COMA

Christina Amalia
Pembimbing :
dr. Anik Widijanti, Sp.PK(K)
INTRODUCTION
Coma is defined as the total absence of wakefulness
(arousal) and awareness: unarousable
unresponsiveness.
To distinguish coma from transient states (eg, seizure)
this set of conditions must last at least 1 h
Most cases of coma are due to metabolic disorders or
exogenous drug intoxication
The most important single sign distinguishing toxic-
metabolic coma from primary brain disease is the
presence of pupillary light responses

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DEFINITION
Clinical Levels of Altered Conciousness
Persistent
vegetative state
Coma Brain death
Deep sleeplike state, cant be
Stupor aroused
Unresponsive, can be aroused to near-
normal state with appropriate stimuli
Drowsiness
Light sleep, easy arousal,
persistence of alertness for brief
periods

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ETIOLOGY
Structural

Brain abscess
Brain tumor
Brainstem
hemorrhage
Brainstem infarction
Herniation

Types of cerebral herniation

(A) uncal; (B) central; (C) transfalcial; (D) foraminal

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ETIOLOGY
Structural

Cerebral artery Multifocal

occlusion leukoencephalopathy
Cerebral vasculitis Sagittal sinus thrombosis
Hydrocephalus Subarachnoid
Intracranial hemorrhage
hemorrhage Trauma

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Etiology
Non-structural
Drugs Alcohol, Amphetamines,
Anticholinergics, Antidepressants
Barbiturates, Benzodiazepines,
Opiates, Sedative, Tranquilizers
Toxins Carbon monoxide, Cyanide, Ethylene
glycol
Lead, Methanol
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Etiology
Metabolic Diabetic ketoacidosis, Hepatic failure,
Hypercapnia, Hypoxia
Hypo-/Hypernatremia, Hypo-
/Hypercalcemia, Hypoglycemia
Nonketotic hyperosmolar coma, Renal
failure (uremia)
Encephalopathy
Infection Encephalitis, Meningitis, Sepsis
Other Diffuse ischemia, Fat embolism
Hypotension, Seizure (postictal)
Pathogenesis
Almost all instances of diminished alertness can
be traced to widespread abnormalities of the
cerebral hemispheres or to reduced activity of a
special thalamocortical alerting system termed
the reticular activating system (RAS)

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Pathogenesis

Principal causes of coma:

1. lesions that damage the RAS in the upper
midbrain or its projections
2. destruction of large portions of both cerebral
hemispheres
3. suppression of reticulocerebral function by
drugs, toxins, or metabolic derangements such
as hypoglycemia, anoxia, uremia, and hepatic
failure

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Diabetic Ketoacidosis Coma

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 Hyperosmolar Hyperglycemic
Nonketotic Coma

Relative insulin deficiency + illness Dehydration blood

or injury vol <<

glucose use in cells

glucose production in Severe hyperglycemia
liver

Lethargy, mental
Hyperglycemia confusion, shock
Coma
Glucosuria
urination >>
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Hypoglycemic
Coma

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Hepatic Coma

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 History
In many cases, the cause of coma is immediately evident
(e.g. trauma, cardiac arrest, or reported drug ingestion)
In the reminder, certain points are especially useful:
1. the circumstances and rapidity with which neurologic
symptoms developed
2. the antecedent symptoms (confusion, weakness,
headache, fever, seizures, dizziness, double vision, or
vomiting)
3. the use of medications, illicit drugs, or alcohol
4. chronic liver, kidney, lung, heart, or other medical
disease

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General physical examination
Fever suggests a systemic infection, bacterial
meningitis, heat stroke, malignant hyperthermia due to
anesthetics or anticholinergic drug intoxication
Hypothermia is observed with exposure; alcoholic,
barbiturate, sedative, or phenothiazine intoxication;
hypoglycemia; peripheral circulatory failure
Tachypnea may indicate systemic acidosis or
pneumonia or rarely infiltration of the brain with
lymphoma

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 Abberant respiratory pattern
Cheyne-Stokes signifies bihemispheral damage or
metabolic suppresion
Kussmaul breathing usually implies metabolic acidosis
but may also be occur with pontomesencephalic lesions

Marked hypertension suggests hypertensive

encephalopathy, but it may also be secondary to a rapid
rise in intracranial pressure (ICP)

Hypotension is characteristic of coma from alcohol or

barbiturate intoxication, internal hemorrhage, myocardial
infarction, sepsis, or profound hypothyroidism

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 Funduscopic examination can detect subarachnoid
hemorrhage (subhyaloid hemorrhages), hypertensive
encephalopathy (exudates, hemorrhages, vessel-crossing
changes, papilledema), and increased ICP (papilledema)

Cutaneouspetechiae suggests thrombotic

thrombocytopenic purpura, meningococcemia, or a
bleeding diathesis associated with an intracerebral
hemorrhage

Cyanosis, reddish or anemic skin coloration are other

indications of an underlying systemic disease responsible
for the coma

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Neurologic examination
Level of consciousness (Glasgow Coma Scale)

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Brainstem Reflexes

Reflex Technique Normal Response

Pupils Response Direct and
to light consensual
constriction
Oculocephalic Turn head Eyes move
(dolls eyes) from side conjugately in
to side opposite
direction
Gag Stimulates Symmetric elevation
soft palate

