coma english

8/2/2019 Coma English

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COMA AND RELATEDDISORDERS OF

CONSCIOUSNESS

Prof. M. Gavriliuc,Department of Neurology, Medical

and Pharmaceutical NicolaeTestemitsanu State University,

Republic of Moldova


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ANATOMICAL BASIS OF CONSCIOUSNESS


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Normal Consciousness. This is the

condition of the normal person whenawake. In this state the individual isfully responsive to stimuli andindicates by his behavior and speechthe same awareness of self and

environment as that of the examiner.This normal state may fluctuateduring the course of the day from oneof keen alertness or deep

concentration with a markedconstriction of the field of attention toone of mild general inattentiveness.From this state, the normal individual

can be brought immediately to a state

of full alertness and function.

Description of States of Normal and ImpairedConsciousness


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Inattention and Confusion.In

these conditions the patientdoes not take into account allelements of his immediateenvironment. Patientdenotes an inability to thinkwith customary speed andclarity, usually marked bysome degree ofinattentiveness and

disorientation. Confusionmost often results from aprocess that influences thebrain globally such as a toxic

or metabolic disturbance or adementia.



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Drowsiness and Stupor.Drowsinessdenotes

an inability to sustain a wakeful state withoutexternal stimuli. Inattentiveness and mildconfusion are the rule, both improving witharousal. The lids droop without closingcompletely; there may be snoring, the jaw and

limb muscles are slack, and the limbs arerelaxed. This state is indistinguishable fromlight sleep, with slow arousal elicited byspeaking to the patient or applying a tactile

stimulus. Stupordescribes a patient who can

be roused only by vigorous and repeatedstimuli, at which time he opens his eyes, looksat the examiner, and does not appear to beunconscious; response to spoken commands iseither absent or slow and inadequate.



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an individual exhibits no voluntary

movement or behavior.Somehistorians believe that the

description of Jesus resurrectinghis friend Lazarus from the dead

may represent one of the firstreports of an individual in coma. Inaddition, more recent descriptions,documented approximately 150years ago, discuss the diagnosis of

apparent death as a possiblesynonym for coma (Kiss 1991).

Coma, from the Greek word "koma," meaning deep sleep,is a state of extreme unresponsiveness, in which


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COMA. The patientwho appears to be asleep and is at the

same time incapable of being aroused byexternal stimuli or inner needs is in a stateof coma. There are variations in thedegree of coma; in its deepest stages, noreaction of any kind is obtainable: corneal,

pupillary, pharyngeal, tendon, and plantarreflexes are all absent, and tone in thelimb muscles is diminished. With lesserdegrees of coma, pupillary reactions,

reflex ocular movements, and corneal andother brainstem reflexes are preserved invarying degree, and muscle tone in thelimbs may be increased.


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Physiology and Morbid Anatomy of Coma

Coma-producing alterations in the brain are of three main types:

1. one clearly morphologic,

consisting either of discreteparamedial lesions in the upperbrainstem and lowerdiencephalon,

2.or of more widespread

changes throughout thehemispheres, thus interruptingthe flow of signals to thecerebral cortex from the centralgenerators of the brainstemactivating system. The other

type is metabolic orsubmicroscopic, resulting insuppression of neuronal activity,usually concurrently in thereticular activating system and in

cortical neurons.

1 + 2


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CLINICAL APPROACH TO THE COMATOSE PATIENT

COMA is not a disease per se butis always a symptomaticexpression of an underlyingdisease. Sometimes theunderlying disorder is perfectlyobvious, as with severe cranialtrauma. All too often, however, thepatient is brought to the hospitalin a state of coma and little

pertinent medical information isimmediately available. The clinicalproblem must then be scrutinizedfrom several angles.


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Alterations in vital signs - temperature,pulse, respiratory rate, and blood

pressure - are important aids indiagnosis. Fever is most often due to asystemic infection such as pneumonia orto bacterial meningitis. An excessively

high body temperature (42 or 43C)associated with dry skin should arousethe suspicion of heat stroke oranticholinergic drug toxicity. Fevershould not be ascribed to a brain lesionthat has disturbed the temperature-regulating centers - a very rare

occurrence. Hypothermiais frequentlyobserved in patients with alcoholic orbarbiturate intoxication, drowning,exposure to cold, peripheral circulatoryfailure, and myxedema.


