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CH0576: The Biology of Disease-Dr Rosemary Bass Biology of Trauma Copyrighted work available under Creative Commons by-nc-nd 2.0 UK.

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Presentation on theme: "CH0576: The Biology of Disease-Dr Rosemary Bass Biology of Trauma Copyrighted work available under Creative Commons by-nc-nd 2.0 UK."— Presentation transcript:

1 CH0576: The Biology of Disease-Dr Rosemary Bass Biology of Trauma Copyrighted work available under Creative Commons by-nc-nd 2.0 UK

2 What do we mean by trauma? Physical trauma- wound/shock caused by sudden physical injury - can be caused by violence/accident Psychological trauma- something that causes psychological injury Link between the two forms of trauma - 25% trauma patients experience significant early psychological reactions. Some long term effects Physical trauma is emphasis of this lecture

3 Different kinds of Physical Trauma Today will talk about: - Brain trauma - Vascular trauma Other kinds of trauma:Skeletal, Thoracic Aortic Splenic Hepatic (any part of the body can undergo a sudden violent injury impacting on any part of skeleton or internal organ)

4 What causes major trauma?

5 In 2005 there were a total of 1,349 road accidents in Newcastle of which 9 were fatal, 96 serious and 1,244 slight. Newcastle upon Tyne Road Safety (City Council data)

6 Sports & Brain Trauma American Football - chronic brain trauma pattern in former NFL players (Amen et al (2011) J Neuropsychiatry Clin Neurosci. 23(1):98) Rugby Skiing Cycling – Bicycle accidents account for 800/500,000 injuries treated at hospitals in USA each year (risk of brain injury decreased 88% by wearing a helmet)

7 European Brain Injury Consortium (EBIC) study, 52% of head injuries were related to MVAs Trauma: Consequences of MVA (Motor Vehicle Accidents) Vascular trauma is also another extremely common result of MVA ( Vascular trauma is also another extremely common result of MVA ( see e.g. Gupta et al ANZ J. Surg. (2001) 71, 461–466) ● Brain Trauma ● Haemorrhage Physiological and metabolic consequences First MVA fatality was a pedestrian killed in 1889

8 Brain Trauma

9 Traumatic Brain Injury (TBI): definitions and risk factors Glasgow Coma scale used to define injury: GCS Mild TBI – Mild Concussion GCS 9-12 Moderate TBI – Haemorrhage or Contusion (most MVA) GCS 3-8 Severe TBI – Cognitive/physical disability or death Risk Factors: Age: 15-24, 6 mon - 2yrs, elderly 2:1 Male: Female High crime areas Trauma categories: Blunt: (closed, non-missile) – falls Open (penetrating, missile)

10 Incidence of death from head injury approx 7 /100,000 Head injury is major cause of morbidity in MVA survivors In a study where 3000 head injuries were assessed according to GCS when arrived at hospital: GCS Mild TBI – Mild Concussion 2668 GCS 9-12 Moderate TBI – Haemorrhage or Contusion 133 GCS 3-8 Severe TBI – Cognitive/physical disability or death 102 After 1 year 1397 were still disabled - 90% of these had initially been assess as having mild injuriesAfter 1 year 1397 were still disabled - 90% of these had initially been assess as having mild injuries

11 We Now Know The Brain is Vital for Life & Correct Body Functioning Wasn’t always so... Queen Hatshepsut Ancient Egyptians thought that the heart was the location of personality and intelligence

12 The Brain is Vital for Life & Correct Body Functioning Examples: Limbic System Endocrine Function Cognitive Function Personality Control of motor functions – motor cortex

13 Purves et al Neuroscience Limbic System involved in emotions esp. relating to survival, primitive behavioural responses Sensory systems

14 Endocrine System Hypothalamus = “Commander in chief” Produces “releasing hormones” which act on the anterior pituitary to control homeostasis by downstream regulation of other hormones Also provides link between nervous system and endocrine system

15 Most hormones from the anterior pituitary control other endocrine organs The exceptions are Growth Hormone and Prolactin

16 Cognitive Function Thought processing Memory Learning Speech Reading/Comprehension Self-awareness Mental Imagery Language Not completely mapped but associated with brain structures including the hypothalamus, amygdala, cerebral cortex

