ActualityActuality

• Increasing spectrum of diseases secondary to critical illness

• 1/3 of intensive care units (ICU) patients, 55% mortality rate

• Increase length of stay and disability• Systematic approach to identify

potentially reversible etiologies and prognostic factors

• Increased survival among medical and surgical.

Concept of extreme Concept of extreme conditionsconditions

Mechanisms of InjuryMechanisms of Injury. . Brain injuryBrain injury

Level of ConsciousnessLevel of Consciousness ComaComa Spinal injurySpinal injury ShockShock

Concept of extreme Concept of extreme conditionsconditions

► Intensive-care medicine or critical-care medicine is a branch Intensive-care medicine or critical-care medicine is a branch of medicine concerned with the diagnosis and management of medicine concerned with the diagnosis and management of life threatening conditions requiring sophisticated organ of life threatening conditions requiring sophisticated organ support and invasive monitoring.support and invasive monitoring.

► A critically ill patient is one at imminent A critically ill patient is one at imminent risk of deathrisk of death; the ; the severity of illness must be recognised early and appropriate severity of illness must be recognised early and appropriate measures taken promptly to assess, diagnose and manage measures taken promptly to assess, diagnose and manage the illness.the illness.

► The approach required in managing the critically ill patient The approach required in managing the critically ill patient differs from that required in less severely ill patients with differs from that required in less severely ill patients with immediate resuscitation and stabilisation of the patientis immediate resuscitation and stabilisation of the patientis condition taking precedence.condition taking precedence.

► Priorities are:Priorities are:

hypoglycaemia and dysrhythmiashypoglycaemia and dysrhythmias

analysis of the deranged physiologyanalysis of the deranged physiology

establishing the complete establishing the complete diagnosis in stages as furtherdiagnosis in stages as further

history and the results of history and the results of investigations become availableinvestigations become available

careful monitoring of the patientis careful monitoring of the patientis condition and response to treatmentcondition and response to treatment

adhering to advanced life support guidelines and the adhering to advanced life support guidelines and the principles of cardiorespiratory managementprinciples of cardiorespiratory management

urgent treatment of life-threatening urgent treatment of life-threatening emergencies such as hypotensionemergencies such as hypotension

hypoxaemiahypoxaemia

hyperkalaemiahyperkalaemia

prompt resuscitationprompt resuscitation

Mechanisms of InjuryMechanisms of Injury• Injury to brainInjury to brain tissue can result from a number of conditions, tissue can result from a number of conditions,

including trauma, tumors, stroke, and metabolic including trauma, tumors, stroke, and metabolic derangements.derangements.

• Brain damageBrain damage resulting from these disorders involves several resulting from these disorders involves several common pathways, including the effects of hypoxia and common pathways, including the effects of hypoxia and ischemia,ischemia, cerebral edema, and injury caused by increased cerebral edema, and injury caused by increased intracranialintracranial pressure. pressure.

• In many cases, the mechanisms of injury areIn many cases, the mechanisms of injury are interrelated.interrelated.

BRAIN INJURY• The brain is protected from external

forces by the rigid confines of the skull and the cushioning afforded by the cerebrospinal fluid (CSF).

• The metabolic stability required by its electricallyactive cells is maintained by a number of regulatory mechanisms, including the blood-brain barrier and autoregulatory mechanisms that ensure its blood supply.

• Nonetheless, the brain remains remarkably vulnerable to injury.

• One third of all trauma deaths• 15-45 years of age• 49%-road traffic accidents,28%-

falls,23%-gun shot injuries and other causes

• Inpatient case fatality rates all head injuries - 2.6%to6.5% severe injuries - 15 to 50%• Good outcome-Glasgow outcome scale

of 1or 2

IntroductionIntroduction

Category Description % of ptsGood/

moderateSevere/

vegetativeDead

No CT data 2.3 5.9 0.0 94.1

Diffuse injury I

No visible pathology on CT

7.0 61.6 28.8 9.6

Diffuse injury II

Cisterns visible, shift 0 – 5 mm, no high or mixed density lesion > 25 cm3

23.7 34.5 52.0 13.5

Diffuse injury III

(swelling)

Cisterns compressed or absent, shift 0 – 5 mm, no high or mixed density lesion > 25 cm3

20.5 16.4 49.7 34.0

Diffuse injury IV

(shift)

Shift > 5 mm, no high or mixed density lesion > 25 cm3

4.3 6.2 37.6 56.2

Evacuated mass lesion

Any lesion surgically evacuated

37.0 22.8 38.4 38.8

Nonevacua-ted mass

High or mixed density lesion > 25 cm3 not surgically evacuated

4.8 11.1 36.1 52.8

Brainstem injury

(no brainstem reflexes by physical exam)

0.4 0.0 33.3 66.7

Can be minor or serious Even small lacerations

can lead to significant blood loss.

› This blood loss may be severe enough to cause hypovolemic shock.

They are often an indicator of deeper, more serious injuries.

Significant force applied to the Significant force applied to the head may cause a head may cause a skull fractureskull fracture..

May be May be openopen or or closedclosed, , depending on whether there is an depending on whether there is an overlying laceration of the scalpoverlying laceration of the scalp

Injuries from bullets or other Injuries from bullets or other penetrating weapons often result penetrating weapons often result in skull fractures.in skull fractures.

Signs of skull fracture include:Signs of skull fracture include:

•Patient’s head appears deformedPatient’s head appears deformed

•Visible cracks in the skullVisible cracks in the skull

•Ecchymosis Ecchymosis (bruising) that develops (bruising) that develops under the eyes (under the eyes (raccoon eyesraccoon eyes))

•EcchymosisEcchymosis that develops behind that develops behind one ear over the mastoid process one ear over the mastoid process ((Battle’s signBattle’s sign))

Account for about Account for about 80% of all skull 80% of all skull fracturesfractures

Radiographs are Radiographs are often required to often required to diagnose a linear diagnose a linear skull fracture skull fracture because there are because there are often no physical often no physical signs.signs.

