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Approach to. Contents Clinical Evaluation History Examination Lab Evaluation Management.

Dec 29, 2015

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Alban Baker
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Page 1: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

Approach to

Page 2: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

Contents

Clinical Evaluation History

Examination

Lab Evaluation

Management

Page 3: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

Basics

Wakefulness depends on the integrity of both cerebral hemi- spheres and the ascending reticular activating formation of the brain stem.

Page 4: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

Cont..

The management of an unconscious patient is never an easy task in clinical practice

The duty of physician is Arrive at diagnosis Predict the eventual outcome

Page 5: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.
Page 6: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

History

Page 7: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

i) Onset of coma (abrupt, gradual)

ii) Recent complaints ( headache, depression, focal weakness,

vertigo )

iii) Recent injury

iv) Previous medical illness ( diabetes,uraemia, heart disease )

v) Access to drugs ( sedatives,psychotropic drugs )

Page 8: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

Examination

Page 9: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

General physical Examination

i) Vital signs

ii) Evidence of trauma

iii) Evidence of acute or chronic system illness

iv) Evidence of drug ingestion ( needle marks alcohol breath )

v) Nuchal rigidity (examine with care)

Page 10: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

Neurological Examination

Page 11: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

State of consciousness Obtundation; responds-to verbal

stimuli although slow and inappropriate. Stupor; the subject can be aroused

only by vigorous and repeated noxious stimuli.

Coma; unarousable and unresponsive.

Page 12: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

Respiratory pattern 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 of cerebral herniation.

( e ) Cheyne-Stoke respiration – usually diencephalic lesion central transtentorial herniation and obstructive hydrocephalus.

( d ) Ataxic respiration (completely irregular breathing) brain-stem dysfunction of a diffuse nature

Page 13: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

Pupillary size and reaction

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

Small symmetrical pupils reactive to light metabolic diseases and drug overdose.

Unequal pupil fixed to light intracranial mass lesion producing 3rd nerve palsy e.g

in unilateral uncal herniation.

Page 14: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

Eye movements

Vestibulo-ocular reflexes – douching of one ear with cold water produces ipsi-lateral deviation of both eyes with a contralateral quick phase nystagmus lasting for 1—2 minutes. Use of hot water produces the opposite effect i.e. contralateral deviation with ipsilateral quick phase nystagmus. Bilateral douching with cold water gives rise to downward deviation with upward nystagmus and with hot water the opposite response. Absence or abnormal response indicates brain-stem dysfunction.

Oculo-cephalic reflexes (Doll's eye movement ) - Normal response consist of deviation of both eyes to the opposite direction of head rotation. Again absence or abnormal response indicates brain-stem dysfunction.

Page 15: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

Motor Responses

This is elicited by applying peripheral noxious stimuli e.g. pinching of limbs rubbing the sternum to elicit pain.

( a ) Appropriate response – brushing away the source of stimulus.

{ b ) Inappropriate response - decerebrate or decorticate rigidity. Motor response is also of localising value. Paralysed limb will show no response and presence of hemiplegia can therefore be evident. Decerebrate rigidity indicates brain-stem damage and if bilateral is usually associated with a very poor prognosis. Complete flaccidity with no response to noxious stimuli is often indicative of severe central nervous system depression due to drug overdose.

Page 16: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

Laboratory Evaluation

Page 17: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

Supratentorial lesions

Skull radiograph Computerised tomographic scan

CTscan) Carotid angiography EEG ( electroencephalogram )

Page 18: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

Infratentorial lesions

Skull radiograph CT scan Vertebral angiography EEG Ventriculography

Page 19: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

Diffuse neuronal lesions Examination of CSF ( cerebro spinal fluid ) Serum glucose, calcium, Na, K, magnesium Blood gases and PH Liver and renal functions Drug levels

