Neurotrauma and intensive care Flashcards

Question

GOS 2

Answer 1

Severe disability (conscious but dependent)

Answer 2

Moderate disability (independent but disabled)

Answer 3

Good recovery | (Can resume normal activities)

Answer 4

Lower severe disability

Answer 5

Upper severe disability

Answer 6

Lower moderate disability

Answer 7

Upper moderate disability

Answer 8

Lower good recovery

Answer 9

Upper good recvoery

Answer 10

Mood disturbance Cognitive impairment Personality changes Social Family effects

Answer 11

Mechanical load that translates into deformation of cerebral tissue which then initiate cellular responses that lead to disturbances in autoregulation and metabolism

Answer 12

Skull # EDH Contusions (coup or contrecoup)

Answer 13

High positive pressure at coup site and transmission of force vector through the brain parenchyma, generating a slapping effect to the contrecoup site. At the cellular level, high negative pressure at the contrecoup site, the development of cavitation bubbles known as contrecavitations and the brain parenchyma bouncing against the inner posterior skull are associated with contrecoup lesions.

Answer 14

More severe at the crest of gyrus than at the sulcus Associated with swelling that subsides with time

Answer 15

Occurs due to inertial forces during translational or rotational motion. CSF significantly increases convolutional gliding and shear strain Brain displacement lags behind skull and dura and occurs in different regions of the brain parenchyma itself causing WM damage.

Answer 16

More mobile relative to the region of the skull base White matter is stiffer than grey matter and thus more strain is distributed at the interface.

Answer 17

Vascular, neural and dural elements (e.g. distal ICA, optic and oculomotor nerves, olfactory nerves and pituitary stalk) that tether the brain to the skull are most susceptible. Splenium of the corpus callosum Dorsolateral brainstem can also experience DAI due to a similar trajectory to that of the skull base.

Answer 18

General translational and angular motion of the head. Rotational insults induce shear straing.

Answer 19

When a single inertial load combineswith a minor trauma impact load

Answer 20

Occurs with gradual compression (e.g. closing elevator door) Steady load results in skull fractures and cerebral injuries that are deeper than cortical contusions from an impact load. In contrast to blunt impact trauma, energy from crushing trauma tends to be transmitted to the foramina and hiatus of the middle cranial fossa, causing damage to associated cranial nerves, SNS and intima of blood vessels.

Answer 21

Focal or diffuse Anatomical

Answer 22

2% of all brain injuries More common in patients \<50 Particularly in paediatric patients primarily due to meningeal and diploic bein haemorrhage

Answer 23

Either due to fracture of the squamous part of temporal bone causing MMA laceration Venous sinus injury Fracture haematoma EDH constrained by periosteum which passes through the cranial sutures so EDH do not cross suture line

Answer 24

Dura is tightly adherent to skull Lower venous pressure

Answer 25

Type 1- acute Type 2- subacute Type 3- chronic

Answer 26

A hyperdense lesion with swirl sign indication of bleeding, rise in pressure eventually produces a tamponade of the bleeding site and progresses to type II, a homogenous hyperdense and organised clot. Type II is characterised by a low-density collection to blood resorption by perivascular tissue along with a contrast-enhanced membrane consisting of neovascularity and granulation tissue.

Answer 27

Contralateral hemiparesis Ipsilateral oculomotor nerve paresis Decerebrate rigidity Arterial hypertension Cardiac arrhythmias Respiratory disturbanecs if uncorrected leading to apnoea and death.

Answer 28

Tearing of dural bridging veins Tearing of superficial pial arteries

Answer 29

Crescent-shaped, hyperdense collection

Answer 30

Isodense Symptomatic improvement 7-21/7

Answer 31

Subacute SDH

Answer 32

\>21/7 Hypodense May not present symptomatically until there is significant mass effect

Answer 33

Chronic SDH

Answer 34

Stereotypic motor disorders Impaired oculomotor reflexes and following uncal herniation, unilaterally fixed and dilated pupils. Arterial bleeds are associated with larger clots near the Sylvian fissure

Answer 35

Reaccumulation Infection (e.g. osteomyelitis, meningitis, ventriculitis)

Answer 36

Time to evacuation Age Extent of neurological deficit Sex Post-op ICP

Answer 37

0.25-1g/kg body weight Restrict mannitol use prior to ICP monitoring to patients with signs of transtentorial herniation or progressive neurological deterioration not attributable to extracranial causes