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Slow breathingpoints to opiate orbarbiturate intoxication and occasionally to

hypothyroidism, where-as deep, rapidbreathing should suggest the presence of

pneumonia, diabetic or uremic acidosis(Kussmaul respiration), pulmonary edema,or the less common occurrence of anintracranial disease that causes central

neurogenic hyperventilation. The rapidbreathingof pneumonia is oftenaccompanied by an expiratory grunt,

cyanosis, and fever. Diseases that elevateintracranial pressure or damage the brainoften cause slow, irregular respiration orperiodic CSR. The various disorderedpatterns of breathing and their clinical

significance are described further on.


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BREATHING PATTERNS ANDLOCALIZATION:


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The pulse rate, if exceptionally slow,should suggest heart block, or - if

combined with periodic breathing andhypertension - an increase in

intracranial pressure. Markedhypertension is observed in patientswith cerebral hemorrhage and

hypertensive encephalopathy and, attimes, in those with greatly increasedintracranial pressure. Hypotension isthe usual finding in states of depressed

consciousness that are due to diabetes,alcohol or barbiturate intoxication,internal hemorrhage, myocardialinfarction, dissecting aortic aneurysm,septicemia, Addison disease, or

massive brain trauma.


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Inspection of the skin.

Cyanosis of the lips and nail beds -inadequate oxygenation.

Cherry-red coloration - carbon monoxidepoisoning.Multiple bruises - cranial fracture andintracranial trauma.

Telangiectases and hyperemia of the face andconjunctivae alcoholism.Marked pallor - internal hemorrhage.A maculohemorrhagic rash - meningococcalinfection, staphylococcal endocarditis,typhus, or Rocky Mountain spotted fever.Excessive sweating - hypoglycemia or shock.Excessively dry skin - diabetic acidosis,uremia, or drug overdose with anticholinergic

effect.


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The odor of the breath may

provide a clue to the etiologyof coma. The odor of alcoholis easily recognized (exceptfor vodka, which is odorless).The spoiled-fruit odor of

diabetic coma, theuriniferous odor of uremia,the musty fetor of hepaticcoma, and the burnt almond

odor of cyanide poisoning aredistinctive enough to beidentified by physicians whopossess a keen sense ofsmell.


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The predominant

postures of the limbsand body, thepresence or absenceof spontaneousmovements, the

position of the headand eyes, and therate, depth, andrhythm of respiration

should be noted.

Neurologic Examination of the Stuporous or Comatos Patient


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The state of responsiveness is

then estimated by noting thepatient's reaction to calling hisname, to simple commands, orto noxious stimuli such assupraorbital or sternal

pressure, pinching the side ofthe neck or inner parts of thearms or thighs, or applyingpressure to the knuckles. By

grading these stimuli, one mayroughly estimate both thedegree of unresponsivenessand changes from hour to

hour.



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Vocalization may persist in

stupor and is the firstresponse to be lost as comaappears. Grimacing and deftavoidance movements of thestimulated parts are preserved

in light coma; their presencesubstantiates the integrity ofcorticobulbar andcorticospinal tracts. Yawning

and shifting of body positionsindicate a minimal degree ofunresponsiveness.


Glasgo Coma Score


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The GCS is scored between 3 and 15, 3 being the worst, and 15 the best. Itis composed of three parameters : Best Eye Response, Best VerbalResponse, Best Motor Response, as given below :Best Eye Response. (4) Best Verbal Response. (5)E1.No eye opening. V1. No verbal responseE2. Eye opening to pain. V2. Incomprehensible sounds.E3. Eye opening to verbal command. V3. Inappropriate words.E4. Eyes open spontaneously. V4. Confused

V5.Orientated

Best Motor Response. (6)M1. No motor response.M2. Extension to pain.M3. Flexion to pain.M4. Withdrawal from pain.M5.Localising pain.

M6. Obeys Commands.Note that the phrase 'GCS of 11' is essentially meaningless, and it is

important to break the figure down into its components, such asE3V3M5 = GCS 11. A Coma Score of 13 or higher correlates with a mildbrain injury, 9 to 12 is a moderate injury and 8 or less a severe braininjury.

Teasdale G., Jennett B., LANCET (ii) 81-83, 1974.

Glasgow Coma Score


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Examination of the cranialnerves and brainstemreflexes has localizing

value. Localization canprovide insight intopathophysiology as there areregional differences insusceptibility to variouspathologies.

