СOMА is a condition of complete unconsciousness from which a patient cannot be roused even by the most painful stimuli. Less degree of coma is called stupor.
Head injury, cerbrovascular accidents, meningitis, encephalitis, tumour, abscess, epilepsy, hypertensive encephalopathy, systemic infection and infestation, e.g. cerebral malaria, typhoid , typhus etc.
Stokes-Adams syndrome, coronary thrombosis.
Pulmonary embolism, carbon-dioxide narcosis or pulmonary encephalopathy.
Matabolic and Endocrinal
Diabetic coma, hypoglycaemic coma, hepatic coma, renal failure, hypothermic coma, heat hyperpyrexia, ecclampsia, hypopituitary coma, hypothyroid coma, electrolyte imbalance etc.
Alcohol, opium, barbiturates etc.
CLINICAL GRANDING OF COMA
(ii) To speech.
(iii) To pain.
Best verbal response
(iii) Inappropriate words
(iv) Incomprehensive sounds.
Best motor response
(i) Obey commands.
(ii) Localises pain.
(iii) Flexion to pain.
(iv) Extension to pain.
CLINICAL FEATURES OF COMA
History from Relations
(i) Hypertension, nephritis, diabetes, liver discase, chronic respiratory illness.
(ii) Injury or poisoning, drugs.
(iii) Similar attacks in the past.
(iv) Mode of onset: Sudden or gradual with or without fever.
(v) History of occupation.
General examination OF COMA
(i) Any injury. One should look for the discolouration of the skin behind the ear which is often associated with skull fractures particularly of posterior cranial fossa which is called Battle’s sign.
(ii) Any bleeding from nose, ear, mouth.
(iii) Jaundice, Cyanosis.
(iv) Any smell of acetone, alcohol, opium, paraldehyde, or fetor hepaticus in the breath.
(v) Pulse, respiration, temperature, BP.
(vi) Response to painful stimuli: Purposive limb withdrawal indicates integrity of the sensory pathway. In pyramidal lesion unilateral absence of response is seen in spite of stimuli given on both sides. In presence of bilateral pyramidal lesion or brainstem lesion bilateral absence of motor response is seen in internal capsular lesion or lesion of rostral cerebral peduncle decorticate posture is seen. In lesions of midbrain or rostral pons decerebrate poture is seen while in extensive lesion of brain stem extending down to pons decerebrate posture in upper limbs with flaccidity or slight flexor response in lower limbs will be present.
(i) Pupil-unequal or not, size, shape, reflexes. In presence of hypothalamic involvement there will be Horner’s syndrome; small reactive pupils will be seen in bilateral diencephalic or pontine lesion. With lesion of 3rd cranial nerve with uncal herination there will be absence of light reflex or consensual light reflex. In many metabolic encephalopathies pupils are smaller than normal but reaction to light is preserved. Fixed and dilated pupils seen with Atropin, or Scopolamine poisoning but in Morphin or Opium poisoning they are pin-pointed. After CPR if the pupils are dilated and fixed it bears a poor prognosis
(ii) Eye movement, conjugate deviation of head and eyes (oppositive to site of lesion). Doll’s head manoeuvre (brain stem lesion) is also helpful, conjugate ocular deviation indicates ipsilateral Hemisphere lesion or contralateral pontine lesion. Downward conjugate deviation indicates mesencephalic lesion. Nonconjugate ocular deviation indicates brain stem lesion. Eye movement to passive head turning or caloric stimulation are also important. Normal conscious subjects with open eyes do not exhibit controversive conjugate eye movement in response to brisk rotation of head side to side or flexion extension of head. With cortical lesion in stuporosed subjects brisk Doll’s head eye response is seen. In brain stem lesion oculocephalic Response is lost. In testing oculovestibular reflex by caloric stimulation in normal subjects jerky nystagmus develops which persists for 2-3 minutes with slow component to the tested ear. When the brain stem is intact but the patient is unconscious the fast component of nystagmus disappears and the eyes are tonically deviated to the tested ear for about 2-3 minutes and then come to their original position. When the brain stem is damaged the Response is bizarre and finally disappears. Oculocephalic and oculovestibular reflex responses are intact in metabolic coma.