Answer 38

Looked at the use of bifrontotemporoparietal decompressive craniectomy in adults under the age of 60y with refractory intracranial hypertension and diffuse brain injury Within 72h of injury Australia, NZ and Saudi Arabia

Answer 39

DECRA trial showed that patients undergoing craniectomy had worse ratings on the GOS-E at 6 months than those receiving standard care (P = 0.03), although the rates of death were similar at 6 months (19% and 18%, respectively). Reduced ICP

Answer 40

NEJM Hutch 2016 In patients with traumatic brain injury (TBI) and intracranial hypertension refractory to medical management, does decompressive craniectomy as a last-tier intervention improve outcomes as measured by the Extended Glasgow Outcome Scale (GOS-E)?

Answer 41

. This trial showed that craniectomy increased the number of favorable outcomes compared to continued medical management and that for every 100 patients managed surgically vs medically there were 22 more survivors. Of these 22, 27% were in a vegetative state, 36% had lower severe disability (dependent on others for care) and 36% had upper severe disability (independent at home) or better. This informs the debate around historical concerns that decompressive craniectomy simply increases the number of patients who survive in a vegetative state. While surgical intervention did result in more vegetative patients than medical management, it also resulted in higher rates of upper severe disability, which is considered a favorable outcome. The rates of moderate disability and good recovery were similar to those who received medical management.

Answer 42

In patients with severe blunt traumatic brain injury (TBI) does early and sustained cooling compared with standard care improve neurological outcomes at 6 months? JAMA 2018

Answer 43

aAm for normothermia in my patients with TBI Significantly: hypothermia did not improve 6 month outcome, but increased pneumonia, ventilation days, bradycardia and noradrenaline use Hypothermia did not reduce ICP

Answer 44

Minor head injury that leads to a small haematoma from tearing of the stretched bridging veins that span the subdural space and are thus unsupported in those with cerebral atrophy. The initial insult is often forgotten. In a subset of patients an inflammatory neomembrane forms and potentiates ongoing haemorrhage and swelling of the enclosed haematoma by the breakdown of blood products and the development of an osmotic gradient across the neomembrane. The clinical presentation can thus be several weeks after the initial insult

Answer 45

Headache Hemiparesis Speech disturbance Behavioural disturbance Coma if large and untreated

Answer 46

More likely to progress to coma rapidly and are consequently treated at a lower absolute volume.

Answer 47

Most commonly over the cerebral convexity but can be interhemispheric or over the tentorium and more rarely in the posterior fossa.

Answer 48

One or two burrholes Mini-craniotomy Closed drainage systems

Answer 49

Infection Seizures Recurrence

Answer 50

The recurrence rate of subdurals can be reduced by subdural drain for 48h with no significant increase in morbidity.

Answer 51

Frequent finding in closed head injuries due to direct damage to cortical vessels. Correlates with poorer outcome and more severe injury, Appears to be a reflection of a greater degree of violence at injury rather than secondary injury

Answer 52

May contribute to cerebral swelling Haemodynamically significant vasospasm (can be observed as early as 2 days post-injury) Disturbance of cerebral autoregulation

Answer 53

Associated with the progression of associated cerebral contusions More time spent on ICU Less likely to be discharged home 1.5x more likely to due during acute hospitalisation In penetrating TBI there is a significant association between SAH and poor outcome.

Answer 54

1.5-3% of all head trauma Predominantly severe.

Answer 55

Damage to septum pellucidum, choroid plexus and subependymal forniceal veins are seen at post-mortem exams in patiets with primary IVH

Answer 56

22% regain independence

Answer 57

Focal or mutlifocal Cortical or subcortical regions Herniating contusions Intermediary contusions

Answer 58

Cerebral contusion

Answer 59

Occur when one tissue is displaced from one cranial compartment to another, typically along the margin of the falx, the tentorium or the foramen magnum, leading to compression of the herniating tissue.

Answer 60

Subcortical lesions affecting the corpus callosum, basal ganglia, hypothalamus and brainstem.

Answer 61

24h Associated with marked reduction of CBF to the contused cortex which normalises 7/7 after injury during which focal areas of hyperaemia can appear. Can be delayed as long as 10/7.