Linear skull fracturesLinear skull fractures

Result from high-Result from high-energy direct energy direct trauma to the trauma to the head with a blunt head with a blunt objectobject

Frontal and Frontal and parietal bones are parietal bones are most susceptiblemost susceptible

Bony fragments Bony fragments may be driven may be driven into the braininto the brain

Compressed skull fracturesCompressed skull fractures

Associated with Associated with high-energy high-energy traumatrauma

Usually occur Usually occur following diffuse following diffuse impact to the headimpact to the head

Signs include CSF Signs include CSF drainage from the drainage from the ears, raccoon ears, raccoon eyes, and Battle’s eyes, and Battle’s signsign

Basilar skull fracturesBasilar skull fractures

Result when Result when severe forces are severe forces are applied to the applied to the headhead

Often associated Often associated with trauma to with trauma to multiple body multiple body systemssystems

Brain tissue may Brain tissue may be exposed to the be exposed to the environmentenvironment

Open skull fracturesOpen skull fractures

Hypoxia and IschemiaHypoxia and IschemiaHypoxia and hypotension are the 2 major causes Hypoxia and hypotension are the 2 major causes of secondary CNS injury following head trauma.of secondary CNS injury following head trauma.The The brainbrain relies on the ability of the cerebral circulation to relies on the ability of the cerebral circulation to

deliverdeliver sufficient oxygen sufficient oxygen for its energy needs. for its energy needs.

Although the brainAlthough the brain makes up only 2% of the body weight, it makes up only 2% of the body weight, it receives one sixth ofreceives one sixth of the resting cardiac output and accounts for the resting cardiac output and accounts for

20% of the oxygen20% of the oxygen consumption.consumption.

By definition, By definition, hypoxiahypoxia denotes a denotes a deprivation ofdeprivation of oxygenoxygen with with maintained blood flow and ischemia, a situationmaintained blood flow and ischemia, a situation of greatly of greatly

reduced or interrupted blood flow. reduced or interrupted blood flow.

The cellular effectsThe cellular effects of hypoxia and ischemia are quite different, of hypoxia and ischemia are quite different, and the brain tendsand the brain tends to have different sensitivities to the two to have different sensitivities to the two

conditions. conditions.

Hypoxia interferes with the delivery of oxygen, and ischemia interferes with the delivery of oxygen and glucose as well as the

removal of metabolic wastes.

Hypoxia and IschemiaHypoxia and Ischemia• HypoxiaHypoxia usually is seen in conditions such as exposure to usually is seen in conditions such as exposure to

reducedreduced atmospheric pressure, carbon monoxide poisoning, atmospheric pressure, carbon monoxide poisoning, severesevere anemia, and failure to oxygenate the blood. anemia, and failure to oxygenate the blood.

• Contrary toContrary to popular belief, popular belief, hypoxiahypoxia is fairly well tolerated, is fairly well tolerated, particularly inparticularly in situations of chronic hypoxia. situations of chronic hypoxia.

• Neurons Neurons are capable of substantialare capable of substantial anaerobic metabolism anaerobic metabolism and are fairly tolerant of pure hypoxia;and are fairly tolerant of pure hypoxia; it commonly produces it commonly produces euphoria, listlessness, drowsiness,euphoria, listlessness, drowsiness, and impaired problem and impaired problem solving. solving.

• UnconsciousnessUnconsciousness and and convulsionsconvulsions may occur when hypoxia is may occur when hypoxia is sudden and severe. sudden and severe.

• However,However, the the effects of severe hypoxia effects of severe hypoxia ((i.e.i.e., , anoxiaanoxia) on brain ) on brain function seldomfunction seldom are seen because the condition rapidly leads are seen because the condition rapidly leads to to cardiaccardiac arrest and ischemiaarrest and ischemia..

Hypoxia and IschemiaHypoxia and Ischemia

• Unconsciousness occursUnconsciousness occurs within seconds of severe global ischemia, such as that resulting from complete cessation of blood flow, as in cardiac arrest. If circulation is restored immediately, consciousness is regained quickly. However, if blood flow is not promptly restored, severe pathologic changes take place.

• Energy sources (i.e., glucose and glycogen) are exhausted in 2 to 4 minutes, and cellular ATP stores are depleted in 4 to 5 minutes. Approximately 50% to 75% of the total energy requirement of neuronal tissue is spent on mechanisms for maintenance of ionic gradients across the cell membrane (e.g., sodium-potassium pump), resulting in fluxes of sodium, potassium, and calcium ions.

• Excessive influx of sodium results in neuronal and interstitial edema. • The influx of calcium initiates a cascade of events, including release of intracellular

and nuclear enzymes that cause cell destruction.

Focal ischemiaFocal ischemia involves ainvolves a single single area of the brain, area of the brain, as in strokeas in stroke. .

Collateral circulationCollateral circulation may provide may provide low levels of blood flow during focal low levels of blood flow during focal

ischemiaischemia.. The residual perfusion The residual perfusion may provide sufficient substrates tomay provide sufficient substrates to

maintain a maintain a low level of metabolic low level of metabolic activity, preserving neuronalactivity, preserving neuronal

integrityintegrity..

Global ischemiaGlobal ischemia occurs when occurs when blood flow is inadequate toblood flow is inadequate to meet meet the metabolic needs of the entire the metabolic needs of the entire brain. In contrast to personsbrain. In contrast to persons with with focal ischemia, those with global focal ischemia, those with global

ischemia ischemia have nohave no collateral collateral circulation during the ischemic circulation during the ischemic eventevent. The result is. The result is a spectrum of a spectrum of

neurologic disorders. neurologic disorders.

Hypoxia and

Ischemia

• Within the brain, certain regions and cell populations are more susceptible than others to hypoxic-ischemic injury.

• For example, neurons are more susceptible to injury than are the glial cells.

