Approach to Unconsious Pt

8/4/2019 Approach to Unconsious Pt

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BY:DR.AMMARAH YASMEEN

HOUSE OFFICERMEDICAL UNIT IV CHK


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Define basic terms.

Explain neuroanatomy precisely.

Review causes of unconsciousness. Clinical approach to follow in E.R.

Review key aspects of history, physicalexamination and lab evaluation.

Definitive management.


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It has been defined, at one time or another,as: subjective experience; awareness; theability to experience feelings; wakefulness;having a sense ofselfhood; or as the

executive control system of the mind. Two components of conscious behavior

content- the sum of cognitive and affective function arousal- appearance of wakefulness

The three most widely accepted states ofconsciousness are sleeping, dreaming andwaking.


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DROWSINESS:A decreased level of consciousness characterized bysleepiness and difficulty in remaining alert but easyarousal by stimuli. It may be caused by a lack of sleep,

medications, substance abuse, or a cerebral disorder.

OBTUNDATION:A greatly reduced level of consciousness. The patient isnot yet comatose but is close, arousing only with very

strong stimulus.STUPOR:A state of impaired consciousness characterized by amarked diminution in the capacity to react to

environmental stimuli.COMA:Is a state of extreme unresponsiveness, in which anindividual exhibits no voluntary movement or behavior.


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Unconsciousness implies a mental state thatinvolves complete or near-complete lack ofresponsiveness to people and otherenvironmental stimuli. Being in a comatose

state or coma is a type of unconsciousness.


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Wakefulness depends on the integrity ofboth cerebral hemispheres and theascending reticular activating formation ofthe brain stem.

It receives input from numerous somaticafferents.

It projects to midline thalamic nuclei (which

are in a circuit with cortical structures) andthe limbic system.


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ARAS acts as a gating system, increasing or

decreasing thalamic inhibitory influence onthe cortex alters effect of sensory stimuli ascending

alters descending cortical stimulation

Function of ARAS-Thalamic-Cortical systemdepends on: anatomic integrity of structures

metabolic integrity (circulatory integrity)

communicative integrity (neurotransmitterfunction)


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Coma (unconsciousness) impliesdysfunction of: ARAS or

Both hemi-cortices

Anatomically, this means Central brainstem structures (bilaterally) from

caudal medulla to rostral midbrain

Both hemispheres


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Braintumor

epilepsy

infectionsCardiovascular

disease

trauma

metabolicdisturbances

Thiaminedeficiency

Causes ofunconciousness


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NEUROLOGICAL Trauma

Infections meningitis, encephalitis,malaria, typhoid, rabies, trypanosomiasis.

Tumours cerebral / meningeal tumors Vascular subdural / subarachnoid hgr,

stroke, hypertensive encephalopathy

Epilepsy nonconvulsive status / postictal

state


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METABOLIC Drugs, poisoning e.g CO ,alcohol etc. Hypoglcemia, hyperglycemia (keto acidoti

or HONK) Hypoxia, carbondiaoxide narcosis (COPD) Septicemia Hypothermia Myxedema ,addisonian crisis

Hepatic / uremic encephalopathy Thiamine deficinecy


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CARDIOVASCULAR Cardiac arrest

OTHERS Stroke(hypovolemic), syncope, Psychogenic

(hysteric)


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ABC

Immediate management

History

Examination

Investigations


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ABC

A Open the

airway

B breathing C circulation

Examining the Airway forobstruction and CervicalSpine Control in theevent of any possible

trauma for e.g fracture.Maintainairway.oropharyngealendotracheal.

Breathingshallow.?........Aspiration?Look, Listen and

Feel for adequaterespiratory effort.Supplement with O2to correct hypoxia ifsaturations arebelow 95%.

If trauma check forbleeding thenchecking thecirculation. If a carotid

pulse is not palpablethen resuscitationshould be commenced.


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Maintain i.v line and support the ciculationif required with I.V fluids.

oxygen inhalation

Protect the cervical spine unless trauma isknown not to be the cause.

Check blood glucose; give 50mL 50%dextrose IV stat if hypoglycemia is possible.


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I.V thiamine if history of alcohlism.

Control and treat seizures if present.

I.V naloxone (0.4mg-2mg IV) for opiateintoxication; I.V flumazenil forbenzodiazepine intoxication.