Answer 62

Caused by angular acceleration leading to damage of axonal integrity. Diffuse brain injury is seen in up to 50% of TBIs Defined as diffuse damage in the cerebellar hemispheres, corpus callosum, brainstem and cerebellum. Long tract structures (axons and blood vessels) are, particularly at risk.

Answer 63

Adams 1-3 Based on MR

Answer 64

Grey-white matter interface (commonly parasagittal white matter of frontal lobes and periventricular temporal lobes)

Answer 65

Frontal and temporal lobes Those without lucid intervals

Answer 66

Focal lesions in the corpus callosum (commonly posterior body and splenium)

Answer 67

Brainstem (commonly dorsolateral and rostral midbrain, cerebellar peduncles, medial lemnisci and corticospinal tracts)

Answer 68

Grade I and II typically show marked improvement in GCS within 2/52 Grade III requires 2 months for recovery

Answer 69

Established by immunostaining for B-APP and autopsy and identifying axonal retraction balls in deep white matter.

Answer 70

Transient neurological disturbance caused by rapid linear and/or rotational acceleration and deceleration forces resulting in a disruption in cerebral structure of vascular phsyiology. Can be clinically based on LOC, loss of memory, alteration in mental state, focal neurological deficit.

Answer 71

Non-blunt projectile breaching cranium and dura mater. Associated with worse Px

Answer 72

When a projectile also causes an exit wound

Answer 73

Generates wave of compression and re-expansion (cavitation wave) and inflicts focal shearing damage, parenchymal contusions and haematomas

Answer 74

Track crossing ventricle Involving both hemispheres Crossing the geographical centre of the brain Associated vascular injury

Answer 75

3.5ml O2/ 100g/ min

Answer 76

Aerobic metabolism is the primary method of energy production. Disturbed after TBI with a significant increase in anaerobic glycolytic turnover and elevated extracellular lactate. Hyperglycolysis contributes to prolonged elevated lactate: glucose, CSF lactic acidosis and impaired mitochondrial function Duration and extent of hyperglycolysis may correlate with the severity of the injury.

Answer 77

Reduces in comatose patients with TBI

Answer 78

Law of laminar flow in a cylindrical tube. Can be used to describe CBF after TBI CBF = k[CPP x d(4)]/ 8xlxv Where K is a constant d is the vessel diameter l is artery length v is blood viscosity.

Answer 79

Autoregulation is impaired or absent in the majority of severe TBI patients at some point in their clinical course When autoregulation is lost, the brain becomes vulnerable to systemic pressure disturbances leading to secondary insults (e.g. ischaemia from reduced CBF or oedema from excessive CBF)

Answer 80

Hct and serum fibrinogen affect CBF and induce an autoregulatory response under normal physiological circumstances. Increase in viscosity causes an increase in arterial dilatation as it reduces metabolic supply. Following acute cerebral infarction, HCt and fibrinogen are associated with reduced CBF

Answer 81

The Process by which the PaCO2 affects CBF and the cerebral vasculature Hypercarbia results in vasodilation Hypocarbia in vasoconstriction

Answer 82

Changes in perivascular pH via carbonic anhydrase

Answer 83

The normal response to acetazolamide administration is vasodilation and augmentation of CBF to 30-60% over 10-15 minutes A failure to vasodilate in response to acetazolamide implies maximal vasodilation.

Answer 84

Hyperaemia and metabolic acidosis in CSF are associated with the acute phase of TBI (first 24h) Persistent loss of CO2 reactivity risks severe neurological compromise.

Answer 85

Causes both changes in CBF and AVDO2

Answer 86

Identified hypoxia (20%) and hypotension (18%) of TBI patients.

Answer 87

Arterial hypotension Hypoxaemia Reduced CPP Raised ICP Pyrexia

Answer 88

Glutamate activates NMDAR triggering neuronal depolarisation with unchecked Ca influx into mitochondria due to impaired ATP synthesis. Mitochondrial dysfunction leads to damaged tissue energy failure. These intracellular changes lead to cerebral oedema, raised ICP, vascular compression and herniation.

Answer 89

Measured with microdialysis Marker of anaerobic respiration and correlates with outcome after TBI. The raised ratio can be due to cerebral ischaemia or mitochondrial dysfunction. Lactate is metabolised to pyruvate in the mitochondria of axons and astrocytes

Answer 90

Studies of patients with GCS \<^ report a 25% incidence of reduced oxidative metabolism and metabolic crisis (LPR \>40) despite absence of systemic ischaemia which suggest LPR is an indicator of widespread mitochondrial dysfunction causing metabolic depression following TBI.

