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ByProf. Nabil Lymon

Professor of Internal MedicineMansoura University

Approach to Diagnosis and Management

of Comatosed Patient

Approach to Diagnosis and Management

of Comatosed Patient

introductionintroductionThe state of consciousness or alertness

depends on:An intact reticular activating system (R.A.S): this is a

collection of unclei present in the brain stem,

hypothalamus & thalamus. It receives impulses from

the pathways carrying sensations from the outside

world & transmits them through ascending fibres to

the cerebral cortex. Its function is the activation of

cerebral cortex.

An intact cerebral cortex.

Interruption of the state of

consciousness may occur at one or both

these levels:

R.A.S: a small lesion is sufficient to produce

Cerebral cortex: an extensive lesion is

necessary to produce coma.

DefinitionDefinitionComa is sleep like state in which the patient makes

no purposeful response to the environment and from which

he or she cannot be aroused. The eyes are closed and do

not open spontaneously. The patient does not speak and

there is no purposeful movement of the face or limbs.

Verbal stimulation produces no response. Painful

stimulation may produce no response or non purposeful

reflex movements mediated through spinal cord or

brainstem pathways.

ClassificationClassification Old classification based on:

Degree of disturbance of consciousness. Response of the patient to external stimuli.

Glasgow coma scale: in this scale the level is evaluated according to the patient’s response to external stimuli, using 3 criteria:

Eye opening Verbal response. Motor response

Each response is given a score. The total score is summed to give an overall value of the level of consciousness from 3-14.

StateconsciousnessResponse to external

stimuli Lethargy or drowsiness

ImpairedVerbal response to increased verbal stimulation

StuporImpairedVerbal response only to vigorous & continuous stimulation

Semi-comaLostNo verbal response, only reflex response to painful stimuli

Coma Lost No verbal or reflex response to painful stimuli

Eye Opening ConsciousnessResponse to external stimuli

Spontaneous 4Oriented 5Obeys orders 5

In response to speech 3Confused 4Localises to pain 4

In response to pain 2

Words, no sentences 3Flexes to pain 3

None 1Sounds, no words 2Extends to pain 2

None 1None 1

According to this scale: coma (score3) is defend as a state of loss of consciousness where there is no eye opening, no vebral or motor response to external stimuli

Causes of comaCauses of coma

OrganiOrganicc

HystericHystericalal

IntracraniIntracranialal

ExteracranExteracranialial

Intracranial causesIntracranial causes The coma is associated with signs of

lateralisation:Unequal pupilsDeviation of the eyes to one sideFacial asymmetryTilting of the head to one side.Unilateral hypo or hypertoniaAsymmetric deep reflexes.Unilateral +ve Babinski.Unilateral focal or jacksonian fits.

Hysterical ComaHysterical Coma No apparent organic lesion. All vital signs are normal:

PulseTempB.P.

No particular smell of breath No finding on chemical analysis. Coma is usually incomplete.

Traumatic: head injury with:

Cerebral concussion.

Contusion

Laceration.

Inflammatory

Encephalitis

○ Acute onset

○ Fever

○ Headache

○ Confusion

○ Focal cerebral signs.

ContCont_______________________._______________________. Meningitis

FeverHeadacheNeck stifness+ve Kernig’s signC.S.F. changes

Cerbral abscess:Gradual onset of low feverSigns of increased intracranial tensionFocal cerebral signsSeptic focus (e.g. otitis media)

VascularVascular Susbarachnoid haemorrhage

Sudden onsetSevere headacheNeck stiffness+ve Kernig’s signBloody C.S.F.

Cerberal haemorrahage Sudden onsetVomitingFocal signs (e.g hemiplegia or fits)Deeping coma

Cont___________________. Cerebral thrombosis

Basilar artery occlusionDeep comaDecerbrate rigidityRespiratory embarrassment

Cerebral embolism Acute onsetSource of emboli e.g. mitral stenosisA.FBacterial endocarditisFocal signs as hemiplegia

ContCont______________________.______________________. Hypertensive encephalopathy:

Hypertension

Rentinal changes

Convulsions

Subdural haematoma

Usually middle aged and elderly

Headache and fluctuation of consciousness precedes the

coma

Papiloedema and focal signs may be present + history of

head trauma.