• Among the neurons, the pyramidal cells of the hippocampus, the Purkinje cells of the cerebellum, and the neurons of the globus pallidus of the basal ganglia are particularly sensitive to generalized ischemic-hypoxic injury.

• The reason for this selectivity is uncertain but appears to be related at least to some extent on local levels and metabolism of certain excitatory neurotransmitters such as glutamate.

Cerebral EdemaCerebral Edema

Cerebral edema, Cerebral edema, or brain swelling, or brain swelling, is an increase in is an increase in tissue volumetissue volume secondary to secondary to abnormal fluid abnormal fluid accumulation. accumulation.

There areThere are basically two types basically two types of brain edema: of brain edema: vasogenic or vasogenic or cytotoxic.cytotoxic.

VasogenicVasogenic EdemaEdema Vasogenic edemaVasogenic edema results from an increase results from an increase in the extracellular in the extracellular

fluid that surrounds brain cells. fluid that surrounds brain cells. It occursIt occurs with conditions such aswith conditions such as::

Vasogenic edemaVasogenic edema occurs occurs primarily primarily in the in the whitewhite matter of the matter of the brainbrain, possibly because the white matter , possibly because the white matter is moreis more compliant compliant than the gray matterthan the gray matter and offers and offers less resistance toless resistance to fluid fluid accumulationaccumulation. .

Vasogenic edemaVasogenic edema can be localized, as in the can be localized, as in the case of abscesses case of abscesses or neoplasms, or it may be more generalized.or neoplasms, or it may be more generalized.

The functional manifestations of vasogenic edema includeThe functional manifestations of vasogenic edema include::

tumorstumors

prolonged prolonged ischemiaischemiahemorrhagehemorrhage

infectious processes (infectious processes (e.g.e.g., meningitis), meningitis) that impair that impair the function of the blood-brain barrier and allowthe function of the blood-brain barrier and allow water and plasma proteins to leave the capillary water and plasma proteins to leave the capillary

and move intoand move into the interstitium.the interstitium.

brain injurybrain injury

focalfocal neurologic neurologic

deficitsdeficits

disturbancesdisturbances in in consciousnessconsciousness

severesevere intracranial intracranial hypertensiohypertensio

nn

Cytotoxic Edema Cytotoxic edema involves the swelling of involves the swelling of brain cells. It involves an brain cells. It involves an increase in fluid increase in fluid

in the intracellularin the intracellular spacespace, , chiefly the gray matter, although the white matter may, although the white matter may be be involved. involved.

Cytotoxic edema can result from can result from hypoosmotichypoosmotic statesstates, such as water intoxication or , such as water intoxication or severe ischemia, that impairsevere ischemia, that impair the function of the sodium-potassium membrane pump.the function of the sodium-potassium membrane pump. This causes rapid accumulation of sodium in the cell, followedThis causes rapid accumulation of sodium in the cell, followed by movement of water by movement of water along the osmotic gradient. Dependingalong the osmotic gradient. Depending on the nature of the insult, cellular edema can on the nature of the insult, cellular edema can occuroccur in the vascular endothelium or smooth muscle cells, astrocytes,in the vascular endothelium or smooth muscle cells, astrocytes, the myelin-the myelin-forming processes of oligodendrocytes, orforming processes of oligodendrocytes, or neurons. neurons.

Major changes in cerebral function, such as Major changes in cerebral function, such as stupor and coma, occur with , occur with cytotoxic edema. .

The The edema associated with ischemia may be severe enough to produce may be severe enough to produce cerebral infarction with necrosis of brain tissue..

Cerebral EdemaCerebral Edema

Definition of TermsDefinition of Terms ConfusionConfusion : :

– impaired attentionimpaired attention and and concentration, manifest concentration, manifest disorientation in time, place and disorientation in time, place and personperson, impersistent thinking, , impersistent thinking, speech and performance, reduced speech and performance, reduced comprehension and capacity to comprehension and capacity to reasonreason

– Fluctuate in severity, typically worse Fluctuate in severity, typically worse at night ‘sundowning’at night ‘sundowning’

– Perceptual disturbances and Perceptual disturbances and misinterpret voices, common objects misinterpret voices, common objects and actions of other personsand actions of other persons

ConfusionConfusion is also found in is also found in dementia (progressive failure of dementia (progressive failure of language, memory, and other language, memory, and other intellectual functions)intellectual functions)

Level of ConsciousnessLevel of Consciousness

Alert:Alert: normal awake and responnormal awake and responsive statesive state

Drowsiness:Drowsiness: state of apparent state of apparent sleep, briefly arousal with oral sleep, briefly arousal with oral commandcommand

LethargicLethargic:: resembles resembles sleepiness, but not becoming sleepiness, but not becoming fully alert, slow verbal response fully alert, slow verbal response and inattentive. Unable to and inattentive. Unable to adequately perform simple adequately perform simple concentration task (such as concentration task (such as counting 20 to 1)counting 20 to 1)

Level of ConsciousnessLevel of Consciousness Somnolent: Somnolent: easily aroused by voice easily aroused by voice

or touch; awakens and follows commor touch; awakens and follows commands; reqands; requireduired stim stimulationulation to maintain to maintain arousalarousal

Obtunded/StuporousObtunded/Stuporous:: arousable arousable only with repeated and painful only with repeated and painful stimulation; verbal output is stimulation; verbal output is unintelligible or nil; some purposeful unintelligible or nil; some purposeful movement to noxious stimulationmovement to noxious stimulation

Comatose:Comatose: no arousal despite vigorono arousal despite vigorous stimus stimulationulation, no purposeful moveme, no purposeful movementnt - only posturing, brainstem reflexes - only posturing, brainstem reflexes often absentoften absent

Dementia Confusional stateDementia Confusional state

Memory problemMemory problemClouding of Clouding of

consciousnessconsciousness

FluctuateFluctuate

AcuteAcute

Varies little Varies little

from time to from time to

timetime

Longstanding Longstanding naturenature

DementiaDementia Confusional stateConfusional state

Causes of confusional Causes of confusional statestate

Medical or Medical or surgical diseasesurgical disease• Metabolic disorders Metabolic disorders