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HISTORY Onset of symptoms (abrupt or gradual) How found suicide note, seizures. Fever Headache Vomiting.types.. Trauma Recent altered behaviour..?

H/o diabetes? Hypertension? controlled? Poison..? Prior suicidal attempts?


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Drugs?o Insulin, OHAo

Antipsychoticso Sedativeso Steroidso Anti coagulantso Diuretics

Acute or Chronic alcohol intake Seizure disorder Prior episode of coma Elderly nothing predictable

Past medical history- chronic liver ,kidney,lung, heart disease, diabetes or psychiatricillness.


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EXAMINATION


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APPEARANCE ODORo Alcoholo Fruity .DKAo Uriniferous .Uremiao

Musty fetor of Hepatic comao Burnt almond odor of Cyanideo Organophosphate


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COLOURo Pallor

Severe internal hemorrhage,Hypothyroidism , Hypopituitarism, CKD

o Cyanosis of lips and nailso Cherry red.COo Facial plethora . alcoholismo

Maculo hemorrhagic rashMeningococcemia , Typhus,RMSF, Staph endocarditis


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DIFFUSE PETECHIAE-TTP, DIC, Fat embolism

ECHYMOTIC PATCHES-Drug induced

-CLD

-DIC-Trauma


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LARGE BLISTERS-If the patient has been motionless for a time

-Acute barbiturate, alcohol, or opiate intoxication

FACIAL PUFFINESS-CKD

-Myxedema, Hypopituitarism

NAIL-Splinter hemorrhage

-White nail

-Half and half nail

-Clubbing


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FEVER-Pneumonia, sepsis, meningitis

Jaundice

Features of chronic liver disease

Central obesity, striae

Nasal bleed, CSF leak

Aural bleed


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VITALS1.PULSE

Tachycardia Hypovolemia/haemorrhage Hyperthermia Intoxication Bradycardia Raised intracranial pressure Heart blocks


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2. TEMPERATUREIncreased

Sepsis Meningitis ,encephalitis Malaria ,Pontine haemorrhage Drugs with anticholinergic activity Heat stroke

Decreased Hypoglycemia Hypothermia (less than 31 C) Myxedema Alcohol, barbiturate ,sedative or phenothiazine

intoxication.


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3.BLOOD PRESSUREIncreased

Hypertensive encephalopathy Cerebral haemorrhage Raised intracranial pressure

Decreased Hypovolemia Myocardial infarction Intoxication/poisoning Profound hypothyroidism, Addisonian crisis


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4. RESPIRATORY RATEIncreased (tachypnae)

Pneumonia Acidosis (DKA, renal failure)

Pulmonary embolism Respiratory failure

Decreased Intoxication/poisoning


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The neurological examination focuses onthe following components.

Glasgow coma scale

Breathing patterns.

Pupillary responses.

Eye movements.

Motor responses.


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GCS SCORE: 3 severe injury


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An abbreviated coma scale is used in theassessment of critically ill patient (primaryservey)

AVPUA alert

V respond to voice stimulus

P respond to pain

U - unresponsive


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Normal pupillary size, shape, and light

reflexes indicate integrity of midbrainstructures and a cause of coma other than amass lesion


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Medium to dilated symmetrical pupils fixed tolightStructural disease of the brain stem.

Small symmetrical pupils reactive to lightMetabolic diseases and drug overdose.

Unequal pupil fixed to lightUnilaterally enlarged pupil (>5.5 mm diameter)

happens in ipsilateral 3rd nerve compressionIntracranial mass lesion producing 3rd nervepalsy e.g in unilateral uncal herniation.


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Morphine extremely pin point

Barbiturate pin point

Organophosphate

Atropine Dilated nonreacting

Tricyclics even to

physostigmine


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1.VESTIBULO-OCULAR REFLEX (Caloricresponse) With 10 mL of cold water douching one ear

produces ipsi-lateral deviation of both eyes with a

contralateral quick phase nystagmus lasting for 12 minutes. Use of hot water produces the oppositeeffect i.e. contralateral deviation with ipsilateralquick phase nystagmus.

In comatose patients, the fast corrective phase ofnystagmus is lost and the eyes are tonicallydeflected to the side irrigated with cold water oraway from the side irrigated with warm water; thisposition may be held for 2 to 3 min.