17 Control of motor functions Posterior parietal cortex LevelFunctionStructures HighStrategyAssociation areas of neocortex, basal ganglia MiddleTacticsMotor cortex, cerebellum LowExecutionBrain stem, spinal cord CNS has hierarchy of control levels Forebrain at top, spinal cord at bottom

18 Wilder Penfield Canadian Neurosurgeon (& others) Mapped using electrical stimuli during brain surgery

19 Where brain injury is & severity will determine dysfunction

20 Windscreen Coup Contrecoup Coup Contrecoup Brain injury after blunt trauma Coup: a. Direct trauma to brain b. Tearing of subdural veins c. trauma to brain base a b c Contrecoup: a. damage to hind brain b. shearing forces through brain

21 Section through head: Brain, skull and associated membranes Location of Haematomas (haemorrhage) Extradural (epidural) haematoma (dura and skull) Subdural haematoma (arachnoid and dura) Intracerebral (in brain matter) Contusion (bruise) – capillary damage and blood seepage into brain (Contains CSF)

22 Focal Brain Injury: Contusions – Epidural haematoma Caused by direct blow to the head (most common cause MVA)Caused by direct blow to the head (most common cause MVA) Contusions, brain lacerations & haemorrhage in a brain compartmentContusions, brain lacerations & haemorrhage in a brain compartment 85% cases due to tear in middle meningeal artery85% cases due to tear in middle meningeal artery 90% cases consequence of temporal fracture90% cases consequence of temporal fracture Blood clot over the dura: Distension/compression of other brain regions

23 Focal Brain injury: Contusions – Subdural haematoma Most common causes: MVA, falls in elderly, or due to alcohol 48 hours, top of brain 10-20% of TBI, tearing of bridging veins

24 Focal Brain Injury: Contusions – Intracerebral haematoma lshtm.ac.uk/ 2-3% of people with head injury – hours post impact Frontal Temporal - Infarction, necrosis, multiple haemorrhages, oedema, ICP (intracranial pressure) Behavioural changes: memory deficits, attention, motivation, emotion, sometimes hypersexuality

25 Diffuse brain injury [axonal injury (DAI)]: 3 categories: Mild : post-traumatic coma for 6-24 hours - Residual cognitive, psychological, sensorimotor deficits Moderate: Prolonged coma lasting > 24 hours - Impairment in cortex and diencephalon (thalamus, hypothalamus – midbrain) - Axonal tearing - Most common form and closely associated with MVA Severe: 64% survival rate, very prolonged loss of consciousness - Mechanical disruption of axons extending into brainstem Prolonged traumatic coma > 6 hours -Usually caused by sudden head movement -For example shaken baby syndrome

26 Pathological indicators of DAI: Axon Retraction ball Specimen stained with Bielschowsky stain Appear 12 hours to several days post injury 2-3 weeks Gliosis Reactive Gliosis (scarring), increase number of supporting cells at sites of axonal damage

27 Pathophysiology of TBI: Primary damage - impact - Injury to Neurons, Glia; (mechanical disruption debris & leakage) - vascular response (increased capillary endothelial permeability) Secondary damage – compromised circulation, brain shift - Cerebral oedema, brain swelling, haemorrhage, infection, ICP - Cerebral ischemia (focal/global) & tissue hypoxia Ischemic neurons cause glial permeability to Na + (cytotoxic)Ischemic neurons cause glial permeability to Na + (cytotoxic) Metabolic failure Ca 2+ influx, phospholipase activationMetabolic failure Ca 2+ influx, phospholipase activation Lactic acidosisLactic acidosis Tertiary damage – cardiorespiratory consequence - Apnea, hypotension, abnormal ECG

28 Metabolic and cellular event leading to Cerebral Ischemia haemorrhage RBC breakdown Hemoglobin and iron Increased free radical formation Secondary injury Tissue hypoxia Arachidonic acid release Decreased CBF Neutrophils Vasospasm/oedema Leukotriene production Activation of Kallikrein- kinin Vasoconstriction, thrombosis formation RBC and Platelet aggregation 5-HT release

29

30 Vascular Trauma Gupta et al ANZ J. Surg. (2001) 71, 461–466 Survey of 153 patients admitted to Royal Perth Hospital during a 6 year period Location & cause of vascular trauma: Neck Thorax Abdomen Upper limb Lower limb

