1. Head Injury, Cranial Surgery and IICP
Intracranial problems include injuries and increased ICP.
NUR 2549

2. Unconsciousness
An abnormal state in which client is unaware of self or environment
Can be for very short time to long term coma
Care is designed to
Determine the cause
Maintain bodily functions
Support vital functions
Protect client from injury
Can be like fainting all the way to unarousable, all ranges in between. Not a diagnosis or disease, but manifestation of many pathophysiologic processes: trauma, metabolic disturbances, mass lesions, infections.
Care focuses on determining and correcting cause, maintaining function, protection from injury and hazards of immobility

3. Etiology
Arousal
State of being awake that depends on a group of neurons in the brainstem
Can maintain level of wakefulness even without functioning cortex
Consciousness involves 2 aspects: arousal and content. Arousal refers to state of wakefulness dependent on activity of RAS (reticular activating system). This is a network of nerve fibers and cell bodies in the reticular formation in the central brainstem with connections to many parts of the nervous system. An intact RAS can maintain a state of wakefulness, even if cortex is not functioning.

4. From Human
Physiology
RAS is located in
brain stem

5. Etiology Content part of consciousness
Ability to reason, think and feel
Also to react to stimulus with purpose and awareness
Controlled by cerebral hemispheres (higher centers)
Intellect and emotional function are also controlled in the same area.
Content refers to the ability to reasons, think, feel and react to stimuli with purpose and awareness. These are mediated by the cerebral hemispheres “higher centers”, where intellect and emotional functions are controlled.
Interruption of impulses from the RAS or alteration of the functioning of the cerebral hemispheres can cause unconsciousness.
Impaired consciousness will result from any condition that alters the function of the hemispheres or that depresses or destroys the upper brainstem.

6. Causes of unconsciousness can be grouped by cause: supratentorial mass lesions, subtentorial mass lesions, destructive lesions, metabolic and diffuse cerebral disorders.
Supratentorial mass lesions: generally interfere with consciousness by compressing and shifting cerebral contents, cause pressue on upper brainstem containing RAS. Occur above the tentorium (a fold of dura mater separating the cerebellum and the cerebrum), may be trauma, subarachnoid hemorrhage, intracerebral hemorrhage or infarction, tumors and abscesses. Most serious consequence of supratentorial mass lesion is herniation of cerebral hemisphere through tentorial notch, causing compression of brainstem, results in ischemia and infarction.
Subtentorial masses or destructive lesions occuring below the tentorium compress or destroy the RAS above the midpons, Pontine or cerebellar hemorrhage, infarction, tumor, abscess can cause brain compression, upward herniation through tentorial notch, downward herniation into foramen magnum.
Metabolic and diffuse cerebral disorders can cause altered conscious states. Can disturb cerebral metabolismna dregulation of cellular nutrition, electrolyte balance, oxygen and carbon dioxide regulation, and enzymatic. Problems are uremia, diabetes mellitus, hypoglycemia, alcohol intoxication, drug overdose (barbiturates), lead poisoning.

7. Major Reactions Two reactions affecting cerebral metabolism occur:
Cerebral ischemia /anoxia – brain isn’t getting enough oxygen and compensatory mechanisms take place
Cerebral edema results because the brain compensates by dilating blood vessels trying to get more oxygen
Regardless of the cause of unconsciousness, 2 processes affecting cerebral metabolism usually occur: cerebral ischemia-anoxia, and cerebral edema. Problem common to all metabolic brain diseases is decreased oxygen uptake. Must institute measure to ensure adequate systemic circulation, treat cerebral edema and increased ICP with hyperosmotic drugs and steroids.