NeoplasticNeoplastic Primary e.g. meningioma or glioma

Metastatic

Bilaterak papilloedema is usually present.

History of pervious fits:

Absence of focal signs of cerbral lesion

Dilated puplis

Bilateral externsor plantar response.

EpilepsyEpilepsy

EXTRACRANIAL CAUSESEXTRACRANIAL CAUSES1. Toxic: Barbiturates: respiratory depression, circulatory failure &

subnormal temperature. Opiates: pin–point pupil, respiratory depression, slow weak pulse

& cold skin. Belladonna (atropine): hot flushed dry skin, fever, dilated pupil,

delirium. Salicylates: hyperventilation, fever, bleeding tendency & dilated

pupils. Alcohol: characteristic odour, cold skin, increased level in the

blood. Co poisoning: cherry red skin, no respiratory distress in spite of

07 lack. Tranquilizers & hypnotics.

2. Hypoxic

Pulmonary disease.

CO2 narcosis.

3. Ischaemic

Cardiac arrest.

Cardiac arrhythmias

Myocardial infarction.

Hypotensive drugs

4. MetabolicHypo & hyperglycemia (D.M.).Hypo & hyperthermia (heat stroke).Uraemia.Cholaemia.

5. EndocrinalHypopituitarism.Hypothyroidism.Hypo & hyperparathyroidism.Addissoes crisis.

6. FeversMeningitis, encephalitis.Malaria specially cerebral type.Septicaemia.Status typhosus.

CAUSES OF FEBRILE CAUSES OF FEBRILE COMACOMA Infective: encephalitis, meningitis & other hyperpyrexias.

Vascular: pontine haemorrhage, subarachnoid

haemorrhage.

Metabolic: diabetic ketoacidosis, hepatic cirrhosis.

Endocrinal: thyrotoxic & Addissonian crisis.

Toxic: Belladonna & salicylate poisoning.

Sun stroke & heat stroke.

Coma with 2ry infection due to hypostatis pneumonia,

U.T. infection or bed sores.

CLINICAL APPROACH TO A CASE CLINICAL APPROACH TO A CASE OF COMAOF COMA

History taken from the patient's relatives.

Onset: may be:

Sudden e.g. cerebral haemorrhage or

embolism.

Subacute e.g. cerbral thrombosis.

Gradual e.g. brain tumour.

ContCont_________________________._________________________.

Head initiry: cerebral concussion, laceration or

haemorrhage.

Convulsions: post-ictal coma, brain tumour or

overdose of antiepileptics. 4. Drug intake:

insulin overdose, drug intoxication (e.g.

barbiturates . ..).

Exposure to the sun as during the Pilgrimage in

Mecca (sun stroke).

GENERAL EXAMINATIONGENERAL EXAMINATION Hyperthemia: causes of febrile coma

poisons e.g. Afropine

TCAs

Salicylats

Hypothermia: Hypopituitarism, Hypothyroidism.

Barbiturate, opiate or alcohol poisoning.

Peripheral circulatory failure: cardiac causes.

PulsePulse Bradycardia: brain tumour, opiate

poisoning, myoexedma Tachycardia: hyperthyroidism, uraemia

atropine

Blood pressure:

High B.P.: hypertensive encephalopathy.

Low B.P.: Addissionian crisis, Alchol &

barbiturate poisoning.

RespirationRespiration

Slow, deep, stertorous: in morphine &

barbiturate poisoning.

Rapid, deep (Kussmaul) respiration: in

diabetic or uraemic acidosis.

Hyperpnoea regularly alternating with

apnoea (Chyne-Stokes respiration): lesions

affecting both cerebral hemispheres.

ContCont____________________.____________________. Central neurogenic hyperventilation: similar

to Kussmaul's respiration but the cause is a

lesion at the junction between midbrain &

pons.

Apneustic breathing: prolonged pause at full

inspiration due to pontine lesion.

Ataxic breathing: phases of deep & shallow

breathing alternate irregularly: due to

medullary lesion.

Odour of breathOdour of breath Acetone odour: in diabetic ketosis coma. Fetor hepaticus: in hepatic coma. Uriniferous odour: in uraemic coma. Alcohol odour: in alcohol intoxication. Others:

PhenolCyanideKeroseneOpium poisoning.

Inspection of skinInspection of skin

Injuries or bruises: in traumatic causes

 Dry skin in ketosis, atropine poisoning

Moist skin: in hypoglycaemic coma.