COMA


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The Pupillary Reactions

A unilaterally enlarged pupil (> 5 mm diameter) is the mostimportant indicator of progressive horizontal displacement of

the midbrain or medial temporal lobe. The earliest sign ofcompression is usually a loss of light reaction alone; withcontinued compression, the pupil may become oval or pear-shaped.With massive midbrain lesions, both pupils dilate to morethan 5 mm and become unreactive to light; contrariwise,

normal pupillary size, symmetry, and shape and thepreservation of light reflexes indicate integrity of midbrainstructures. Pontine tegmental lesions cause extremely mioticpupils (


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Oculocephalic reflexes (doll's-eye movements)

are elicited by briskly turning ortilting the head and consist of

conjugate movement of the eyesin the opposite direction, are notpresent in the normal alertperson. Elicitation of these

reflexes in a comatose patientprovides two pieces ofinformation: one, evidence ofintactness of the ocular motornerves and of the midbrain and

pontine tegmental structures thatintegrate ocular movements, andtwo, loss of cortical inhibition thatnormally holds these movements

in check.


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Vertical globe deviationwith neck flexion and

extension can be usedto uncover upperbrainstem lesions thatcause coma. Similarly,

lid elevation shouldoccur with upward eyemovement during neckflexion if the uppermidbrain is

undamaged.


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Although the failure to elicit eyemovements implies brainstem

dysfunction, sedative oranticonvulsant intoxicationserious enough to cause comamay symmetrically obliterate the

brainstem mechanisms foroculocephalic reactions and, inextreme cases, even theoculovestibular responses,described below. Asymmetry in

elicited eye movements,however, remains a dependablesign of focal brainstem disease.


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CORNEAL REFLEXOften the corneal reflexesdisappear in the deep stages of

coma of any cause, asbrainstem function is depressed.Unilateral loss of the cornealreflex denotes an ipsilateral

pontine lesion but may alsooccur contralateral to a largehemispheral lesion and bemisinterpreted as an ipsilateralbrainstem lesion. Lower

brainstem reflexes are seldomhelpful in the analysis of coma.

Si f I d I t i l P


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Signs of Increased Intracranial Pressure

A history of headache before the onset ofcoma, recurrent vomiting, and subhyaloid

retinal hemorrhages are the bestimmediate clues to the presence ofincreased intracranial pressure, usuallyfrom one of the types of cerebral

hemorrhage. Papilledema develops within12 to 24 h in cases of brain trauma andhemorrhage, but, if pronounced, it usuallysignifies brain tumor or abscess, i.e., alesion of longer duration. Increased

intracranial pressure produces coma byimpeding global cerebral blood flow.


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Laboratory Procedures in Comatos Patient

In patients with evidenceor even a suspicion ofincreased intracranial

pressure, a CT scan orMRI should be obtained asa primary procedure.


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Laboratory Procedures in Comatos PatientIf poisoning is suspected,aspiration and analysis of

the gastric contents issometimes helpful, butgreater reliance should beplaced on chromatographic

analysis of the blood andurine. Accurate means areavailable for measuring theblood concentrations ofphenytoin, barbiturates,

alcohol, and a wide rangeof other toxic substances.


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Laboratory Procedures in Comatos PatientLumbar puncture,although carrying a certain

risk of promoting furtherherniation, is neverthelessnecessary in someinstances to rule out

bacterial meningitis,encephalitis, or a primarysubarachnoid hemorrhagethat is not visible by CT,although such a patient

would not likely becomatose.


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Laboratory Procedures in Comatos PatientUrine of low specific gravity and high proteincontent is found in uremia. Urine of high

specific gravity, glycosuria, and acetonuriaare found almost invariably in diabetic

coma. Blood counts are made, and inmalarial districts a blood smear is examined

for parasites. Neutrophilic leukocytosisoccurs in bacterial infections and also withbrain hemorrhage and infarction, althoughthe elevation in the latter conditions rarelyexceeds 12,000 WBC/mm3. Venous blood

should be examined for glucose, urea,carbon dioxide, bicarbonate, ammonium,sodium, potassium, chloride, calcium, andSGOT (serum glutamic oxaloacetic

transaminase) in appropriate cases.


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Classification of Coma and Differential Diagnosis

I. Diseases that cause no focal or lateralizing neurologicsigns, usually with normal brainstem functions. CT scan

and cellular content of the CSF are normal.

A. Intoxications: alcohol, barbiturates and other sedativedrugs, opiates, etc.

B.Metabolic disturbances: anoxia, diabetic acidosis,uremia, hepatic coma, hypoglycemia, addisonian crisis,profound nutritional deficiency.

C.Severe systemic infections:pneumonia, typhoid fever,malaria, septicemia, Waterhouse-Friderichsen syndrome.