8. Behavior
Document accurately what the client’s behavior is. Example: if the client opens eyes on command but not spontaneously, chart it as such. Be descriptive.
State of unconsciousness is defined by behavior and pattern of brain activity on EEG. In deepest unconsciousness, patient does not respond to painful stimuli, corneal and pupillary reflexes are absent, cannot swallow or cough, incontinent of urine and feces. EEG pattern shows decreased or absent neuronal activity-this patient is in a coma.
Behavior: picture states of unconsciousness as a continuum from hypoexcitable state of coma to hyperexcitable state of seizure. Normal alertness is between these 2 states, abnormalities range from slight disorientation to coma. Rather than relying on terms along the continuum that may be confusing like “lethargy”, describe LOC by noting specific behaviors. When deviation occurs, need systematic approach to assessment, Glasgow Coma Scale. See page 1610 in Lewis.

9. Glascow Coma Scale Used to document assessment in three areas
Eyes
Verbal response
Motor response
Normal is 15 and less than 8 indicates coma
Because of confusion and ambiguity about terms describing altered states of consciousness, GCS developed in areas assessed respond to definition of coma as inability to speak, obey commands, or open eyes with verbal or painful stimulus. Specific responses are given a number, can be graphed to see if patient is stable, improving, deteriorating. Nurse responsibility is to elicit the best response on each of the scales, higher scores mean higher level of brain functioning. Fully alert person is 15, 8 or less indicates coma.
GCS is specific and structured, saves time by using number ratings rather than lengthy descriptions, can discriminate between different or changing states.
GCS assess arousal aspect of consciousness.

10. From Rehabilitation
Nursing

11. From Rehabilitation
Nursing

12. Other Assessment
Assess bodily function including respiratory, circulatory and elimination
Pupil checks – are pupils equal and how they react to light
Extremity strength
Corneal reflex test
Always assess circulation and respirations first! Other neuro assessments are pupillary checks, extremity strength testing, corneal reflex testing.

13. Intracranial Pressure
Monro-Kellie hypothesis (applies only to children with a rigid skull and not neonates)
Skull is an enclosed space with three variables
Brain tissue
Blood
Cerebrospinal fluid
CP is the force exerted against the skull by it’s contents: brain tissue, blood, CSF.
Mechanisms that control total volume in cranial vault contribute to maintenance of normal ICP.
Brain tissue accounts for 80% of total volume, composed of neurons and glial cells plus interstitial and intracellular fluids. The blood brain barrier assists in keeping brain volume constant by prohibiting osmotically active substances from escaping the vascular space and entering the interstitial fluid.
Cerebral blood volume accounts for 10% of total cranial volume, affected by cerebral blood flow, factors affecting diameter of cerebral vessels and venous outflow. Vessel diameter is affected by small changes in carbon dioxide levels, a slight increase causing vasodilation and increased cerebral blood flow. Obstruction or impaired venous outflow via internal jugular veins results in back up and increase in cerebral blood volume.
Cerebrospinal fluid is 10% of total cranial volume. Constant volume of only ml even though production is ml/day. Produced by choroid plexus in ventricles, reabsorbed via arachnoid villi.
Only slight or transient increase in pressure can be tolerated before neurologic function may be impaired. IICP or intracranial hypertension is when intracranial pressure exceeds 10mm mercury, with a presssure range of mm mercury possibly requiring intervention. Pressures over 30mm mercury warrant immediate attention.
Monroe-Kelly hypothesis states intracranial pressure remains stable as long as the volume added is balanced by the volume displaced. So total volumes of CSF, blood and brain tissue are variable when compensatory mechanisms are intact. Limited compensation is possible by displacement of brain tissue, generally more effective in slowly expanding masses (tumor or chronic subdural hematoma). Increase CSF absorption and decreased production, displacement of CSF into spinal subarachnoid space, collapse of cerebral veins and dural sinuses, increased venous outflow, slight compression of brain tissue tolerated.

14. Intracranial Pressure
The skull cannot expand to allow for extra space occupying tissue or fluid
If one of the three components increases the other two must decrease in order to compensate
Any increase in volume of one component without decrease of another will result in IICP. (Mass lesions increase brain tissue volume: tumor, abscess, hematoma. Increase in CSF volume if unable to circulate CSF out or be reabsorbed: acute transition hydrocephalus, chronic increase in CSF).
Initially compensatory mechanisms allow intracranial pressure to remain normal, despite increase in volume of one of components in cranial vault. Adaptation is limited, as ICP rises, decompensation occurs resulting in compression and ischemia.