Cherry-red colour: in CO poisoning and

cyanide poisoning

Needle markers on limbs: in drug addiction

ContCont____________________.____________________. Rashes: in waterhouse freidreichson’s

meningitis, in endocarditis & other exanthemata.

Bullae may be seen in babiturates, TCAs and

Copoisoning.

Cyanozed in opium and barbiturate poisoning

Pale cold clammy skin in cocaine toxicity.

Cold flushed in alcohol toxicity

C.N.S. ExaminationC.N.S. Examination

Signs of lateralization: denoting an

intracranial cause for the coma.

Pupillary signs:

Dilated, irreactive to light.

○ Unilateral 3rd nerve compression, as in uncal

herniation.

○ Bilateral: .eg. atropine poisoning.

ContCont____________________.____________________.Constricted:

○ Unilateral: Horner's syndrome however,

alone, this syndrome does not cause coma.

○ Bilateral:

Reactive to light: metabolic coma.

Irreactive to light: pontine haemorrhage,

morphine poisoning (pin–point pupil).

ContCont___________________.___________________.

Fundus examination: for papilloedema in

cases of increased I.C.T.

Signs of meningeal irritation: Neck

stiffness, opisthotonus. +ve Kernig's &

Lassegue's signs in cases of meningitis &

subarachnoid haemorrhage.

Laboratory Laboratory InvestigationInvestigation Blood examination:

Blood picture: leucocytosis in bacterial infections.

Blood film for malaria parasites.

Blood levels of sugar, creatinine,

Blood gases: pH, HCO-3.

Toxicological studies in cases of poisoning.

Analysis of gastric contents for possibility of

poisoning.

Urine analysis for sugar, acetone & albumin.

C.S.F. examination: e.g. bloody in S.A.H.,

purulent in bacterial meningitis

Plain x–ray skull: e.g. sellar changes in T

I.C.T., fractures in trauma.

C.T.-Scan & M.R.I show the site, size and

nature of intracranial lesions.

Emergency Emergency managementmanagement Immediately

Ensure adequancy of airway, ventilation and

circulation

Draw blood for serum glucose, electrolytes, liver

and renal function tests, PT, PTT and CBC.

Start IV and adminster 25 g of dextrose, 100 mg

of thiamine and 0.4 – 1.2 mg of naloxone IV.

Draw blood for arterial blood gas determinations.

Treat seizures.

NextNext If signs of meningeal irritation are present

perform LP to rule out meningitis

Obtain a history if possible.

Perfom detailed general physcial and

neurologic examination.

Order CT scan if history or findings suggest

structural lesion or subarachnoid hemorrhage.

LaterLater ECG Correct hyper or hypothermia. Correct severe acid base and elctrolyte

abnormalities. Chest X-ray. Blood and urine toxicology studies, EEG.

Significance of Significance of endotracheal tubeendotracheal tube Maintain the airway patient

Suction of secretions

Oxygenation & mechanical retaliation

Some emergency drugs can be given

through it tube e.g. Naloxone

Atropine

Epinephrine

conclusionconclusion Coma is produced by disorders that affect

both cerbral hemispheres or the brainstem

reticular activiting system.

The possible causes of coma re limited:

mass lesion, metabolic encephalopathy,

infection of the brain (encephalitis) or its

coverings (meningitis) and sub arachnoid

hemorrhage.

ContCont___________________.___________________. The examination of a comatose patient should be

focused and brief: assess whether the pupils

constrict in response to light, whether eye

movements can be elicited by rotating the head

(doll’s head maneuver) or by irrigating the

tympanic membrane with cold water (caloric

stimulation), the nature (especially bilateral

symmetry or asymmetry) of the motor response

to a painful stimulus and the presence or

absence of signs of meningeal irritation.

ContCont____________________.____________________. Immediately exclude hypoglycemia.

Patients who can open their eyes are not in

coma.

A sudden onset of coma suggest a vascular

origin, especially a brainstem stroke or

subarachnoid hemorrhage.

Rapid progression from hemispheric signs such

as hemiparesis, hemisensory deficit or aphasia

to coma within minutes to hours is characteristic

of intracerbral hemorrhage.