• HepaticHepatic• UremicUremic• Hypo- and Hypo- and hypernatremiahypernatremia• HypercalcemiaHypercalcemia• Hypo- and Hypo- and hyperglycemiahyperglycemia• HypoxiaHypoxia• HypercapniaHypercapnia

Infectious illnessInfectious illness•PneumoniaPneumonia•EndocarditisEndocarditis•Urinary tract Urinary tract infectioninfection•PeritonitisPeritonitis

Congestive heart Congestive heart failurefailure Postoperative and Postoperative and posttraumatic statesposttraumatic states Drug intoxicationDrug intoxicationOpiatesOpiatesBarbituratesBarbituratesOther sedativesOther sedatives

Diseases of nervous Diseases of nervous systemsystem• Cerebrovascular Cerebrovascular disease, tumor, abscessdisease, tumor, abscess• Subdural hematomaSubdural hematoma• MeningitisMeningitis• EncephalitisEncephalitis• Cerebral vasculitisCerebral vasculitis• Hypertensive Hypertensive encephalopathyencephalopathy

Definition of TermsDefinition of Terms

COMACOMA - - reduced alertness and responsiveness represents reduced alertness and responsiveness represents a continuum that in severest forma continuum that in severest form,, a deep sleeplike state from a deep sleeplike state from

which the patient cannot be aroused.which the patient cannot be aroused.

STUPORSTUPOR - l - lesser degrees of unarousability in which the esser degrees of unarousability in which the Patient can be awakened only by vigorous stimuli, Patient can be awakened only by vigorous stimuli,

accompanied by motor behavior that leads to avoidance accompanied by motor behavior that leads to avoidance of uncomfortable or aggravating stimuli.of uncomfortable or aggravating stimuli.

DrowsinessDrowsiness - which is familiar to all persons, - which is familiar to all persons, simulates light sleep and is characterized by easy arousal simulates light sleep and is characterized by easy arousal

and the persistence of alertness for brief periods.and the persistence of alertness for brief periods.

Drowsiness and stuporDrowsiness and stupor are usually attended by are usually attended by some degree of confusion.some degree of confusion.

By definition, coma (decreased By definition, coma (decreased arousal) is produced by:arousal) is produced by:

Bilateral hemispheric damageBilateral hemispheric damage

Suppression by hypoxia, Suppression by hypoxia, hypoglycemia, drugs or toxinshypoglycemia, drugs or toxins

Brain stem lesion or metabolic Brain stem lesion or metabolic derangement that suppresses derangement that suppresses Reticular Activating System Reticular Activating System

(RAS)(RAS)

Level of consciousness Pattern of breathing (Cheyne-Stokes) Pupillary changes Oculomotor responses (ie. Doll’s eyes) Motor responses

PosturingPosturing DecorticateDecorticate

Flexion of arms, wrists, Flexion of arms, wrists, fingersfingers

Adduction of upper Adduction of upper extremitiesextremities

Extension of lower Extension of lower extremitiesextremities

DecerebrateDecerebrate Extremities in Extremities in

extensionextension Pronation of forearms Pronation of forearms

and plantar extension and plantar extension of feetof feet

GLASGOW COMA SCORE GLASGOW COMA SCORE

MortalityMortality

MorbidityMorbidity

Brain death – brain stem death – no potential for recovery – no control of homeostasis

Cerebral death – death of cerebral hemispheres not including the brain stem – vegetative state

Recovery of consciousness Residual cognitive dysfunction Psychosocial domain Vocational domain

Prognosis of comaPrognosis of coma

► RecoveryRecovery from coma depends primarily on the from coma depends primarily on the causes, rather than on the depth of coma causes, rather than on the depth of coma

► IntoxicationIntoxication and metabolic causes carry the best and metabolic causes carry the best prognosis prognosis

► ComaComa from traumatic head injury far better than from traumatic head injury far better than those with coma from other structural causesthose with coma from other structural causes

► ComaComa from global hypoxic-ischemic carries least from global hypoxic-ischemic carries least favorable prognosis favorable prognosis

► At At 33rdrd day day, no papillary light reflex or GCS < 5 is , no papillary light reflex or GCS < 5 is associated with associated with poor prognosis poor prognosis

Conditions mimic coma

•Brain death•Locked-in syndrome•Vegetative state •Frontal lobe disease •Non-convulsive status epilepticus •Psychiatric disorder (catatonia,

depression)

Vegetative StateVegetative StateSignifies an awake but Signifies an awake but unresponsive state. Most of unresponsive state. Most of these patients were earlier these patients were earlier comatose and after a period of comatose and after a period of days or weeks emerge to an days or weeks emerge to an unresponsive state in which unresponsive state in which their eyelids are open, giving their eyelids are open, giving the appearance of wakefulness. the appearance of wakefulness. Yawning, grunting, swallowing, Yawning, grunting, swallowing, limb and head movements limb and head movements persist, but there are few, if any, persist, but there are few, if any, meaningful responses to the meaningful responses to the external and internal external and internal environment-in essence, an environment-in essence, an "awake coma.“"awake coma.“Respiratory and autonomic Respiratory and autonomic functions are retained.functions are retained.Cardiac arrest and head injuryCardiac arrest and head injury are the most common causes.are the most common causes.

Locked-in stateLocked-in state Describes a Describes a pseudocomapseudocoma in which in which an awake patient has no means of an awake patient has no means of producing speech or volitional limb, producing speech or volitional limb, faceface, and pharyngeal movements in , and pharyngeal movements in order to indicate that he or she is order to indicate that he or she is awake, but vertical eye movements awake, but vertical eye movements and lid elevation remain unimpaired, and lid elevation remain unimpaired, thus allowing the patient to signal. thus allowing the patient to signal.

