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COMA

Francis M. Filloux, MD

OBJECTIVES:

1.   Understand the pathophysiologic mechanisms of impaired consciousness.  Distinguish between "structural" and "metabolic" causes/manifestations of coma. 

2.   Be aware of the differential diagnosis of coma. 

3.   Be familiar with the basic clinical evaluation of the comatose patient. 

4.   Memorize an algorith for the management of a comatose patient.

I. Definitions:  

      A.  An impairment of consciousness in which the patient is in a state of unarousable unresponsiveness.  Coma is the most advanced of a series of states in which there is progressive impairment of consciousness: lethargy ---> (confusion/delirium)---> obtundation/stupor ---> coma ---> death.  (Obviously the outcome is potentially serious).

      B.   Other terms: 

            1.   Persistent vegetative state:  brainstem circuits maintain vital functions but awareness (consciousness) is absent.

            2.   Delirium:  impaired consciousness with confusion, agitation and hallucinations.

            3.   Stupor:  pathological sleepiness with decreased activity (same thing as obtundation).

            4.   Akinetic mutism:  term with various uses:  most often: complex neurobehavioral state in which the patient has sleep/wake cycles and can maintain vital functions, but does nothing (absence of the impulse to act).  Often due to bilateral, inferior (orbital) frontal lobe lesions.

            5.   Abulia: similar to 4.

            6.   Locked in syndrome ("coma vigile"):  not a form of coma-- consciousness is preserved, but patient's motor function is sufficiently impaired to prevent outward expression of thought and behavior.  (Due to extensive or transverse high brainstem lesions).  

II.   Pathological conceptualization.

      A.  Consciousness represents the reciprocal interaction and successful functioning of two neural components:

            1.   The Ascending Reticular Activating System (ARAS)-- provides AROUSAL or A-WAKEFULNESS (ALERTNESS).

            2.   The cerebral cortex -- provides AWARENESS.

      B.   Sufficient impairment of either of these two "systems" (or both) produces coma.

      C.  VERY SIMPLISTICALLY you can think of causes of coma in two very general categories according to this scheme:

            1.   coma due to injury or compression of the ARAS = STRUCTURAL COMA.

            2.   coma due to generalized impairment of cerebral cortex (+/- the brainstem) = METABOLIC COMA.

            3.   In general, the former represents the more urgent emergency (more potentially life-threatening) than the latter.

      D.  Specific conditions causing coma:  remember these by recalling that processes which impair either of the above two "systems" can cause coma.  See tables.

Table 1:  Common Causes of Coma Categorized

Supratentorial Mass Lesions                                            

·         hematomas

·         strokes

·         tumor

·         abscess

Infratentorial Mass Lesions

·         brainstem stroke

·         brainstem hemorrhage

·         brainstem tumor

·         brainstem abscess

·         same processes in cerebellum

 

Diffuse Cerebral or Metabolic

·         hypoxia/ischemia

·         concussion

·         meningitis/encephalitis

·         seizure (post-ictal states or status)

·         subarachnoid hemorrhage

·         endocrine disturbances

·         endogenous toxins/deficiencies

                -- uremia

                -- hepatic failure

                -- hypoglycemia, etc...

·         exogenous toxins/ drugs  

Table 2: Mnemonic for Causes of Coma: "SPITE ME NOT"

S     space-occup. lesions                    M    metabolic                              N     neoplastic             

P     psychiatric                                    E      electrical/epileptic                O     oxygen/other

I       infectious/inflamm.                                                                            T     toxic                       

T     trauma

E      endocrine

      E.   Structural lesions can cause coma in one of two ways:  

            1.   Directly by injuring the ARAS itself (e.g., brainstem stroke or hemorrhage).

            2.   Indirectly by compressing the ARAS from the outside.  This process is due to herniation whereby a mass lesion or swelling causes displacement of cerebral structures utimately compressing the midbrain and brainstem, often in a rostro-caudal pattern.  Several types of herniation are described: 

                  a.   Cingulate Gyrus herniation: (figure 1A, topmost arrow a)

                        1.   cingulate gyrus displaced underneath falx, crossing midline.

                        2.   compresses ipsilateral internal cerebral vein and anterior cerebral artery.

                        3.   results in congestion, ischemia and edema.

                  b.   Central herniation: (figure 1B)

                        1.   swelling of hemispheres and basal ganglia bilaterally (ususally)

                        2.   compresses diencephalon and adjoining midbrain caudally through the tentorial notch.

                        3.   results in diencephalic and midbrain (upper brainstem) damage secondary to compression, ischemia and or hemorrhage (traction on penetrating vessels of midbrain and pons).

                  c.   Uncal herniation: (figure 1A, lower arrows)

                        1.   mass or swelling of cerebrum (often unilateral) pushes hippocampal gyrus and uncus over incisura into tentorial notch.

                        2.   compresses ipsilateral third nerve (causing "blown pupil" ... see below).

                        3.   results in damage to brainstem (pons and midbrain).

                  d.   Foramen magnum herniation (tonsillar herniation):

                        1.   posterior fossa mass or swelling.