15. Intracranial Pressure
Other factors that influence intracranial pressure
Arterial pressure
Venous pressure
Intraabdominal and intrathoracic pressure
Posture
Temperature
Blood gases (left off handout)
Compression of veins caused by an increase in ICP results in reduction of total cerebral blood volume.
Displacement of cerebrospinal fluid from cranial subarachnoid space to spinal subarachnoid space (especially lumbar region) is also compensatory mechanism, plus increased rate of reabsorption as pressure gradient increases between subarachnoid space and venous sinuses.

16. Normal Intracranial Pressure
Pressure exerted by total volume from:
Brain tissue
Blood
Cerebrospinal fluid
Normal manometer reading –
Normal transducer reading – 0-15mm Hg

17. Cerebral Blood Flow
Amount of blood going through 100g of brain tissue in 1 minute – cerebral blood flow is 50ml/min per 100g
Brain uses 20% of the body’s oxygen
Brain uses 25% of body’s glucose

18. Autoregulation of Cerebral Blood Flow
Blood vessels alter their diameter to ensure a constant cerebral blood flow
Lower limit for MAP is 50mm Hg.
Below this, cerebral flow decreases and there is risk of ischemia
Upper limit is MAP of 150mmHg. Above this the cerebral blood vessels are maximally constricted. Blood vessels cannot constrict more to control high pressure. Blood brain barrier is disrupted and cerebral edema and ICP results
MAP= DBP + 1/3 Pulse Pressure
Autoregulation is automatic alteration in diameter of cerebral blood vessels to maintain a constant blood flow to the brain during changes in systemic arterial pressure. Purpose is to ensure consistent cerebral blood flow to maintain cerebral perfusion pressure in normal limits.
Lower limit of systemic arterial pressure at which autoregulation is effective in a normotensive person is MAP of 50mm Hg. Lower causes symptoms of cerebral ischemia: syncope and blurred vision.
Upper limit of systemic arterial pressue for autoregulation to be effective is 150mm Hg. When pressure higher than this, vessels are maximally constricted, vasoconstrictor response is lost, blood brain barrier is disrupted, results in IICP.
MAP is diastolic blood pressure plus 1/3 pulse pressure (systolic BP minus diastolic BP)
BP 122/84: MAP 97

19. Cerebral Perfusion Pressure (CPP)
Pressure needed to maintain blood flow to the brain
MAP-ICP=CPP
Normal CPP is
CPP>100 is hyperperfusion and IICP
CPP< 60 hypoperfusion
CPP<30 incompatible with life
CPP (cerebral perfusion pressure) is pressure needed to ensure blood flow to the brain. Equals MAP-ICP. As CPP decreases, autoregulation fails, cerebral blood flow decreases. CPP below 30 mm Hg results in cellular ischemia, death. Autoregulation normally maintains adequate cerebral blood flow and perfusion pressure by 3 mechanisms: changes in ICP, cerebral vasodilation, metabolic factors. See Lewis 1612
Low CPP indicates client is experiencing cerebral ____________________

20. Elastance – stiffness of the brain
High elasticity –high elastance ICP increases with small increases in volume
Low elasticity – brain compensates and ICP stays stable
Elastance is the brain’s ability to accommodate changes in volume, represents stiffness of the brain. High elastance=large increases in pressure with small volume increase.

21. Compliance Low compliance is same as high elastance
High compliance – ICP remains stable
Blood pressure
If MAP is low, blood vessels in brain dilate to bring in more blood
If MAP is high, blood vessels constrict to shunt away blood from brain
Compliance is the inverse of elastance, the expandability of the brain. With low compliance=large increases in pressure with small volume changes (same as high elastance). A lot of stiff or too little stretch cause the same thing-IICP. A compliant brain has the ability to compensate for added volume and maintain normal ICP. Degree of compliance varies from patient to patient, over time in each patient; this is why turning or suctioning may result in large changes in ICP in one patient and not another.