Vertical eye movement and lid Vertical eye movement and lid elevation remain unimpaired.elevation remain unimpaired.Etiology: infarction or Etiology: infarction or hemorrhage of the ventral hemorrhage of the ventral pons, pons, which transects all which transects all descending corticospinal and descending corticospinal and corticobulbar pathwayscorticobulbar pathways. . Such patients have written entire Such patients have written entire treatises using treatises using Morse code.Morse code.

Akinetic mutism

• PPartially or fully awake artially or fully awake patient who is able to patient who is able to form impressions and form impressions and think but remains think but remains immobile and mute, immobile and mute, particularly when particularly when unstimulated. unstimulated.

• Causes: Causes: damage in the damage in the regions of the medial regions of the medial thalamic nuclei, the thalamic nuclei, the frontal lobes (particularly frontal lobes (particularly situated deeply or on the situated deeply or on the orbitofrontal surfaces), orbitofrontal surfaces), or from hydrocephalus. or from hydrocephalus.

Abulia• Aboulia or abulia (from the Greek

"αβουλία", meaning "un-will"), in neurology, refers to a lack of will or initiative and can be seen as a disorder of diminished motivation (DDM).

• Aboulia falls in the middle of the spectrum of diminished motivation, with apathy being less extreme and akinetic mutism being more extreme than aboulia. A patient with aboulia is unable to act or make decisions independently. It may range in severity from subtle to overwhelming. It is also known as Blocq's disease (which also refers to abasia and astasia-abasia).

• Mental and physical slowness and lack of impulse to activity that is in essence a mild form of akinetic mutism with the same anatomic origins.

CatatoniaCatatonia CatatoniaCatatonia is a state of neurogenic motor is a state of neurogenic motor

immobility, and behavioral abnormality manifested immobility, and behavioral abnormality manifested by by stupor. It was first described, in 1874, by . It was first described, in 1874, by Karl Ludwig Kahlbaum in in Die Katatonie oder das Die Katatonie oder das SpannungsirreseinSpannungsirresein ( (Catatonia or Tension InsanityCatatonia or Tension Insanity). ).

HHypomobile and mute syndrome associated with a major ypomobile and mute syndrome associated with a major psychosis. psychosis.

Patients appear awake with eyes open but make no Patients appear awake with eyes open but make no voluntary or responsive movements, although they blink voluntary or responsive movements, although they blink spontaneously, swallow, and may not appear distressed. spontaneously, swallow, and may not appear distressed.

EEyes are half-open as if the patient is in a fog or light yes are half-open as if the patient is in a fog or light sleep. sleep.

NO NO clinical evidence of brain damageclinical evidence of brain damage..

Brainstem Reflexes pupillary responses to light,spontaneous and elicited

eye movements, corneal responsesPUPILLARY LIGHT RESPONSES:

Simmetrically reactive round pupils:

Exclude midbrain damage (2 to 5 mm )

Enlarged pupil (>5 mm), unreactive or poorly reactive:

Intrinsic midbrain lesion (ipsilateral) by mass effect (contralateral).

Unilateral pupillary enlargement: Ipsilaterall mass.

Oval and slightly eccentric pupils:

Early midbrain third nerve compression.

Bilaterally dilated and unreactive Severe midbrain damage by transtentorial

pupils: herniation or anticholinergic drugs toxicity.

Reactive bilaterally small but not pinpoint (1 to 2.5 mm):

Metabolic encephalopathy, deep bilateral hemispheral lesions as hydrocephalus or thalamic hemorrhage

Very small but reactive pupil(Less than 1 mm): 

Narcotic or barbiturate overdose or bilateral pontin damage.

Ocular MovementsOcular MovementsEye movements are the second sign of importance in determining

if the brainstem has been damaged.

EYE MOVEMENTS

Adducted eye at rest:Lateral rectus paresis due to VI nerve lesion. If is bilateral is due to intracraneal hypertension.

Abducted eye at rest, plus ipsilateral pupilary enlargement :

Medial rectus due to III nerve dysfunction.

Vertical separation of the ocular Pontin or cerebellar lesion

Globes. (Skew deviation) :

Coma and spontanous conjugate horizontal roving movements :

Midbrain and pons intact

“Ocular bobbing”. Brisk downward and slow upward movement of the globes with loss of horizontal eye movements :

Bilateral pontine damage

“Ocular dipping”. Slower, arrhytmic downward followed by a faster upward movement with normal reflex horizontal gaze :

Anoxic damage to the cerebral cortex.

Thalamic and upper midbrain lesions: Eyes turned down and inward.

Brainstem ReflexesRespiratory pattern

Shallow, slow, well-timed regular

Suggest metabolic or drug depression.

Breathing:

Rapid, deep (Kussmaul) breathing:

Metabolic acidosis or ponto-mesencephalic lesions.

Cheyne-Stokes breathing, with light

Mild bihemispherical damage

or metabolic supression.

Coma:

Agonal gasps: Bilateral lower brainstem damage. Terminal respiratory pattern.

Anatomy and Physiology- Anatomy and Physiology- General Structure and General Structure and

FunctionFunction

Spinal Column:Spinal Column:• Made up of 26 vertebrae stacked

on top of one another• Divided into 5 areas; cervical, cervical,

thoracic, lumbar, sacral, and coccyxthoracic, lumbar, sacral, and coccyx• “Joint” at the superior end of the spinal

“Long Bone” VERY FLEXIBLE:VERY FLEXIBLE:• Allows flexion, extension, and rotation of

the head• The head acts as a weighted lever

during acceleration/ deceleration• Common site of spinal injuries

Bony spinal injuries may or may not be associated with spinal cord injury These bony injuries include:

Compression fractures of the vertebrae Comminuted fractures of the vertebrae Subluxation (partial dislocation) of the vertebrae

Other injuries may include: Sprains- over-stretching or tearing of ligaments Strains- over-stretching or tearing of the muscles

Cutting, compression, or stretching of the spinal cord Causing loss of distal function, sensation, or motion Caused by:

Unstable or sharp bony fragments pushing on the cord, or Pressure from bone fragments or swelling that interrupts the blood

supply to the cord causing ischemia

Immediate and irreversible loss of sensation and motionImmediate and irreversible loss of sensation and motion

Cutting, compression, or stretching of the spinal cordCutting, compression, or stretching of the spinal cord

Occurs at the time of impact/injuryOccurs at the time of impact/injury

Injury DelayedInjury Delayed Occurs later due to swelling, ischemia, or movement of Occurs later due to swelling, ischemia, or movement of sharp or unstable bone fragmentssharp or unstable bone fragments May be avoided if spine immobilized during extrication, May be avoided if spine immobilized during extrication, packaging, treatment, and transportpackaging, treatment, and transport

Complete injury to specific spinal tracts with reduced Complete injury to specific spinal tracts with reduced function distallyfunction distally

Other tracts continue to function normally with distal function Other tracts continue to function normally with distal function intactintact

Mechanism of InjuryMechanism of Injury Physical manner and forces Physical manner and forces

involved in producing injuries or involved in producing injuries or potential injuriespotential injuries

Valuable tool in determining if the Valuable tool in determining if the a particular set of circumstances a particular set of circumstances could have caused a spinal injurycould have caused a spinal injury

Mechanisms likely to produce Mechanisms likely to produce spinal injuries occur in MVAs, spinal injuries occur in MVAs, falls, violence, and sports falls, violence, and sports (including diving accidents)(including diving accidents)

Hyperextension Hyperextension - - Excessive/abnormal bending back Excessive/abnormal bending back of the head beyond its normal of the head beyond its normal range of motionrange of motion

Hyperflexion Hyperflexion - Excessive/abnormal bending - Excessive/abnormal bending forward of the chin toward the chest. This is forward of the chin toward the chest. This is one mechanism seen when patients are one mechanism seen when patients are ejected from moving vehiclesejected from moving vehicles

Flexion injuriesFlexion injuriesThe most common fracture mechanism in cervical The most common fracture mechanism in cervical injuries is injuries is hyperflexion.hyperflexion.

Anterior subluxationAnterior subluxation occurs when the posterior occurs when the posterior ligaments rupture. ligaments rupture. Since the anterior and middle columns remain Since the anterior and middle columns remain intact, this fracture is stable.intact, this fracture is stable.

Simple wedge fractureSimple wedge fracture is the result of a pure is the result of a pure flexion injury. The posterior ligaments remain intact. flexion injury. The posterior ligaments remain intact. Anterior wedging of 3mm or more suggests fracture. Anterior wedging of 3mm or more suggests fracture. Increased concavity along with increased density Increased concavity along with increased density due to bony impaction. Usually involves the upper due to bony impaction. Usually involves the upper endplate.endplate.

Unstable wedge fracture Unstable wedge fracture is an unstable flexion is an unstable flexion injury due to damage to both the anterior column injury due to damage to both the anterior column (anterior wedge fracture) as the posterior column (anterior wedge fracture) as the posterior column (interspinous ligament). (interspinous ligament).

Unilateral interfacet Unilateral interfacet dislocation dislocation is due to both is due to both flexion and rotation. flexion and rotation.

Bilateral interfacet Bilateral interfacet dislocation dislocation is the result of is the result of extreme flexion. BID is unstable and is associated extreme flexion. BID is unstable and is associated with a high incidence of cord damage.with a high incidence of cord damage.

Flexion teardrop fracture Flexion teardrop fracture is the result of extreme is the result of extreme flexion with axial loading. It is unstable and is flexion with axial loading. It is unstable and is associated with a high incidence of cord damage. associated with a high incidence of cord damage.

Anterior atlantoaxial dislocation Anterior atlantoaxial dislocation

Hyperotation Hyperotation - - Excessive/abnormal Excessive/abnormal rotation. This may rotation. This may produce injuries in any produce injuries in any area of the spine.area of the spine.

Axial LoadingAxial Loading- Sudden/excessive compression of the spine. Examples include falling and landing on your feet or ejection from a vehicle and landing on your head

Axial compression injuriesAxial compression injuries Jefferson fracture is a burst fracture of the ring of C1 with lateral displacement of both articular masses. Burst fracture at lower cervical level

Axial Distraction - Sudden/excessive elongation of the spine caused by stretching or tearing anywhere along the spinal column. Example: hanging.

This is a hang man’s fracture suffered This is a hang man’s fracture suffered by a woman that was ejected from by a woman that was ejected from her car in a roll-over MVA. She her car in a roll-over MVA. She apparently got hung up on the apparently got hung up on the shoulder belt and got hung.shoulder belt and got hung.

Lateral radiograph of type II Lateral radiograph of type II Hangman's fracture (pars Hangman's fracture (pars interarticularis fracture of C2 – interarticularis fracture of C2 – Levine and Effendi's Levine and Effendi's classification classification 20,2120,21); it is an ); it is an unstable spine because of the unstable spine because of the discontinuity of central axial discontinuity of central axial spinal pillarspinal pillar

ShockShock is a condition in which the cardiovascular is a condition in which the cardiovascular system fails to perfuse tissues adequatelysystem fails to perfuse tissues adequately

An impaired cardiac pump, circulatory system, An impaired cardiac pump, circulatory system, and/or volume can lead to compromised blood flow and/or volume can lead to compromised blood flow to tissuesto tissues

These three parts can be called the “perfusion triangle.”– When a patient is in

shock, one or more of the three parts is not working properly.