Page 20: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

Management

Page 21: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

Initial Management

Airway Breathing Circulation Deformity Exposure

Page 22: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

Definitive Management In general, management of the comatose patient

depends on the cause. However, while the patient is undergoing evaluation, it is essential to :

pressure area care care of the mouth, eyes and skin physiotherapy to protect muscles and joints risks of deep vein thrombosis risks of stress ulceration of the stomach nutrition and fluid balance urinary catheterization monitoring of the CVS infection control maintenance of adequate oxygenation, with the

assistance of artificial ventilation

Page 23: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

You are in emergency department when an unconscious patient land in emergency with B.P 90/50 pulse 92/min and attendants tell u that the patient suddenly fell unconscious, how will you approach ?

Page 24: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

APPROACH

ABC

Immediate management

Examination

History

Investigations

Page 25: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

ABC

ABC

A –Open theairway

B –breathing C –circulation

Page 26: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

Immediate management

Maintain i.v line, oxygen inhalation

Blood sample for RBS

Control seizures

Consider i.v glucose, thiamine, naloxone, flumazenil

Page 27: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

Examination

Examination

•Vitals•Skin petechial rash

•Injection marks

•Neurological assessment•Neck rigidity•Fundoscopy

•Brainstem reflexes

•Detailed medical examination

Page 28: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

CONTD.

Vitals1.Pulse

tachycardia Hypovolemia/haemorrhage hyperthermia Intoxication

bradycardia Raised intracranial pressure Heart blocks

Page 29: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

CONTD.

2.Temperature increased Sepsis Meningitis ,encephalitis Malaria ,Pontine haemorrhage

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

phenothiazine intoxication.

Page 30: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

CONTD.

3.Blood pressureincreased

Hypertensive encephalopathy Cerebral haemorrhage Raised intracranial pressure

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

crisis

Page 31: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

CONTD.

4.Respiratory rateIncreased(tachypnae)

Pneumonia Acidosis (DKA, renal failure) Pulmonary embolism Respiratory failure

Decreased Intoxication/poisoning

Page 32: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

CONTD.

Skin petechial rash Meningococcal meningitis

Endocarditis

Sepsis,thrombotic thrombocytopenic purpura

Rickettsial infectionRMS (rocky mountain spotted fever)

Page 33: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

CONTD.

Multiple injection marks Drug addiction

Acute endocarditis

Hepatitis B /C with encephalopathy

HIV

Page 34: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

CONTD.

Neurological assessment;

General posture

Level of conciousness

Page 35: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

CONTD.

Posture; Lack of movements on one side

Intermittent twitching

Multifocal myoclonus

DECORTICATION

DECEREBRATION

Page 36: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

CONTD.

Level of conciousness Glasgow coma scale (GCS)Best motor response Best verbal responseEye opening GCS score 3 –severe injury less than or equal to 8 –

moderate injury 9 to 12 – minor injury

Page 37: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

CONTD.

An abbreviated coma scale is used in the assessment of critically ill patient (primary servey)

AVPUA –alertV – respond to voice stimulusP – respond to painU - unresponsive

Page 38: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

Brainstem reflexes

Pupillary responses to light

Spontaneous and elicited eye movements

Corneal responses

Respiratory movements

Page 39: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

CONTD.Ocular movements

Conjugate deviation of eyes to a side – ipsilateral hemisphere frontal leison or contralateral pontine leison. Rarely eyes may turn paradoxically away from the side of deep hemisphere leison (WRONG-WAY EYES)

Downward conjugate deviation of eyes – mesencephalic leison.

Page 40: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

CONTD.

Eyes turn down and inward in – thalamic hgr and upper midbrain leison.

Ocular bobbing – is diagnostic of pontine hgr.

Ocular dipping - indicates diffuse cortical anoxic damage.

Dysconjugate ocular deviation – brainstem leison.

Page 41: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

CONTD.

Oculocephalic reflex (Doll’s eyes response) – brisk in cortical depression ,lost in brainstem leison.