ContCont____________________.____________________. A more protracted course leading to coma

(days to a week or more) is seen with

tumor abscess or chronic subdural

hematoma.

Coma preceded by a confusional state or

agitated delirium without lateralizing signs

or symptoms is probably due to a

metabolic derangement.

Treatment of D.K.AA. Prevention the patient is given guidelines

to prevent this problem such as:1.The daily dose of insulin is mandatory and its

negligence is dangerous.

2.When the patient can't follow his usual diet due to severe illness e.g. pneumonia, he must eat or drink whatever he can tolerate. The patient must test for urine glucose and ketone bodies every 4 hours and if the tests show the need for extrainsulin, we can add 20% to the original dose (e.g. if the patient's usual dose is 40 U we can add 8 U).

B. Curative1. Fluid replacement

a. Suitable regimen is as follow:- 1 litre in the In 1/2 h, followed by 1 litre in 1 h, another 1 litre in 1 h, 1 litre in 2 h, 1 litre in 3 h, and 1 litre in 4 h.

b. 2 the total amount of the fluid deficit is given in 8 hours and the other 2 over the next 16 h.

c. Normal saline is used at the start and changed to dextrose saline when blood glucose reaches 180 mg%.

2. Insulin regimen we can use one of these two methods: a. I V. insulin infusion by the use of infusion pump:- soluble insulin

is diluted in 0.9 saline and 0.1 U/kg/h (6U/h) is given by the infusion. The infusion is continued until the patient is well enough (S.C.insulin is given before eating) and the insulin infusion is discontinued after meal.

b. IM. route (soluble insulin) :- 20 U at the start, then 6 U/h till blood glucose reaches 200 mg%.

Cont_______________________._3. Electrolyte correction

a. Kcl which is given from the second hour after insulin

therapy as follow:

- 20 mmol is added to every litre saline if K level is 3-4 meq/L.

- 40 mmol is added to every litre saline if K level is less than 3

meq/L.

- It is contraindicated to add K if there is oliguria or K level > 5

meq/L.

b. Na HCO3:- 65 mmol over 30-60 min and can be repeated

every hour when the PH <7.1

4. Treatment of the precipitating factors e.g infection.

5. Treatment of the complications:- see later.

Complications1. Acute fatty infiltration of the liver.

2. Infection

a. Rhinocerebral infection with mucormycosis may complicate this condition

b. Treatment with amphotricin B + necrotic tissue removal, improve the survival to about 60%.

3. Shock due to severe dehydration.

4. Vascular thrombosis due to dehydration and increased viscosity of the blood.

5. Pulmonary edema which may occur by the volume overload due to excess fluid.

6. Cerebral edema "rare but fatal"

Cause: It occurs 4-16 h. after initiation of therapy due

to rapid decrease of blood glucose level which lead to

movement of water into the intracellular space leading

to brain edema.

Cl.p.: Increased ICT leads to papilledema,

ophthalmoplegia, confusion, coma.

Prevention: Avoid the rapid decrease of blood

glucose and distribute the fluid replacement over 24

hours.

Treatment: Brain dehydrating measures e.g mannitol

1-2 gm/kg over 20 min.

II. Hyperglycemic hyperosmolar non ketotic

coma (HONK)Pathogenesis

A. It occurs in middle aged and elderly patients due

to the presence of low level of insulin which is

sufficient for prevention of lipolysis and ketosis

and not enough to prevent hyperglycemia.

B. The predisposing factors: see diabetic

ketoacidosis.

Clinical picture

1. Severe hyperglycemia and dehydration

which may lead to renal impairment.

2. Neurologic manifestations such as

convulsions, stupors and coma.

3. Thrombotic complications may occur due

to increased viscosity of the blood.

Treatment

1. The same as in diabetic ketoacidosis but

we give z tonic saline to decrease the

serum osmolality which exceed 340

mosm/L (N.290 mosm/L).

2. Lower rate of insulin infusion 3U/h.

3. Lower rate of S.C. heparin to prevent

thrombosis.

III. Lactic acidosis1. Occur with: biguanide therapy especially

phenformin.

2. The patient presents with acidosis (Kausmaull

respiration), late CNS and CVS inhibition.

3. Plasma ketostix value: < ++ exclude diabetic

ketoacidosis as a cause of metabolic acidosis.

4. Treatment:- by large amounts of bicarbonates.

Thank You

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