HOW TO APPROACH AN UNCONSCIOUS PATIENT IN EMERGENCY Nikhilesh Jain Director and Chief Intensivist Dept. Of Critical Care Medicine CHL Hospitals, Indore

Today's goals

 To develop an understanding of a comatose patient assessment on a first contact basis    Understand the finer nuances of managing strokes Looking for differentials in a comatose patient Initial management of the above subsets

Neural basis

   State of awareness of self and surrounding and cannot be readily defined in terms of anything else The use of terms other than coma and stupor to indicate the degree of impairment of consciousness is beset with difficulties and more important is the use of coma scales (Glasgow Coma Scale and FOUR score) Coma is characterized by total absence of arousal and awareness lasting for at least one hour

Definitions of levels of arousal (conciousness)

     Alert (Conscious) Appearance of wakefulness, awareness of the self and environment Lethargy mild reduction in alertness Obtundation - moderate reduction in alertness. Increased response time to stimuli.

Stupor Deep sleep, patient can be aroused only by vigorous and repetitive stimulation. Returns to deep sleep when not continually stimulated .

Coma (Unconscious) behaviorally Sleep like appearance and unresponsive to all external stimuli (Un arousable unresponsiveness, eyes closed)

Disorders of consciousness

Clinical pearls General examination:

On arrival to ER immediate attention to: 1.

Airway 2.

3.

4.

Circulation establishing IV access Blood should be withdrawn: estimation of glucose # other biochemical parameters # drug screening

Subsequent Assessment

    Attention is directed towards Assessment of pt.

Severity of coma Diagnostic evaluation All possible info Relatives, paramedics and people who have witnessed the episode esp. regarding mode of onset Prior medical history- DM/Drug history/Epilepsy Examination- remote trauma, needle marks, log roll

Points of interest

   In case of TBI neck stabilization takes precedence GCS for initial management especially in TBI Brainstem and motor function

Clues in general examination

  Pulse Bradycardia – Brain tumours, myxoedema, opiates Tachycardia- Hyperthyroidism, Uremia BP High- Hypertensive encephalopathy Low- Addisonian crisis, Alcohol, Barbiturate  Temp Low- Hypopituitarism, hypothyroidism, CPZ, environmental exposure, elderly, cold water immersion High- Infection, Metabolic, vascular, environmental

Some more clues………

 Skin- Injuries, bruises, dry, moist, cherry red , needle marks and rash  Pupils- Size, equality and reaction to light Most metabolic encephalopathies give small pupil with preserved light reflex Structural lesions are more commonly associated with pupillary asymmetry and loss of light reflex

Mucosal examination

        Petechiae &ecchymosis Hypermelanosis Cherry red skin Gray blue cyanosis Telangiectasia Ecthyma gangrenosum Splinter hemorrhages' Pigmented macules TTP,ITP,DIC,meningococcemia, Addisons, chemotherapy, porphyria, melanoma CO poisoning Methemoglobinemia Chronic alcoholism, vascular malformations Pseudomonas sepsis Anemia, sepsis ,leukemia, endocarditis Tuberous sclerosis , neuro fibromatosis

Daily assessments Pupils

Binstem reflexes

4-pupil & corneal reflex present 3-open pupil wide & fixed 2-pupil/corneal reflexes absent 1-pupil & corneal reflex absent 0-absent pupil, corneal & cough reflexes

Respiration

4-not intubated, regular breathing pattern 3-not intubated, cheyne-stokes breathing pattern 2-not intubated, irregular breathing pattern 1-breathes above ventilator rate 0-breathes at ventilator rate Eye response 4-eyelid open or opened, tracking or blinking to command 3-eyelids open, not tracking 2-eyelids closed, open to loud voice, not tracking 1-eyelids closed, open to pain, not tracking.

0-eyelids remain closed with pain Motor response 4-thumbs up, fist, or peace sign to command 3-localizing to pain 2-flexion response to pain 1-extensor posturing 0-no response to pain or generalized

How to interpret Pupils

Herniation signs

What about breathing patterns?

Abnormal breathing patterns in coma

Cheynes - Stokes Central Neurogenic Midbrain Apneustic Pons Ataxic Medulla ARAS

What about motor system?

