like hysteria, depressive state or schizophrenia. (ii) Usually occurs In presence of audence. (iii) Not True unconsciousness but severe state of stupor. (ivj Unusual attitudes. (v) Absence of physical signs. (vl) Fluttering of eyelids. resistance To opening and rolling upward of eyeballs. (vii) Normal pupillary reactions. Management of coma. 1. Removal or control of cause - e.g. - Gastric lavage and dureilcs In narcotic poisoning; removal of patient to uncontaminated atmosphere and Inhalation of oxygen and 5% carbon dioxide in carbon monoxide poisoning; Ice bath or covering the patient with ice water sheets and placing under a fan In heal stroke. 2. Ensure proper respiration - (i) Keep tongue forward.. (II) Oxygen Inhalation. (Hi) Respiratory stimulants like doxapram or nlkethamlde. When there is deep coma, secretions and vomit II inhaled into the lungs, will soon result in death. The patient must be nursed In the semi-prone or lateral position with frequent changes from one side to the other. 3. Ensure proper circulation - (a) Parenteral fluids - Glucose saline, plasma, or blood transfusion. (b) Vasopressor drugs like dopamine II low blood pressure or shock. 4. Care of bowels and bladder - (I) Indwelting catheter. (i!) Saline or soap enema. 5. Care of skin - (I) Frequent change ol position in bed.(ii) Alcohol or spirit rub and powdering of skin (iii) Care of mouth. 6 Control of secondary infection - with antibiotics especialfy in presence of lever or In apyrexial patients wilh trie object of preventing pneumonia 7 Specitto measures eg lor benzodiazepines or organophosphorus poisoning, meningitis, dabetic coma, etc 8 Neurcsurgeal intervention - if coma progression raises the possibility of hemiation. Pseudo coma states Locked-in-stale - A destructive venlral pontine process - (usually brain stem infarction), interrupts descendng corticospinal and corticobulbar tracts sparing only the fibres controlling blinking and vertical eye movements A patient who is 'locked in' is conscious but able to communicate only by means of blinks or vertical eye movements It is a de-efferented state of total paralysis below the level of III n Sirrilar states are occasionally seen in severe poly neuropathy and myasthenia gravis Akinetic mutism - Such patients appear awake but are mute and either fail to respond to stimuli or respond only after very long delays It Is usually caused by severe bifronlal lobe cisease. Patients with akinetic mutism have flaccid tone unlike patients In the vegetative stale. Psychogenic unresponsiveness Patient appears unresponsive but is physiologically awake. Neurological examination and FEG are normal. There may be active opposition to attempts at eye opening by the examiner.. Ice water caloric test will reveal slow and quick components ol the nystagmus. Persistent vegetative slate - In the vegetative state, palienl breathes spontaneously, and shows cycles of eye opening and closing, buT is unaware of the self and the environment. A vegetativa stale may be seen transiently in recovery from coma, but it may persist to death. It is usually seen In patients with diffuse bilateral cerebral hemtsphere disturbance Most conmonty alter head injury or after cardiac arrest. Brain Death Preconditions lor dagnosis -1. PalientB condition is due to irremediable brain damage of known etiology. 2. Patient should be deeply comatose, and the effects ol depressant cfrugs, primary hypothermia or potentially reversible metabolic and
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