D. Circulatory collapse(shock) from any cause.

Cl ifi i f C d Diff i l Di i


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I. Diseases that cause no focal or lateralizing neurologicsigns, usually with normal brainstem functions. CT scan

and cellular content of the CSF are normal.

E. Postseizure states.

F. Hypertensive encephalopathy and eclampsia.

G. Hyperthermia or hypothermia.

H. Concussion.

I. Idiopathic recurring stupor and coma.

J. Acute hydrocephalus.



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II. Diseases that cause meningeal irritation with orwithout fever, with an excess of WBCs or RBCs in the CSF,

usually without focal or lateralizing cerebral or brainstemsigns. Computed tomography or MRI, which preferably

should precede lumbar puncture, may be normal orabnormal.

A. Subarachnoid hemorrhage from ruptured aneurysm,arteriovenous malformation, occasionally trauma.

B. Acute bacterial meningitis.

C. Some forms of viral encephalitis.



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III. Diseases that cause focal brainstem or lateralizingcerebral signs, with or without changes in the CSF.

Computed tomography and MRI are usually abnormal.

A. Hemispheral hemorrhage or infarction.B. Brainstem infarction due to thrombosis or embolism.

C. Brain abscess, subdural empyema.D. Epidural and subdural hemorrhage and brain

contusion.E. Brain tumor.

F. Miscellaneous:cortical vein thrombosis, some forms of viral

encephalitis, focal embolic encephalomalacia due to bacterialendocarditis, acute hemorrhagic leukoencephalitis, disseminated(postinfectious) encephalomyelitis, and others.


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The Persistent Vegetative State

Patients who survived for indefinite periods without regainingany meaningful mental function. For the first week or two after

the cerebral injury, these patients are in a state of deep coma.Then they begin to open their eyes, at first in response topainful stimuli and later spontaneously and for increasinglyprolonged periods. The patient may blink in response to threat

or to light and intermittently the eyes move from side to side,seemingly following objects or fixating momentarily on thephysician or a family member and giving the erroneousimpression of recognition. However, the patient remainsinattentive, does not speak, and shows no signs of awarenessof the environment or inner need; responsiveness is limited toprimitive postural and reflex movements of the limbs. In brief,there is arousal or wakefulness, and alternating arousal-nonarousal cycles are established, but the patient regains

neither awareness nor purposeful behavior of any kind.


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Locked-in Syndrome,and Akinetic MutismA patient is fully conscious and

able to see but unable to feel, ormove because of brainstemdamage. Locked-in patients canoften move their eyes to stimuli

and move their eyesvoluntarily if onlyupwards.


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Brain Death

A state of coma in which the brain was irreversibly damagedand had ceased to function but in which pulmonary and

cardiac function could still be maintained by artificial means.

The central considerations in the diagnosis of brain deathare:

1. absence of cerebral functions (unreceptivity andunresponsivity);2. absence of brainstem functions, including spontaneous

respiration; and3. irreversibility of the state. To these is usually added evidence

of catastrophic brain disease (trauma, cardiac arrest,cerebral hemorrhage, etc.).


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Care of the Comatose Patient

1. The management of shock, if it is present, takes precedence

over all other diagnostic and therapeutic measures.

2. Shallow and irregular respirations, stertorous breathing(indicating obstruction to inspiration), and cyanosis require theestablishment of a clear airway and delivery of oxygen. The

patient should initially be placed in a lateral position so thatsecretions and vomitus do not enter the tracheobronchial tree.Secretions should be removed by suctioning as soon as theyaccumulate; otherwise they will lead to atelectasis and

bronchopneumonia. Arterial blood gases should be measuredand further observed by monitoring of oxygen saturation. Apatient's inability to protect against aspiration and the presenceof either hypoxia or hypoventilation dictates the use ofendotracheal intubation and a positive-pressure respirator.


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1. The management of shock, if it is present, takes precedence

over all other diagnostic and therapeutic measures.

2. Shallow and irregular respirations, stertorous breathing(indicating obstruction to inspiration), and cyanosis require theestablishment of a clear airway and delivery of oxygen. The

patient should initially be placed in a lateral position so thatsecretions and vomitus do not enter the tracheobronchial tree.Secretions should be removed by suctioning as soon as theyaccumulate; otherwise they will lead to atelectasis and

bronchopneumonia. Arterial blood gases should be measuredand further observed by monitoring of oxygen saturation. Apatient's inability to protect against aspiration and the presenceof either hypoxia or hypoventilation dictates the use ofendotracheal intubation and a positive-pressure respirator.