      Asymmetry of tone/movt Asymmetry of plantar responses Tendon reflexes are not so important Motor response to DPS (supraorbital/nail bed) Flexion of upper limb with extension of lower limb (decorticate response) Extension of upper and lower limb (decerebrate response)

Signs of lateralization

    Unequal pupils Deviation of eyes/turning of head to one side Facial /deep reflexes asymmetry Unilateral Hyper/hypotonia ,extensor plantars/focal or jacksonian fits

Epidemiology in a non neurological ICU

     Metabolic encephalopathy-28.6% Seizures-28.1% Hypoxic ischemic encephalopathy-23.5% Stroke-22.1% Sepsis is major cause of neurological complication-38.8%

A major break up

         Acute stroke- 1-4% Meningitis/encephalitis Post reversible leucoencephalopathy Associations of hypertensive crisis/ encephalopathy Seizures -0.8-4% Dys electrolytemias and pH disturbances Renal/hepatic dysfunction Hypoxic ischemic encephalopathy Sepsis (70% in a medical ICU)

Epidemiology in a surgical ICU

    Cholesterol embolization Fat embolus Multifocal ischemic stroke Transplants-organ related/procedure related/therapy related

Supratentorial v/s infratentorial

    Starts with focal cerebral dysfunction Rostral to caudal progression Signs usually localise a single area (Diencephalon / mid brain/brain stem Asymmetrical motor signs       Affect RAS in pontine region Involvement of brain stem nuclei/tract with focal findings Sudden onset of coma Brainstem signs precede/accompany onset of coma Cranial nerve palsies are usual Bizarre resp patterns at onset

Posturing

     Cerebral hemisphere  Decorticate posture Diencephalon supra tentorial  Diagonal posture Upper brain stem  Decerebrate posture Pontine  Abnormal ext arm  Weak flexion leg Medullary  Flaccidity

Common patterns

A word about EEG

  Fast activity is commonly seen with drug overdose whereas slow wave abnormalities are more commonly associated with metabolic and anoxic coma An iso electric EEG is more common with drug induced comas though otherwise it indicates severe cerebral damage

To summarise……….

          Primary ABC Blood for sugar, electrolytes, ABG and osmolality Sample storage for subsequent screens Distinguish between metabolic and structural cause of coma and plan imaging accordingly LP may be needed CXR,ECG and EEG (fast activity/slow wave abnormalities/anoxic coma) Treatment of cause Nursing care Maintain normal physiology Care of skin and prognostication

How do I identify stroke?

Cincinnati scale

LAPPS

What to do next?

        Support ABCs with SOS oxygen Do a pre hospital stroke assessment Establish time of onset Transport to a stroke unit with prior relevant info Neurologic screening assessment Activation of stroke team 12 lead ECG Emergent CT scan Brain

What if my CT is fine?

Rule out stroke mimics

Inclusions of fibrinolytic therapy

What if his BP is high?

Supportive things?

         Admission to a stroke unit Monitoring to maintain normothermia, euglycemia and euvolemia Treatment of acute seizures Induced hypothermia Treatment of UTI/Pneumonia Swallow assessments DVT prophylaxis Treatment of concomitant systemic diseases Decompressive craniotomy has a mortality benefit

Extending the time windows for thrombolysis? (3-4.5 hrs)

   Inclusions remain the same Exclusions include age>80 years, INR< 1.7,NHS scale>25 Even with thrombolysis NHS>20 are known to have poor outcomes

ICH

 Defined as bleeding within the cranial vault

What is my work up gonna be?

Traumatic ICH

    Spinal clearance from a neurosurgeon Racoon eyes/battle sign ENT consult for skull base fractures Neurosurgical inputs with mass effect, on going herniation/obstructive hydrocephalous

Specifics of ICH diagnosis

Initial management

What are my BP targets?

What drugs do I use?

   Wait during the initial 24 hrs Use short acting agents such as esmolol, hydralazine, enalaprilat, nicardipine or labetalol Caution with holding beta blockers and clonidine

Complications?

What about anticonvulsants?

Other Supportive measures

     Treating ICP with mannitol/HTS (periodic monitoring of sodium and osmolality) and MV sos Anticonvulsants Stress ulcer prophylaxis Nutrition Control of temperature, fever and shivering

What if my patient was on an anti thrombotic agent?

When do I think about neurosurgery?

Summing up     ICH is a neurologic emergency which may require neurosurgery Non contrast CT helps Definitive indications of surgery Optimizing medical and critical care interventions goes a long way in improving outcomes

Thank you