22. Metabolic Factors affecting cerebral blood flow
Oxygen tension – When oxygen tension (PaO2) falls below 50, cerebral arteries dilate to increase cerebral blood flow. If this fails to happen, the brain metabolism changes to anaerobic metabolism and lactic acid builds up
Carbon dioxide tension - If the blood becomes acidic, the blood vessels dilate to increase cerebral blood flow (increased CO2 and acidosis are potent vasodilators)
Cerebral arteries dilate to raise oxygen tension, if not anaerobic metabolism begins. Acid environment causes further increase in blood flow.

23. Metabolic Factors Globally Focally
extreme cardiovascular changes (asystole)
Pathophysiologic states (diabetic coma)
Focally
Trauma and tumors
Metabolic factors can alter or abolish autoregulation globally or locally. When autoregulation is lost, cerebral blood flow is not longer kept at a constant level, but is influenced by changes in systemic BP, hypoxia, or hormones. Increasing ICP can progress to unconsciousness, changes in neuro function, brain herniation and death.

24. Stages of Increased ICP
Stage 1 – High compliance and low elastance. Autoregulation is functioning
Stage 2 – Compliance is lower and elastance is increased. An increase in volume places client at risk for IICP
Stage 3 – High elastance and low compliance. Small changes in volume will cause large increase in ICP
Lots of stretch, low stiffness, autoregulation still works.
Lower stretchability, increased stiffness, client at risk for IICP.
Lots of stiffness, little stretch, small changes in volume cause large increases in pressure.

25. Stages of Increased ICP
Stage 4 – ICP rises to terminal levels with little increase in volume. Brain herniates leading to
REST IN PEACE
Where is it going to go? It’s outta here…

26. Increased Intracranial Pressure
From an increase in cranial volume that results from increase in one or more of the following:
Brain tissue
Blood
Cerebrospinal fluid
Let’s review a little…

27. Increased Intracranial Pressure
Cerebral edema – regardless of cause, increases tissue volume, can lead to IICP
Types –
Vasogenic-most common (tumors, abscesses, ingested toxins)
Cytotoxic-local disruption of cell membranes (lesions or trauma)
Interstitial-uncontrolled hydrocephalus, hyponatremia
Cerebral edema is an important factor contributing to IICP. Associated with a variety of conditions, but regardless of cause, results in increase in tissue volume with potential for IICP. 3 types of cerebral edema: vasogenic, cytotoxic, interstitial.
Vasogenic cerebral edema is mostly in white matter, caused by changes in endothelial lining of cerebral capillaries, allow leaking from capillaries into extracellular space, osmotic gradient favors flow of water from blood vessels to extravascular space. Speed and extent of spread of edema depend on BP, site of injury, extent of blood-brain barrier defect.
Cytotoxic cerebral edema usually in gray matter, from lesions or trauma that result in hypoxia or anoxia, sodium depletion, SIADH. Fluid and protein shift from extracellular space into cells with swelling and loss of cellular function.
Interstitial cerebral edema-results from diffusion of ventricular CSF in patient with uncontrolled hydrocephalus, cans be caused by enlargement of extracellular space resulting from systemic water excess. Fluid moves into cells to balance with hypo-osmotic interstitial fluid.
Unless there is a reduction in ICP, brainstem will be compressed, herniation of the brain from one compartment to another can occur.

28. Complications of IICP Inadequate cerebral perfusion
Cerebral herniation
Brain shift : Lateral, downward, or both
Irreversible
Edema and ischemia further increased
Compression of brainstem and cranial nerves may be fatal
Cerebellum and brainstem forced through foramen magnum

29. Clinical Manifestations
Change in level of consciousness is the most sensitive and important indicator of neuro status
May be pronounced or subtle
Early signs may be nonspecific: restlessness, irritability, generalized lethargy
LOC reflects the integrity of the brain as a whole, even subtle changes can be significant. Excess sleepiness can indicate increased ICP is developing.
Evaluate LOC and compare with previous findings: include arousability, content of consciousness, speech.
Determine the level of stimulus needed to arouse the patient (verbal, touch, shaking?)
Content of consciousness: orientation
Ability to follow commands: stick out your tongue, let go of my fingers
Speech: clear, coherent, slurred, garbled, aphasic, incomprehensible sounds, no effort to speak
Report changes immediately!