(iii) Any facial palsy-Nasolabial fold, puffing of check in and out. If there is puffing out of one check with each expiration one should think of paralysis of that side.
(iv) Neck rigidity, general rigidity, decerebrate posture of flaccidity.
(vi) Plantar reflex.
(vii) Ophthalmoscopic examination.
(ii) Source of embolism, e.g. mitral stenosis, strial fibrillation or myocardial infarction.
(i) Rate and character of respiration: Cheyne-Stoke’s respiration is seen in both hemispheric, diencephalic or in metabolic disorders. Hyper-ventillation is seen in lesion of tegmentum of brain stem. Lesion of pons may give rise to apneustic breathing (prominent end respiratory pause) in Basilar artery lesion. In lesion of lower tegmentum of pons or medulla atactic breathing (most irregular breathing with shallow and deep breaths) is seen.
(ii) Presence of any source of embolism, e.g. lung abscess or bronchial carcinoma.
Enlargement of liver and spleen, ascitis.
(i) Blood for total, differential count and detection, of malaria parasite, widal reaction, blood culture specially in cases with fever.
(ii) Estimation of blood sugar, urea, serum bilirubin SGOT and SGPT, serum electrolytes, NH3 etc.
(iii VDRL test for syphilis.
(iv) Urine for albumin, sugar, acetone and casts.
(v) Complete examination of CSF including cytological, bacteriological, serological and colloidal gold test.
(vi) X-ray of the skull, EEG, brain scan and MRI are also helpful.
MANAGEMENT OF COMA
(i) The patient should be kept in a railed cot in a calm and quiet room preferably in ICU.
(ii) A Ryle’s tube can be passed, the stomach contents are aspirated and to be sent for chemical test
(iii) The bladder is to be catheterised and a sample of urine to be sent for sugar, acetone test and other test.
(iv) Change the posture from time to time and patient is to be kept preferably in lateral decubitus to prevent aspiration of gastric contents.
(v) Give oxygen inhalation if there is dyspnoea.
(vi) Tracheostomy may be done if there is airway obstruction.
(vii) Prophylactic antibiotics may be given.
(viii) Liquid paraffine drops on both eyes may be given.
(ix) Inside of the mouth is to be painted with 2% Mercurochrome.
(x) Body powder to be sprinkled over the skin surface.
(xi) If there is low BP, foot end of the bed should be raised and appropriate IV fluid drip to be started with pressure raising agents, e.g, Dopamine.
(xii) Ice sponging may be done if there is hyperpyrexia.
(xiii) Proper fluid, electrolyte, Acid Base balance and nutrition with intravenous glucose, saline solutions are to be made until the patients is able to take food and drinks by mouth. Then nutrition may be maintained by glucose, horlicks, fruit juice, fructose, etc. if there is contraindication. COMA
(xiv) Specific measures particularly in cases of poisoning should be taken.
(xv) The underlying cause is to be treated as far as practicable.
TYPES OF SPECIFIC PNEUMONIA Staphylococcal Pneumonia TYPES OF SPECIFIC PNEUMONIA It may be a primary respiratory infection or secondary to…
ACUTE LOBAR PNEUMONIA It is the commonest of all specific pneumonias. AETIOLOGY Predisposing causes Age: All ages but 50% of…
BRONCHIAL ASTHMA DEFINITION OF BRONCHIAL ASTHMA BRONCHIAL ASTHMA is a chronic reversible inflammatory destructive disease of the airways characterised by…
BRONCHIECTASIS DEFINITION BRONCHIECTASIS is a condition of permanent abnormal dilatation of the larger bronchi. AETIOLOGY AND PATHOGENESIS Acquire Obstruction Obstruction…
CHRONIC BRONCHITIS DEFINITION OF CHRONIC BRONCHITIS Chronic bronchitis may be defined as a disease characterised by cough and sputum for…
ACUTE TRACHEO BRONCHITIS DEFINITION ACUTE TRACHEO BRONCHITIS is Acute inflammation of Tracheo bronchial tree caused by various organisms (bacteria and…