                        2.   forces cerebellar tonsils through foramen magnum.

                        3.   results in compression of medulla and lower cranial nerves (and death).    

            3.   In general, uncal herniation is due to a unilateral cerebral hemisphere mass lesion. Principal initial problems are headache and contralateral neurological dysfunction followed by rapid deterioration of consciousness along with development of a markedly dilated pupil ("blown pupil") as herniation takes place.  This represents a medical/neurosurgical emergency!

            4.   Central herniation is more commonly due to midline, parasagittal lesions or bilateral cerebral lesions.  Consciousness is impaired early, often before dilated pupils develop.  Here there follows a more typical "rostro-caudal" deterioration as progressively lower regions of midbrain and brainstem are affected.

III. Your Job as a Physician: 

      I suppose your ultimate job as a physician is to protect a person's consciousness.  Hence, every physician must know how to recognize, evaluate and manage (at a basic level) the comatose patient.  A patient in coma is doing the best they can to die until proven otherwise.

IV. Evaluation of the comatose patient:  

General tools of the trade:

      A.  Since the obtunded/comatose patient basically does not converse or cooperate, you have to rely on: 1) history from others, and 2) basic observations and neurological examination findings.

      B.   HISTORY:  This is still crucial.  As the patient is being stabilized (see below), the physician and staff try to determine:

            1.   what happened?

            2.   any underlying medical problems?  (e.g., diabetes)

            3.   any medications used or in the home?

            4.   non-prescribed drug use/ exposure?

      C.  While you take the history, you are also examining the patient (and preparing to have a CT scan of brain done). Besides the general exam (any bruises?  alcohol on the breath?  needle tracks on arm? signs of systemic disease?. etc...), you perform a concise neurological examination, to answer the following questions:

            1.   What is the level of consciousness/coma?

            2.   Is there evidence of impending herniation?

            3.   Is brainstem function affected?

            4.   Are there any focal findings that are helpful?

            Question 1:       What is the level of consciousness/coma?  Is there spontaneous activity?  Eye opening?  verbal response?  motor activity?  Does the patient have any response to voice, tactile stimulation, painful stimulation?

            Question 2:       Is there evidence of impending herniation? Is there a "blown pupil":  a dilated, sluggishly reactive or non-reactive pupil?  Are both pupils dilated? (i.e., "fixed and dilated"?)

            Question 3:       Is brainstem function affected?  

                  a.   check pupils:  CN II, sympathetics and parasympathetics (CN III).

                  b.   check oculocephalic maneuver ("doll's eyes"):  (CN III, IV and VI, plus intrinsic brainstem pathways:  MLF).

                  c.   check corneal reflex:  afferent:  CN V;  efferent:  CN VII.

                  d.   check cold water calorics [optional]:  afferent:  VIIIth CN;  MLF and CN III, IV and VI.

                  e.   check "nasal tickle":  afferent CN V; efferent CN VII.

                  f.    check gag reflex:  afferent CN IX;  efferent CN X.

                  g.   assess spontaneous respiratory pattern.

            Question 4:  Are there any focal findings that are helpful?  

                  a.   besides the above CN findings, check resting posture.

                  b.   check motor tone, muscle stretch reflexes, motor response.

      D.  Clinical Patterns Worth Recognizing/Remembering:  In general, the pattern of brainstem/respiratory and motor findings can provide clues to the level or region of structural brain involvement.

            1.   Respiration:  see figure 2

            2.   Pupils:  see figure 3

            3.   Eye-movements (in oculocephalic reflex):  see figure 4

            4.   Posture/ motor response:  see figure 5

            Remember, however, that abnormal brainstem signs (e.g., absent oculocephalic reflex) can be seen in deeper stages of metabolic (toxic) comas, so none of these signs are absolutely specific!

V.  Evaluation and Management of the Comatose Patient:  

      The algorithm below provides a systematic approach to the comatose patient.  It is not perfect nor applicable in all cases, but is a good guide. (see Approach to the Comatose Patient)

VI. Final General Rules:

      A.  General goal is to promptly identify cases in which progressive herniation (rostrocaudal deterioration) will lead to further damage and death unless timely intervention is provided.

      B.   Similarly, early identification of toxic causes in which treatment will prevent irreversible damage or death is helpful. (e.g., aspirin or tricyclic antidepressant intoxication)

      C.  In attempting to separate metabolic from structural causes of coma, the following guidelines are helpful:

            1.   toxic/metabolic comas are often of slower onset and may be preceeded by delirium.

            2.   respiratory impairment often occurs earlier in toxic/metabolic states.

            3.   pupillary responses and oculocephalic reflexes are more likely to be preserved in toxic/metabolic comas.

            4.   focal features are usually absent in toxic-metabolic comas.

            5.   tremor, asterixis and multifocal myoclonus usually limited to toxic-metabolic comas.

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                                              Last updated:  10/05/2002                                                          © 2000-2002 John Rose, MD  University of Utah School of Medicine