain
2 = extension response to pain
1 = no motor response
Verbal response
5 = oriented
4 = confused
3 = inappropriate words
2 = incomprehensible sounds
1 = no verbal response
What are the aspects of the Four SCORE scale?
Eye response
4 = eyelids open or opened, tracking, or
blinking to command
3 = eyelids open but not tracking
2 = eyelids closed but open to a loud voice
1 = eyelids closed but open to pain
0 = eyelids remain closed with pain
Motor response
4 = thumbs-up, fist, or peace sign
3 = localizing to pain
2 = flexion response to pain
1 = extension response to pain
0 = no response to pain or generalized myoclonic status
Brainstem reflexes
4 = pupil and corneal reflexes present
3 = one pupil wide and fixed
2 = pupil or corneal reflexes absent
1 = pupil and corneal reflexes absent
0 = absent pupil, corneal, and cough reflex
Respiration
4 = not intubated, regular breathing pattern
3 = not intubated, Cheyne-Stokes breathing pattern
2 = not intubated, irregular breathing
1 = breaths above the ventilator rate
0 = breaths at ventilator rate or below
Outline the evaluation of a comatose patient
Initial evaluation of the comatose patient should always include assessment with intervention as necessary of the airway, breathing, and
circulatory conditions (A,B,C’s).
The differential diagnosis of coma is extensive. Unless a recognizable infectious or metabolic cause of coma is promptly established, additional testing will be necessary.
Laboratory and toxicologic tests should be obtained as indicated. Initial stat labs would include electrolytes, FBC, arterial or venous blood gas analysis, and possibly toxicologic testing
As the case progresses, neuroimaging may be indicated.
CT and MRI brain scanning may detect hemorrhage, mass effect, or other structural abnormalities.
Vascular imaging may reveal large vessel occlusion.
Initial efforts will be to determine a likely structural or non-structural cause of coma leading to appropriate interventions and consultations.
EEG should be considered in a patient following generalized convulsive status epilepticus with continued altered mental status since status epilepticus may continue with little or no associated motor movements