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3. Concomitantly, an intravenous line is established and blood

samples are drawn for determination of glucose, drugs, andelectrolytes and for tests of liver and kidney function. Naloxone, 0.5mg, should be given intravenously if a narcotic overdose is apossibility. Hypoglycemia that has produced stupor or coma demandsthe infusion of 25 to 50 mL of 50% glucose, followed by a 5%

infusion; this must be supplemented with thiamine.

4. With the development of elevated intracranial pressure, mannitol,25 to 50 g in a 20% solution, should be given intravenously over 10 to20 min and hyperventilation instituted if deterioration from a mass

lesion occurs, as judged by pupillary enlargement or deepeningcoma. Repeated CT scanning allows the physician to follow the sizeof the lesion and degree of localized edema and to detect herniationsof cerebral tissue. With massive cerebral lesions, it may beappropriate to place a pressure-measuring device in the cranium.

C f h C P i


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5. A lumbar puncture should be performed if meningitis or

subarachnoid hemorrhage is suspected, keeping in mind therisks of this procedure and the means of dealing with them. ACT scan may have disclosed a subarachnoid hemorrhage, inwhich case no lumbar puncture is necessary.

6. Convulsions should be controlled by special measure.

7. As indicated above, gastric aspiration and lavage withnormal saline may be useful in some instances of coma due

to drug ingestion. Salicylates, opiates, and anticholinergicdrugs (tricyclic antidepressants, phenothiazines,scopolamine), all of which induce gastric atony, may berecovered many hours after ingestion. Caustic materials

should not be lavaged because of the danger of perforation.

C f h C P i


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8. The temperature-regulating mechanisms may be

disturbed, and extreme hypothermia, hyperthermia, orpoikilothermia may occur. In severe hyperthermia,evaporative-cooling measures are indicated in additionto antipyretics.

9. The bladder should not be permitted to becomedistended; if the patient does not void, decompressionshould be carried out with an indwelling catheter.Needless to say, the patient should not be permitted to

lie in a wet or soiled bed.

C f h C P i


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10. Diseases of the CNS may disrupt the control of

water, glucose, and sodium. The unconscious patientcan no longer adjust the intake of food and fluids byhunger and thirst. Both salt-losing and salt-retainingsyndromes have been described with brain disease.

Water intoxication and severe hyponatremia may ofthemselves prove damaging. If coma is prolonged, theinsertion of a gastric tube will ease the problems offeeding the patient and maintaining fluid and electrolytebalance. Otherwise, approximately 35 mL/kg of isotonic

fluid should be administered per 24 h (5% dextrose in0.45% saline with potassium supplementation unlessthere is brain edema, in which case isotonic normalsaline is preferable).

C f th C t P ti t


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11. Aspiration pneumonia is avoided by prevention of

vomiting (gastric tube and endotracheal intubation),proper positioning of the patient, and restriction of oralfluids. Should aspiration pneumonia occur, it requirestreatment with appropriate antibiotics, and aggressive

pulmonary physical therapy.

12. Leg vein thrombosis - a common occurrence incomatose and hemiplegic patients - often does notmanifest itself by obvious clinical signs. An attempt may

be made to prevent it by the subcutaneousadministration of heparin, 5000 units q 12 h, and by theuse of intermittent pneumatic compression boots.

C f th C t P ti t


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13. If the patient is capable of moving, suitablerestraints should be used to prevent falling out of bed

and self-injury from convulsions.

14. Regular conjunctival lubrication and oral cleansingshould be instituted.

Prognosis of Coma

As a general rule, recovery from metabolic and toxic causes of comais far better than from anoxic coma, with head injury occupying anintermediate prognostic position. If there are no pupillary, corneal, or

oculovestibular responses within several hours of the onset of coma,the chances of regaining independent function are practically nil (seeLevy et al). Other unfavorable prognostic signs are absence ofcorneal reflexes and eye-opening responses and atonia of the limbsat 1 and 3 days after the onset of coma and absence of the cortical

component of the somatosensory evoked responses on both sides.

REFERENCES


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REFERENCES

PLUM F, POSNER JB: Diagnosis of Stupor and Coma,3rd ed. Philadelphia, Davis, 1980.

ADAMS R, VICTOR M: Principles of Neurology, NewYork McGraw-Hill, 1985.

CARONNA JJ, SIMON RP: The comatose patient: Adiagnostic approach and treatment. Int Anesthesiol Clin17(2/3):3, 1979.

WEINER HL, LEVITT LP: Neurology. Fifth edition.

Williams & Wilkins, 1998.

MAIESE K: Metabolic Coma. Neurobase. Third 1999Edition.


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