31 Gupta et al ANZ J. Surg. (2001) 71, 461–466 Similar general physiological responses to different injuries

32 Haemorrhage (and shock): Credit: Anne Weston Red blood cells leaking out of a ruptured blood vessel.

33 Haemorrhage: Intro to cardiovascular haemodynamics Average blood volume litres (males at 5) Large haemorrhages – 30% total BV loss – Hypovolemic shock In shock (in humans) Systolic below 90 mmHg and mean arterial pressure is below 70 mmHg Prolonged hypotension

34 Initial signs of Shock: ● Narrowing of pulse pressure ● Rapid and weak pulse ● Faintness sensation when sitting or standing ● Clammy skin (cold and moist) ● Urine output drops to < 25 mls/hour (despite normal fluid intake)

35 Blood Pressure is Influenced by: CO = cardiac output Blood volume – changes suddenly in vascular injury Blood viscosity PR = peripheral resistance

36 Shock: Compensatory reduction mechanisms BP mean = CO x PR

37 Integrated response to haemorrhage: role of high pressure baroreceptors Located in carotid sinus and aortic arch Decreased firing rate Sympathetic activation Vagal inhibition Increased HR Increased Contractility Venoconstriction Selective arterial constriction Re-establish Arterial Pressure

38 Integrated response to haemorrhage: role of low pressure baroreceptors Decreased blood volume Decreased circulating volume Decreased activity LP baro Increased sympathetic outflow Vasoconstriction e.g. Kidney Info inputs to hypothalamus Stimulates ADH release Reduces renal water excretion Lowered ANP Reduces salt and water loss Regulation of Blood volume and osmolality to maintain CO & BP LP Baroreceptors in: Large systemic veins Pulmonary vessels Heart atrium & ventricles

39 ANP = Atrial Natriuretic Peptide (Atrial Natriuretic Factor)  Cardiac hormone involved in regulating blood pressure  ANP  blood pressure by  salt excretion  blood volume  vessel tension through receptors  ANP expression is triggered by  [salt] and  blood pressure  Feedback loop Corin Hypertension Preeclampsia Pro-ANP ANP Hypertension Receptor Lower blood pressure activation ?

40 Control of Thirst  Blood volume  Osmolarity Hypothalamus  ADH Release Kidneys  H 2 0 Reabsorption

41 Integrated response to haemorrhage: role of chemoreceptors Blood pressure decline drop off of perfusion through Carotid Sinus and Aortic arch. Local hypoxia increases firing rate Marked Increase in sympathetic output Inputs into NTS (nucleus tractus solitarius) Sympathetic activation caused by chemoreceptors much more pronounced than baro’s Brain Ischemia

42 Post-haemorrhage: major restoration of blood volume haemorrhage leads to blood hyperosmolality Stimulates osmoreceptors in the hypothalamus (OVLT) Strong stimulus to drink more water Transcapillary refill Movement of fluid from interstitium to blood plasma Fluid from interstitium to vasculature Appearance of plasma proteins in blood (albumin synthesis by liver) Intracellular water replaces interstitial fluid Raw material supply for Fluid loss

43 Prolonged Hypovolemic shock and multiple organ failure: Hypoperfusion of tissues (oedema) Low blood 0 2 levels Decreased urine production Increased nitrogen ‘waste’ products in blood Tissue necrosis Terminal Impaired Motility ARDS = acute respiratory distress syndrome

44 Summary of Lecture Physiological responses to trauma Brain trauma- Types of injury- blunt trauma (coup, contracoup) - Focal brain injury- epidural haematoma - subdural haematoma - Intracerebral haematoma - Diffuse brain injury - Brain cell death Vascular InjuryHow the body responds to hypovolemic shock

45 References – Textbooks: Boron, W.F. and Boulpaep, E.L. (Latest Edition) Medical Physiology. Saunders Elsevier Dmajanov, I (2009) Pathophysiology. Saunders, Elsevier McCance, K. L. & Huether, S. E. (2006). Pathophysiology. (The Biologic Basis for Disease in Adults and Children). 5 th Edit. Elsevier Mosby. + references provided throughout presentation Ref for Large schematic: Physiological Reviews, Vol. 79, No. 4, October 1999, pp Ischemic Cell Death in Brain Neurons Peter Lipton Bear, Connors, Paradiso. Neuroscience Exploring the Brain (2007) MVAS.html


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