Answer 91

Looks at the pressure reactivity index- response of ICP to CBV. Between -1 and 1 -1 suggests good vasoreactivity. Frequently compromised on the first day after TBI, and the loss of autoregulation in the first 48h has a strong indication for additional secondary injury. Can allow real time CPPopt to maximise autoregulation.

Answer 92

Under normal conditions, the total volume of the intracranial cavity remains constant. Contains three components- blood, CSF and parenchyma An increase in one leads to a compensatory reduction in another to try and maintain a constant ICP. When compensatory mechanisms are exhausted, an exponential increase in ICP occurs.

Answer 93

Vasogenic Cytotoxic Interstitial Osmotic

Answer 94

Vasogenic edema occurs due to a breakdown of the tight endothelial junctions that make up the blood–brain barrier. This allows intravascular proteins and fluid to penetrate into the parenchymal extracellular space. Once plasma constituents cross the barrier, the edema spreads; this may be quite rapid and extensive. As water enters white matter, it moves extracellularly along fiber tracts and can also affect the gray matter. This type of edema may result from trauma, tumors, focal inflammation, late stages of cerebral ischemia and hypertensive encephalopathy.

Answer 95

In cytotoxic edema, the blood–brain barrier remains intact but a disruption in cellular metabolism impairs functioning of the sodium and potassium pump in the glial cell membrane, leading to cellular retention of sodium and water. Swollen astrocytes occur in gray and white matter. Cytotoxic edema is seen with various toxins, including dinitrophenol, triethyltin, hexachlorophene, and isoniazid. It can occur in Reye's syndrome, severe hypothermia, early ischemia, encephalopathy, early stroke or hypoxia, cardiac arrest, and pseudotumor cerebri.

Answer 96

Normally, the osmolality of cerebral-spinal fluid (CSF) and extracellular fluid (ECF) in the brain is slightly lower than that of plasma. Plasma can be diluted by several mechanisms, including excessive water intake (or hyponatremia), syndrome of inappropriate antidiuretic hormone secretion (SIADH), hemodialysis, or rapid reduction of blood glucose in hyperosmolar hyperglycemic state (HHS), formerly known as hyperosmolar non-ketotic acidosis (HONK). Plasma dilution decreases serum osmolality, resulting in a higher osmolality in the brain compared to the serum. This creates an abnormal pressure gradient and movement of water into the brain, which can cause progressive cerebral edema, resulting in a spectrum of signs and symptoms from headache and ataxia to seizures and coma.

Answer 97

Interstitial edema occurs in obstructive hydrocephalus due to a rupture of the CSF–brain barrier. This results in trans-ependymal flow of CSF, causing CSF to penetrate the brain and spread to the extracellular spaces and the white matter. Interstitial cerebral edema differs from vasogenic edema as CSF contains almost no protein.

Answer 98

Three distinct mechanisms Vasogenic- structural damage to BBB causes intravascular flow of protein-rich exudate into the interstitium, increasing extracellular volume without cell swelling. Cytotoxic- ion influxes and increased membrane permeability causes cytotoxic oedema and cellular swelling Osmotic- necrotic tissue is hyperosmolar, causing osmotic-gradient driven fluid accumulation in the cell.

Answer 99

Can initiate more tan 10% reduction in ICP among 86% of patients with autoregulation but only 35% of patients with impaired autoregulation.

Answer 100

Osmotic diuretic Free radical scavenger Improving microvascular flow by dehydrating endothelial cells Reducing HCt as well as the osmotic load.

Answer 101

Intractable ICP (46%)

Answer 102

1g/kg IV Should be given once patient adequately volume resuscitated as can add to hypovolaemia

Answer 103

Systemic Intracranial

Answer 104

Hypoxia Hypotension Hypocapnia Hypercapnia Hypothermia Hyperthermia Hypoglycaemia Hyperglycaemia Hyponatraemia Hypernatraemia Hyperosmolality Infection

Answer 105

Seizure Delayed haenatona SAH Vasospasm HCP Neuroinfection

Neurotrauma and intensive care Flashcards

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