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With brainstem lesions, these vestibulo-ocularreflexes are lost or disrupted.


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Elicitation of these reflexes in a comatose

patient provides two pieces of information:

o Evidence of unimpeded function of theoculomotor nerves and of the midbrain and

pontine tegmental structures that integrateocular movements

o Loss of the cortical inhibition that normally

holds these movements in check


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Sedative or anticonvulsant intoxicationserious enough to cause coma mayobliterate the brainstem mechanisms foroculocephalic reactions

Asymmetry in elicited eye movementsremains a dependable sign of focalbrainstem disease


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Progressive deterioration in response to

corneal touch are among the mostdependable signs of deepening coma.

A marked asymmetry in corneal responsesindicates either an acute lesion of theopposite hemisphere or, less often, an

ipsilateral lesion in the brainstem.


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Restless movements of both arms and both legsand grasping and picking movements -- intactcorticospinal tracts

The occurrence of focal motor epilepsy usuallyindicates that the corresponding corticospinal

pathway is intact Massive destruction of a cerebral hemisphere --

focal seizures are seldom seen on the paralyzedside

Definite choreic, athetotic, or hemiballistic

movements indicate a disorder of the basalganglionic and subthalamic structures, just asthey do in the alert patient


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Non-rhythmic jerking in single or multiple muscle

groups suggests metabolic encephalopathies(hepatic chiefly).


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(A ) HYPERVENTILATION- midbrain and upper pons lesion-metabolic diseases e.g. hepatic coma,

diabetes and generalised raised intracranial

pressure in its early stages.

( B ) HYPOVENTILATION- medullary, upper cervical spinal lesion

-Drug overdose and later stages ofcerebral herniation.


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(C) CHEYNE-STOKES-Massive supratentorial lesion

-Bilateral deep-seated cerebral lesions

-Metabolic disturbances

Presence of CSR signifies bilateral dysfunction ofcerebral structures, usually those deep in thehemispheres or diencephalon, and is seen with

states of drowsiness or stupor.

( D ) ATAXIC RESPIRATION (completelyirregular breathing)

-Brain-stem dysfunction of a diffuse nature


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Headache before the onset of coma Recurrent vomiting

Severe hypertension beyond the patient's

static level Subhyaloid retinal hemorrhages Papilledema develops within 12 to 24 h in

cases of brain trauma and hemorrhage, but if

it is pronounced, it usually signifies braintumor or abscessi.e., a lesion of longerduration


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Indicate the presence of;

Meningitis

Subarachnoid hemorrhage (after 12-24 hrs insome)


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Raised intracranial pressure

Hypertensive changes

Subarachnoid haemorrhage

Diabetic retinopathy


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Full blood counts: Infections.

Biochemistry: Electrolytes, sugar, LFTs,KFTs.

Arterial blood gases: Oxygen, CO2, pH,HCO3.

Blood cultures.

Alcohol levels. Drug screen (urine and blood)


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Lumbar puncture: Infections.

CT Scans in case of trauma, bleeds,hemorrhage.

MRIs where possible.

Thyroid function tests (rarely) Electroencephalogram (EEG) & ECG.

CXR.

Blood films for Malaria.


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Further management depends on the cause always.

Diabetes, hepatic coma, electrolyte imbalances,endocrine causes etc: Correction of metabolicderangements.

Trauma: Neurosurgery. Strokes, heart attacks, respiratory failure, hypoxia,

hypothermia: Correct underlying causes. Medication/drug overdose: Specific antidotes. Meningitis and infections: Antibiotics.

Raised ICP: Mannitol and Dexamethasone.


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Pressure area care Care of the mouth, eyes and skin Physiotherapy to protect muscles and joints

DVT prophylaxis

Risks of stress ulceration of the stomach Nutrition and fluid balance Urinary catheterization

Monitoring of the CVS

Infection control Maintenance of adequate oxygenation


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SUMMARYABC of life support

Oxygen and I.V access

Stabilize cervical spine


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Blood glucose

Control seizures

Consider I.V glucose, thiamine, naloxone,flumazenil


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Brief examination and obtain history

Investigate

Reassess the situation and plan further


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THANK YOU

Approach to Unconsious Pt

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