30. Clinical Manifestations
Changes in vital signs-this is ominous sign
This is a late sign – Cushing’s triad
Increasing systolic blood pressure
Pulse slowing and is bounding
Irregular respiratory pattern
May also have a change in temperature
Changes in VS caused by increasing pressure on thalamus, hypothalamus, pons, and medulla.
Cushing’s triad often do not appear until ICP has been increased for some time or changes suddenly and dramatically. Widening pulse pressure, bradycardia, and irregular respiratory patterns. Need to know Cushing’s triad signs.

31. Clinical Manifestations
Ocular signs
Pupil changes are from pressure on third cranial nerve
Pupils become sluggish, unequal. This is because of brain shift. May also be pressure on other cranial nerves
Compression of oculomotor nerve result in dilation of pupil, sluggish or no response to light, inability to move eye upward, ptosis of eyelid. A fixed, unilaterally dilated pupil indicates herniation of the brain.
Signs of dysfunction of other cranial nerves are: blurred vision, diplopia, changes in extraocular eye movements.

32. Clinical Manifestations
Decrease in motor function
May have hemiparesis or hemiplegia
May see posturing – either decorticate or decerebrate
Decerebrate – more serious from damage in midbrain and brainstem
Decorticate – from interruption of voluntary motor tracts
Motor ability is controlled by nerve tracks originating in the frontal lobes of the brain, with fibers passing through the brain stem to the spinal cord before going to the muscles of the body. Distortion of brain tissue along these pathways can cause motor dysfunction. Patient may exhibit localization to painful stimulus or withdraw from it. Motor strength and tone are assessed in all 4 exxtremities. Decorticate posturing now called abnormal flexion, decerebrate posturing now called abnormal extension.

33. Clinical Manifestations
Headache
From compression on the walls of cranial nerves, arteries and veins
Worse in the morning
Straining and movement makes worse
Brain itself is insensitive to pain. HA often continuous, but worse in the morning, straining or movement may exacerbate.

34. Clinical Manifestations
Vomiting
NOT preceded by nausea- “unexpected”
May be projectile
Nonspecific sign of IICP.

35. Diagnostic Tests CT MRI Cerebral angiography EEG PET
No lumbar puncture if there is ICP because sudden release of pressure can cause brain to herniate
ABG’s – keep O2 at 100% (Lewis 1615) and PCO2 as related to ICP (25-35)
It may be difficult to identify IICP as cause of a coma, loss of consciousness confuses signs, makes it difficult to see the progress of IICP.
Studies to identify the presence and cause of IICP. MRI and CT have revolutionized diagnosis of IICP, can differentiate many conditions that can cause IICP.

36. Drug Therapy
Mannitol – Rapid short acting diuretic that decreases ICP. Decreases total brain water content
Watch fluids and electrolytes closely (I and O and labs)
Don’t give in cases of renal failure or if serum osmolality increased
Mannitol is an osmotic diuretic, used to increase serum osmolarity so fluid is drawn into vascular space from interstitial space in cells, then excreted by kidneys. Has greatest effect on normal brain tissue, decreases bulk. Use in-line filter when administering mannitol because it tends to precipitate into crystals. Indwelling catheter necessary due to rapid diuresis, need for accurate monitoring, minimize patient activity. Anticipate effects in 5-15 minutes, lasting for several hours.