Shock• Inadequate systemic oxygen delivery

activates autonomic responses to maintain systemic oxygen delivery• Sympathetic nervous system

NE, epinephrine, dopamine, and cortisol release• Causes vasoconstriction, increase in HR, and increase of cardiac

contractility (cardiac output)

• Renin-angiotensin axis Water and sodium conservation and vasoconstriction Increase in blood volume and blood pressure

ShockShock

• Cellular responses to decreased systemic oxygen Cellular responses to decreased systemic oxygen deliverydelivery• ATP depletion ATP depletion → ion pump dysfunction→ ion pump dysfunction• Cellular edemaCellular edema• HydrolysisHydrolysis of cellular membranes and cellular death of cellular membranes and cellular death

• Goal is to maintain cerebral and cardiac perfusionGoal is to maintain cerebral and cardiac perfusion• Vasoconstriction of splanchnic, musculoskeletal, and Vasoconstriction of splanchnic, musculoskeletal, and

renal blood flowrenal blood flow• Leads to Leads to systemic metabolic lactic acidosis systemic metabolic lactic acidosis that that

overcomes the body’s compensatory mechanismsovercomes the body’s compensatory mechanisms

Global Tissue HypoxiaGlobal Tissue Hypoxia

• Endothelial inflammation and Endothelial inflammation and disruptiondisruption

• Inability of OInability of O22 delivery to meet delivery to meet demanddemand

• Result: Result: • Lactic acidosisLactic acidosis• Cardiovascular insufficiencyCardiovascular insufficiency• Increased metabolic demandsIncreased metabolic demands

Cell death

Inadequate oxygen delivery

Catecholamines and other responses

Anaerobic metabolism

Cellular dysfunction

Generalized State of Hypoperfusion

What is shock?What is shock?

Shock. Kinds of shock. Shock. Kinds of shock. Mechanisms of disorders of general Mechanisms of disorders of general

hemodynamics and microcirculation at shock.hemodynamics and microcirculation at shock. ShockShock is a state of organ hypoperfusion with resultant cellular is a state of organ hypoperfusion with resultant cellular

dysfunction and death. dysfunction and death. Mechanisms may involve:Mechanisms may involve:decreased circulating volume, decreased circulating volume, decreased cardiac output, decreased cardiac output, vasodilation, vasodilation, sometimes with shunting of blood to bypass capillary exchange beds. sometimes with shunting of blood to bypass capillary exchange beds. SymptomsSymptoms include altered mental status, tachycardia, hypotension, include altered mental status, tachycardia, hypotension,

and oliguria. and oliguria. DiagnosisDiagnosis is clinical, including BP measurement and sometimes is clinical, including BP measurement and sometimes

markers of tissue hypoperfusion (eg, blood lactate, base deficit). markers of tissue hypoperfusion (eg, blood lactate, base deficit). TreatmentTreatment is with fluid resuscitation, including blood products if is with fluid resuscitation, including blood products if

necessary, correction of the underlying disorder, and sometimes necessary, correction of the underlying disorder, and sometimes vasopressors.vasopressors.

STAGES OF SHOCKSTAGES OF SHOCK

Non-progressive StageNon-progressive Stage Reflex compensatory mechanisms are activated.Reflex compensatory mechanisms are activated. Profusion of vital organ is maintainedProfusion of vital organ is maintained

Progressive StageProgressive Stage Tissue hypoperfusion.Tissue hypoperfusion. Circulatory & metabolic imbalances leading to Circulatory & metabolic imbalances leading to

AcidosisAcidosis..

Irreversible StageIrreversible Stage Cellular & tissue injury.Cellular & tissue injury. Even with correction of haemodynamic defects, Even with correction of haemodynamic defects,

survival is not possible.survival is not possible.

Stages of ShockStages of Shock

❇❇ Initial stageInitial stage - - tissues are under perfused, decreased CO, tissues are under perfused, decreased CO, increased anaerobic metabolism, lactic acid is buildingincreased anaerobic metabolism, lactic acid is building

❇❇ Compensatory stageCompensatory stage - R - Reversible. SNS activated by low eversible. SNS activated by low CO, attempting to compensate for the decrease tissue CO, attempting to compensate for the decrease tissue perfusion. perfusion.

❇❇ Progressive stageProgressive stage - - FailingFailing compensatory mechanisms: compensatory mechanisms: profound vasoconstriction from the SNS ISCHEMIA profound vasoconstriction from the SNS ISCHEMIA Lactic acid production is high Lactic acid production is high metabolic acidosis metabolic acidosis

❇❇ Irreversible or refractory stageIrreversible or refractory stage - - Cellular necrosis and Cellular necrosis and Multiple Organ Dysfunction SyndromeMultiple Organ Dysfunction Syndrome may occur may occur

DEATH IS IMMINENT!!!!DEATH IS IMMINENT!!!!

NEUROHUMORAL MECHANISMS MAINTAIN NEUROHUMORAL MECHANISMS MAINTAIN CARDIAC OUTPUT AND BLOOD PRESSURE:CARDIAC OUTPUT AND BLOOD PRESSURE: Baroreceptors reflexesBaroreceptors reflexes Release of catecholamineRelease of catecholamine Activation of renin-angiotensin axisActivation of renin-angiotensin axis ADH releaseADH release Generalized sympathetic stimulationGeneralized sympathetic stimulation

DIFFERENT CLINICAL OUTCOME OF THESE DIFFERENT CLINICAL OUTCOME OF THESE COMPENSATORY MECHANISMS:COMPENSATORY MECHANISMS: TachycardiaTachycardia Peripheral vasoconstriction (cool & pale Peripheral vasoconstriction (cool & pale

skin)skin) Renal conservation of fluidRenal conservation of fluid

WIDESPREAD HYPOXIA:WIDESPREAD HYPOXIA:Anaerobic glycolysisAnaerobic glycolysisProduction of lactic acidosisProduction of lactic acidosispH lead to blunting of vasomotor pH lead to blunting of vasomotor response leading to vasodilatationresponse leading to vasodilatationPeripheral pooling of bloodPeripheral pooling of bloodcardiac outputcardiac output

DIFFERENT CLINICAL OUTCOME DIFFERENT CLINICAL OUTCOME OF THESE FAILING MECHANISMS:OF THESE FAILING MECHANISMS:

Feeble, failing pulseFeeble, failing pulseMental confusionMental confusionUrine outputUrine output