Oculovestibulo responses –two components

1.Conjugate ocular movement – loss in brainstem damage.

2.Nystagmus – loss in damage to cerebral hemisphere

Page 42: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

CONTD.Pupillary changes;

Sr no

pupils causes

1 B/L Pin-point pupils ( less than 1mm)but responsive

Opiates poisoning ,extensive pontine hgr.

2 B/L small pupils but responsive

B/L diencephalon involvement or destructive pontine leison

3 B/L slightly small pupils(1 to 2.5 mm) but responsive

Metabolic encephalopathies ,deep B/L hemisphere leison or thalamic hgr.

4 B/L dilated and fixed Severe midbrain damage, Overdose of atropine,scopolamine,glutethemide.

Page 43: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

CONTD.

Sr. no.

Pupil cause

6 U/L small pupil Horner syndrome

5 Ipsilateral dilated pupil with no direct or consensual reflexes

Compression of 3rd cranial nerve e.g, uncal herniation

7 U/L small and irregular pupilunresponsive

Leison in pretectal area of midbrain

Page 44: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

CONTD.Respiratory movements

Has less localizing value then other brainstem reflexes.

Cheyen-stokes respiration(classic cyclic form ending with a brief apneic period – B/L hemisphere damage or metabolic depression.

Rapid ,deep breathing (Kussmaul) –in metabolic acidosis and in pontomesencephalic leison.

Page 45: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

Neck rigidity;

Meningitis

Subarachnoid haemorrhage

Page 46: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

Fundoscopy

Raised intracranial pressure

Hypertensive changes

Subarachnoid haemorrhage

Diabetic retinopathy

Page 47: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.
Page 48: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

History

Onset of the symptoms

Antecedent symptoms

Use of medications

Chronic liver ,kidney ,lung or heart disease

Page 49: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

CAUSES OF UNCONCIOUSNESS

Braintumor

epilepsy

infectionsCardiovascular

disease

trauma

metabolicdisturbances

Thiaminedeficiency

Causes of unconciousness

Page 50: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

Causes of unconciousness

MetabolicDrugs, poisoning e.g CO ,alcoholHypoglcemia, hyperglycemia (keto

acidoti or HONK)Hypoxia, carbondiaoxide narcosis

(COPD)SepticemiaHypothermiaMyxedema ,addisonian crisisHepatic / uremic encephalopathy

Page 51: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

CONTD.

NeurologicalTraumaInfections – meningitis, encephalitis,

malaria, typhoid, rabies, trypanosomiasis.

Tumours – cerebral / meningeal tumorsVascular – subdural / subarachnoid hgr,

stroke, hypertensive encephalopathyEpilepsy – nonconvulsive status /

postictal state

Page 52: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

Immediate investigations

RBS

Blood CP and ESR

LFTs

Urea and Creatnine

Blood and urine cultures

Page 53: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

Other investigations

CRP

ABGs

Toxic screen , drug levels

Lumbar puncture and CXR

CT scan

Page 54: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

Summary

ABC of life support

Oxygen and I.V access

Stabilize cervical spine

Page 55: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

CONTD.

Blood glucose

Control seizures

Consider I.V glucose, thiamine, naloxone, flumazenil

Page 56: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

CONTD.

Brief examination and obtain history

Investigate

Reassess the situation and plan further

Page 57: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

Take home message

Early management

Prompt diagnosis

Page 58: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

MCQ

Pupillary changes in opiate poisoning

1.B/L pinpoint

2.U/L pin point

3.B/L dilated

Page 59: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

Answer

1. B/L pin point

Page 60: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

MCQ

Myxoedema coma seen in

1.Euthyroid state

2.Hyperthyroid state

3. hypothyroid state

Page 61: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

Answer

3. hypothyroid state

Page 62: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.
Page 63: Approach to. Contents  Clinical Evaluation History Examination  Lab Evaluation  Management.

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