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Brainstem Reflexes

Reflex Technique Normal Response

Oculovestibular Irrigate Sustained deviation
(cold water external of eyes toward
calorics) auditory irrigated ear
canal
Corneal Stimulate Eyelid closure
cornea
Cough Stimulate Cough
cough

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Laboratory Examination
Emergency laboratory tests for non-structural
coma

Venous Complete blood count, glucose, BUN,

blood creatinine, osmolality, liver function
tests, muscle enzyme, thyroid & adrenal
functions, toxicology screens, blood
cultures, electrolytes
Arterial Blood gas analysis, ammonia ,
blood carboxyhemoglobin

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Urine Toxicology, microscopic examination
Gastric Toxicology
aspirate
CSF Cell count, Gram stain, protein,
glucose, culture, viral and fungal
antigens and antibody titers

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Selected causes of Coma

Metabolic Alcoholism blood ethanol, metabolic

Hyperosm acidosis, ketosis
olar Blood glucose >500 mg/dL,
no/mild ketosis,
dehydration
Diabetic blood glucose >500
ketoacidos mg/dL, ketosis, acidosis,
is dehydration

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Metabo Metabolic pH, lactic acid
lic acidosis of
other origin

Hypoglycemia blood glucose (<50

mg/dl)
Hypo- Changes in calcium levels;
/hypercalcemia hypomagnesemia can be
found with hypocalcemia
Hepatic coma blood ammonia, liver
function tests

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Metabo Drugs Presence of any drugs on
lic serum or urine toxicology
screen often at very high
levels
Uremic coma urea and creatinine,
Ischemia metabolic acidosis
Lactic acidosis
Hypo-
/hyperthyroidi Abnormal thyroid function
sm tests

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Encephal Intracranial Blood in CSF
opathy hemorrhage
Trauma - Blood in CSF if traumatic
hemorrhage (+)
Infectious Bacterial, CSF glucose, protein
viral

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DIAGNOSIS
Imaging

Computed tomographic (CT) scanning of the brain is the most

valuable acute test to rule out structural causes of coma
provides detailed images of bony structures of the skull base
It may also show parenchymal shifts and effacement of CSF
spaces
Magnetic resonance imaging (MRI) is the most sensitive method to
image the brain and define diverse pathologies
The image resolution is much better than CT, and it allows
images of the CNS in multiple planes
frequently displays pathologic processes earlier than CT does

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DKA vs HHS
DKA HHS
Hyperglycemia Hyperglycemia
Ketosis Hyperosmolarity
Acidosis

Can and often do occur simultaneously

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DKA vs HHS
Precipitating factors
DKA HHS
Infection Infection
Viral syndrome Pneumonia
Cerebrovascular accident Cerebrovascular accident
Acute pancreatitis Acute pancreatitis
Non-compliance Non-compliance
New-onset diabetes Endocrine
Drugs Drugs
Clozapine Calcium channel blockers
Cocaine Chlorpromazine
Malfunction of insulin pump New-onset diabetes

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DKA vs HHS
Pathophysiology
DKA & HHS can be considered two manifestations of the same
underlying mechanism: insuffiency of insulin effect

Type I diabetes mellitus Type II diabetes mellitus

Absolute insulin deficiency Relative insulin deficiency

DKA HHS

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 DKA vs HHS
Clinical Presentation

DKA HHS

Younger, lean patients with Older, obese patients with

type I DM type II DM
Develop within a day or so Can take days or weeks to
Kussmaul breathing & fruity fully develop
odor No kussmaul breathing &
Dehydration occurs fruity odor
Dehydration occurs, but
more pronounced

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 DKA vs HHS
Clinical Presentation

Symptoms Physical Examination

Polyuria Hypotension
Polydypsia Tachycardia
Blurred vision Dry mucous membranes
Nausea/vomiting Confusion
Abdominal pain Abdominal tenderness
Fatigue
Obtundation

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DKA vs HHS
Laboratory Diagnostic Criteria
DKA
HHS
Mild Moderate Severe
Plasma glucose (mmol/L) 14 14 14 30
Arterial pH 7.25-7.35 7.0-7.24 <7.0 >7.3
Serum HCO3- (mmol/L) 15-18 10-14 <10 >15
Urine ketones ++ ++ ++ +
Plasma ketones ++ ++ ++ +
Total osmolality
Variable Variable Variable 340
(mOsm/kg)*
Anion gap# >10 >12 >12 <12
Alert/ Stupor/ Stupor/
Level of conciousness Alert
+ +
*Formula: 2x[(Na )+(K )]+(urea)+(glucose) drowsy coma
#Formula: (Na+)-[(Cl coma
-)+(HCO -)] (mmol/L)
3

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DKA vs HHS
Typical water & electrolyte deficits

DKA* HHS*
Water (mL/kg) 100 100-200
Sodium (mEq/kg) 7-10 5-13
Chloride (mEq/kg) 3-5 5-15
Potassium (mEq/kg) 3-5 3-7
Phosphate (mEq/kg) 1-1.5 1-2
Magnesium (mEq/kg) 1-2 1-2
Calcium (mEq/kg) 1-2 1-2

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