PROGRESSIVE STAGEPROGRESSIVE STAGE

WIDESPREAD CELLULAR INJURY:WIDESPREAD CELLULAR INJURY: Damage to the organelle of cellsDamage to the organelle of cells Leakage of lysosomal enzymesLeakage of lysosomal enzymes Production of nitric oxide by cellsProduction of nitric oxide by cells Worsened myocardial contractilityWorsened myocardial contractility

DIFFERENT CLINICAL OUTCOME OF DIFFERENT CLINICAL OUTCOME OF CELLULAR INJURY:CELLULAR INJURY:

Septic shock (entry of intestinal flora into Septic shock (entry of intestinal flora into circulation)circulation)

Complete renal shutdown (acute tubular Complete renal shutdown (acute tubular necrosis)necrosis)

Downward clinical spiralDownward clinical spiral

IRREVERSIBLE STAGEIRREVERSIBLE STAGE

COMPENSATORY MECHANISMS: Sympathetic Nervous System (SNS)-

Adrenal Response

SNS - Neurohormonal response SNS - Neurohormonal response Stimulated by Stimulated by baroreceptorsbaroreceptors

Increased heart rateIncreased heart rate

Increased contractilityIncreased contractility

Vasoconstriction (Afterload)Vasoconstriction (Afterload)

Increased PreloadIncreased Preload

COMPENSATORY COMPENSATORY MECHANISMS: MECHANISMS: Sympathetic Sympathetic Nervous System (SNS)-Adrenal Nervous System (SNS)-Adrenal

ResponseResponse SNS - Hormonal: SNS - Hormonal: Renin-angiotension Renin-angiotension systemsystem

Decrease renal perfusionDecrease renal perfusion

Releases renin Releases renin angiotension I angiotension I

angiotension II potent vasoconstriction &angiotension II potent vasoconstriction &

releases aldosterone adrenal cortexreleases aldosterone adrenal cortex

sodium & water retention ( intravascular sodium & water retention ( intravascular volume)volume)

COMPENSATORY MECHANISMS: COMPENSATORY MECHANISMS: Sympathetic Nervous System Sympathetic Nervous System

(SNS)-Adrenal Response(SNS)-Adrenal Response SNS - Hormonal: SNS - Hormonal: Antidiuretic HormoneAntidiuretic Hormone

Osmoreceptors in hypothalamus stimulatedOsmoreceptors in hypothalamus stimulated

ADH released by Posterior pituitary gland ADH released by Posterior pituitary gland

Vasopressor effect to increase BPVasopressor effect to increase BP

Acts on renal tubules to retain waterActs on renal tubules to retain water

COMPENSATORY COMPENSATORY MECHANISMS: MECHANISMS: Sympathetic Sympathetic Nervous System (SNS)-Adrenal Nervous System (SNS)-Adrenal

ResponseResponse SNS - Hormonal: SNS - Hormonal: Adrenal CortexAdrenal Cortex Anterior pituitary releases Anterior pituitary releases

adrenocorticotropic hormone (ACTH)adrenocorticotropic hormone (ACTH) Stimulates adrenal Cortex to release Stimulates adrenal Cortex to release

glucorticoidsglucorticoids Blood sugar increases to meet increased Blood sugar increases to meet increased

metabolic needsmetabolic needs

Types of Shock

• Hypovolemic or Haematogenic

• Traumatic Shock.• Septic• Cardiogenic • Anaphylactic• Neurogenic • Obstructive

Complications of Shock• Acute Respiratory Distress Syndrome

Literature: Literature: 1.1. General and clinical pathophysiology / Edited by Anatoliy V. General and clinical pathophysiology / Edited by Anatoliy V.

Kubyshkin – Vinnytsia: Nova Knuha Publishers – 2011. – P. 642–Kubyshkin – Vinnytsia: Nova Knuha Publishers – 2011. – P. 642–651.651.

2.2. Gozhenko A.I. General and clinical pathophysiology / A.I. Gozhenko A.I. General and clinical pathophysiology / A.I. Gozhenko, I.P. Gurcalova // Study guide for medical students Gozhenko, I.P. Gurcalova // Study guide for medical students and practitioners. Edited by prof. Zaporozan, OSMU. – Odessa. and practitioners. Edited by prof. Zaporozan, OSMU. – Odessa. – 2005. – P. 314–320.– 2005. – P. 314–320.

3.3. Essentials of Pathophysiology: Concepts of Altered Health Essentials of Pathophysiology: Concepts of Altered Health States (Lippincott Williams & Wilkins), Trade paperback States (Lippincott Williams & Wilkins), Trade paperback (2003) (2003) / / Carol Mattson Porth, Kathryn J. Gaspard. – P. 328 – Carol Mattson Porth, Kathryn J. Gaspard. – P. 328 – 336; 725 – 745. 336; 725 – 745.

4.4. Symeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, Symeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, AUS medicine Publishing. – 2010. – P. 531–536. AUS medicine Publishing. – 2010. – P. 531–536.

5.5. Robbins and Cotran Pathologic Basis of Disease 8th edition./ Robbins and Cotran Pathologic Basis of Disease 8th edition./ Kumar, Abbas, Fauto. – 2007. – Chapter Kumar, Abbas, Fauto. – 2007. – Chapter 2020. – P. . – P. 758–775758–775..

6.6. Copstead Lee-Ellen C. Pathophysiology / Lee-Ellen C. Copstead, Copstead Lee-Ellen C. Pathophysiology / Lee-Ellen C. Copstead, Jacquelyn L. Banasik // Elsevier Inc, 4th edition. – 2010. – P. Jacquelyn L. Banasik // Elsevier Inc, 4th edition. – 2010. – P. 927–930, 936–937.927–930, 936–937.

7.7. Pathophysiology, Concepts of Altered Health States, Carol Pathophysiology, Concepts of Altered Health States, Carol Mattson Porth, Glenn Matfin. Mattson Porth, Glenn Matfin. –– New York, Milwaukee. New York, Milwaukee. –– 2009. 2009. –– P.P. 1299–1453 1299–1453..