Approach to comatose patient , patient with low GCS

Approach to comatose patient

1. Approach to a patient with coma Moderator - Dr Vaishak Presenter - Dr Keerti

2. INTRODUCTION Coma is among the most common neurologic emergencies encountered in general medicine and requires an organized approach There exists a continuum of states of reduced alertness, the most severe form being coma, defined as a deep sleeplike state with eyes closed, from which the patient cannot be aroused.

3. Consciousness - state of awareness of self and surroundings Drowsiness simulates light sleep and is characterized by easy arousal that may persist for brief periods. Obtunded: answers /responds to painful stimulus Stupor refers to a lower threshold for arousability, in which the patient can be transiently awakened by vigorous stimuli, accompanied by motor behavior that leads to avoidance or withdrawal from noxious stimuli.

4. THE ANATOMY AND PHYSIOLOGY OF COMA Almost all instances of coma can be traced to either. (1) Widespread abnormalities of the cerebral hemispheres or (2) Reduced activity of the thalamocortical alerting system, the reticular activating system (RAS) The proper functioning of this system, its ascending projections to the cortex, and the cortex itself are required to maintain alertness and coherence of thought. * Unilateral cerebral lesion do not cause unconsciousness *

5. CAUSES OF COMA

6. APPROACH Rapid Initial Examination and Emergency Therapy An initial examination should include a check of general appearance, blood pressure, pulse, temperature, respiratory rate and breath sounds, best response to stimulation, pupil size and responsiveness, and posturing or adventitious movements. The neck should be stabilized in all instances of trauma until cervical spine fracture or subluxation can be ruled out. The airway should be protected in all comatose patients and an intravenous line placed Hypotension, marked hypertension, bradycardia, arrhythmias causing depression of blood pressure, marked hyperthermia, and signs of cerebral herniation mandate immediate therapeutic intervention. supplemental oxygen, intra- venous thiamine (at least 100 mg), and intravenous 50% dextrose in water (25 g).when acute bacterial meningitis is strongly suspected, antibiotics and adjunctive corticosteroids should be administered within 1 hour of hospital admission.

7. History: 1)Assess level of unconsciousness the circumstances and rapidity with which neurologic symptoms developed( infectious vs vascular) (2) Antecedent symptoms (confusion, weakness, headache, fever, seizures, dizziness, double vision, or vomiting) (3) The use of medications, drugs, or alcohol; and (4) Chronic liver, kidney, lung, heart, or other medical disease. (5) The circumstances in which the patient was found

8. GENERAL PHYSICAL EXAMINATION Signs of head trauma: the possibility of coexisting spinal cord injury,raccoon eyes,Battle sign Cutaneous petechiae : thrombotic thrombocytopenic purpura, meningococcemia, or a bleeding diathesis associated with an intracerebral hemorrhage. Cyanosis and reddish or anemic skin coloration :underlying systemic disease or carbon monoxide as responsible for the coma. Fever : systemic infection , bacterial meningitis, encephalitis, heat stroke, neuroleptic malignant syndrome, malignant hyperthermia Hypothermia itself causes coma when the temperature is <31°C (87.8°F) RR : Tachypnea may indicate systemic acidosis ,hypoxia, hypercapnia, acidosis, hyperthermia, hepatic disease, toxins or drugs Hypopnia - brainstem lesion

9. BP hypertension hypertensive encephalopathy, cerebral hemorrhage, large cerebral infarction, or head injury. Cushing reflex - hypertension with bradycardia and respiratory irregularity due to increased ICP(posterior fossa lesion , in children) Hypotension alcohol or barbiturate intoxication, internal hemorrhage or myocardial infarction , sepsis, profound hypothyroidism, or Addisonian crisis. Skin Injuries :bruises,traumatic cause Dry skin : Dka , Atropine Moist skin: Hypoglycemic coma Cherry red : CO poisoning Needle marks : drug addiction Rashes : meningitis, endocarditis

10. Head and neck Evidence of injury Skull should be palpated for depressed fractures. The ears and nose: haemorrhage and leakage of CSF Odour of breath Acetone : DKA Fetor hepaticus : hepatic coma Alcoholic odour : in alcoholic intoxication

11. NEUROLOGIC EXAMINATION State of Consciousnes s The examiner should start with verbal stimuli, softly and then more loudly calling the patient’s name or giving simple instructions to open the eyes. If there is no significant response, more threatening stimuli, such as taking the patient’s hand and advancing it toward the patient’s face, are applied. Finally, painful stimuli may be needed to arouse the patient. All patients in apparent coma should be asked to open or close the eyes and to look up and down; these voluntary movements are preserved in the locked-in syndrome but cannot be elicited in coma—an important distinction.

12. GCS- P

13. Full Outline of UnResponsiveness (FOUR) score An alternative scale referred to as the Full Outline of UnResponsiveness (FOUR) score has been proposed and is based on eye response, motor response, brainstem reflexes (pupillary reaction, corneal reflex, and cough reflex), and respirations.

14. BRAINSTEM REFLEXES The brainstem reflexes that are examined are 1. Pupillary reflex 2. Ocular movements 3. Ocular reflex 4. Respiratory pattern • As a rule, coma due to bilateral hemispheral disease preserves these brainstem activities

15. Pupillary Signs Size Shape Reactive and round pupils of midsize (2.5–5 mm) exclude upper midbrain damage One enlarged (>6 mm) and poorly reactive pupil signifies compression of the third nerve from the effects of a cerebral mass above bilaterally dilated and unreactive pupils: severe midbrain damage, usually from compression by a supratentorial mass Reactive and bilaterally small (1–2.5 mm) but not pinpoint : metabolic encephalopathies Even smaller reactive pupils (<1 mm) characterize opioid : pontine hemorrhage .

16. Ocular movements The position of eyes at rest Presence of spontaneous eye movements (Roving eye movements are slow, conjugate, lateral to-and-fro movements, nystagmus ) The eyes look towards a hemispheric lesion and away from a brain stem lesion

17. oculocephalic reflex The oculocephalic reflexes, elicited by moving the head from side to side or vertically and observing eye movements in the direction opposite to the head movement In the normal oculocephalic reflex (normal or positive doll’s eye phenomenon), the eyes move conjugately in a direction opposite to the direction of movement of the head. Indicates an intact pons mediating a normal vestibulo-ocular reflex These reflexes are normally suppressed in the awake patient

18. The oculovestibular reflex • These are tested by the installation of ice-cold water into the external auditory meatus, having confirmed that there is no tympanic rupture. • A normal response in a conscious patient is the development of nystagmus with the quick phase away from the stimulated side This requires intact cerebropontine connections

19. Respiration Normal respiration depends on (1) a brainstem mechanism, located between the midpons and cervical medullary junction, (2) forebrain Cheyne-Stokes respiration: (hyperpnoea alternates with apneas) is commonly found in comatose patients, often with cerebral disease, but is relatively non-specific( forebrain) Rapid, regular respiration is also common in comatose patients and is often found with pneumonia or acidosis Central neurogenic hyperventilation - rapid breathing, from 40 to 70 breaths/min, usually due to central tegmental pontine lesions Kussmaul breathing is a deep, regular respiration observed with metabolic acidosis. Apneustic breathing is a prolonged inspiratory gasp with a pause at full inspiration. It is caused by lesions of the dorso- lateral lower half of the pons

20. Cluster breathing- which results from high medullary damage, involves periodic respirations that are irregular in frequency and amplitude, with variable pauses between clusters of breaths. Ataxic breathing is irregular in rate and rhythm and usually is due to medullary lesions.

21. Motor System Purposeful and non purposeful movements are noted and the two sides of the body compared. Head and eye deviation to one side, with contralateral hemiparesis, suggests a supratentorial lesion, whereas ipsilateral paralysis indicates a probable brainstem lesion.

22. Posturing

23. Tonic-clonic or other stereotyped movements signal seizure as the probable cause of decreased alertness. Myoclonic jerking, consisting of non rhythmic jerking movements in single or multiple muscle groups, is seen with anoxic encephalopathy ,hepatic encephalopathy . Tetany occurs with hypocalcemia. Cerebellar fits result from intermittent tonsillar herniation and are characterized by deterioration of level of arousal, opisthotonos, respiratory rate slowing and irregularity, and pupillary dilatation.

24. Meningeal irritation signs 1. Neck rigidity 2. Kernig's sign 3. Brudzinski's sign

25. vegetative state signifies an awake-appearing but unresponsive state opens eyes, rolls eyes, grunts,groans. Respiratory and autonomic functions are retained. Yawning, coughing, swallowing, and limb and head movements persist. Extensive cortical gray or subcortical white matter with relative preservation of brainstem Akinetic mutism refers to a partially or fully awake state in which the patient remains virtually immobile and mute but can form impressions and think medial thalamic nuclei or the frontal lobes CONDITIONS THAT MAY MIMIC COME

26. abulia milder form of akinetic mutism characterized by mental and physical slowness and diminished ability to initiate activity. Catatonic patients make few voluntary or responsive movements, although they blink, swallow, and may not appear distressed.

27. locked-in type of pseudocoma ,patient is awake but paralyzed .Can’t speak, can’t move limbs, can’t grunt or groan but retains voluntary vertical eye movements and lid elevation, thus allowing the patient to communicate *alert brain locked in immobile body* 1 vertical pons lesion 2 GBS, periodic paralysis

28. Brain death Absence of cerebral function. ~no response to deep painful stimulus Absence of brain stem function ~ loss of eye movements spontaneous/ oculocephalic, oculovestibular reflex, gag reflex, cough reflex, dilated fixed pupil ~ absence of respiratory movements Irreversibility of the state

29. Laboratories • Obtain ABG, serum electrolytes, glucose, creatinine, complete blood count, liver functions and urinalysis,Platelet count Prothrombin time , aPTT • Drug levels • Toxicology screen of blood and urine if suspected Imaging • A head CT should be obtained to evaluate for structural abnormalities • Brain MRI can be useful if head CT is nondiagnostic and there is suspicion for an ischemic or parenchymal lesion (especially of the posterior fossa)

30. Cerebrospinal fluid (CSF) examination • Lumbar puncture (LP) considered in patients with fever and/or new headache • A fundus examination and/or head imaging prior to LP to assess risk of herniation • Basic cerebrospinal fluid (CSF) studies (e.g. protein, glucose, cell count, Gram stain, and aerobic culture) obtained with additional studies depending on the possible etiology

31. Treat the cause Supportive care – antipyretics, anticonvulsants Management of -ICP Mannitol – 0.25 – 1 gm/kg of 20% solution (1.25 – 5 ml/kg) bolus iv. Frusemide, glycerine Steroids –vasogenic edema Hyperventilation -lowers CBV- inc CPP Maintain PCO2 between 25 – 30 mm Hg Nursing care:Position Nutrition Care of eyes Care of skin Chest physiotherapy Care of bowel & bladder Physiotherapy

32. Thank you