37. Drug Therapy Loop diuretics – reduce blood volume and tissue volume
Corticosteroids – Decadron most common steroid used. Watch for side effects. Should be on antacids or H2 receptor blockers to prevent ulcers.
Lasix and Bumex inhibit sodium and chloride reabsorption in the ascending limb of the loop of Henle, reduce blood volume and utimately tissue volume, cause reduction in rate of CSF production.
Corticosteroids used extensively for cerebral edema, Decadron most common. Theory is that they act by stabilizing cell membrane, prevent formation of inflammatory products, improve neuronal function by improving cerebral blood flow and restoring autoregulation. Evidence of effectiveness is limited per Lewis. Complications include hyperglycemia, increased infections, GI bleeding. Give antacids or histamine receptor blockers, monitor fluid intake due to potential for hyponatremia, monitor glucose levels of blood and urine

38. Drug Therapy
Barbiturates – causes decrease in metabolism and ICP. Causes reduction in cerebral edema and blood flow to brain.
Watch for hangover effects and drowsiness. Side effects make it harder to check LOC. Watch for constipation – do not want client straining.
Skeletal muscle paralyzers may be used (Pavulon)
Antiseizure drugs - Dilantin
Drug therapy to reduce cerebral metabolism, decreases cerebral blood flow and ICP. High dose barbiturates (probably phenobarb) decrease metabolism, decrease ICP, reduce cerebral edema, produce more uniform blood supply to brain. May use Dilantin, seizures increase ICP. Infuse within 1 hour, tends to precipitate, don’t infuse with dextrose.

39. Nutrition Clients need higher amounts of glucose to survive.
Will need nutritional support quickly.
Watch sodium if on Mannitol – may need to give additional salt.
Also may need additional free water if dehydrated – watch I and O closely.
Give low CHO diet to help with CO2
Must meet nutritional needs, regardless of state of consciousness or health. Early enteral feeding following brain injury improves outcomes. Patient with IICP is in hypermetabolic and hypercatabolic state, needs glucose for metabolism of injured brain.
Need nutritional replacements within 3 days after injury. May need added salt, minerals, free water to meet fluid needs. Malnutrition promotes continued cerebral edema!

40. Nutrition Fluid balance is controversial Do not want too dry
Keep normavolemic
Give saline either .45% or normal saline – not glucose to help prevent additional cerebral edema
Controversy about whether patients should be in state of moderate dehydration: may be effective to reduce cerebral, fluids restricted to 65-75% of normal. But---hypovolemia may result in decreased CO and BP, may have impact on cerebral perfusion and oxygen delivery to brain, dehydrated patients do not respond well to vasoactive drugs. May use 5% dextrose in water for piggyback meds, .45% or .9% NS for IV solution

41. Laboratory Work ABGs regularly Electrolytes daily
Base ventilatory support on basis of gases, be aware if moderate hyperventilation is desired.
Disturbances have adverse effect on ICP. Especially monitor: glucose, sodium, potassium, osmolality.

42. Nursing Interventions
Airway and respiratory – suction only as needed and for 10 seconds at a time, only 2 passes. Give 100% O2 prior to suctioning.
Avoid abdominal distention – may need NG tube to decompress stomach
Sedate with care – if not on a vent, use sedation that will not interfere with respiration or mask any neuro changes
Nursing interventions must focus on factors that help control or worsen ICP to help reduce metabolic requirements of the brain. Hypoxia and hypercarbia result in increased cerebral blood flow and volume which contribute to IICP.
Oxygen administration and mechanically assisted ventilation are often used to maintain a PaO2 of mm Hg. Controlled hyperventilation may be used to reduce PaCO2 to mm Hg, causes cerebrovasoconstriction, reduces cerebral blood volume and ICP.
Patent airway is critical, with decrease LOC increased risk of obstruction from tongue or secretion accumulation. Note snoring sounds, oral airway may be helpful for breathing and suctioning.

43. Nursing Interventions
Keep HOB elevated 30 degrees if BP is normal
If BP is low will need to put HOB flat
Keep head in alignment to prevent cutting off venous flow from the head
Don’t elevate knees – this will increase intrathoracic pressure
Turn gently from side to side – if turning raises ICP, client will need to stay on back
Avoid flexion, extension or rotation of head and neck.

44. Nursing Interventions
If client is posturing frequently during care, will need to sedate first and then do only one thing at a time. Minimize stimulation
These clients can become agitated and combative – avoid over stimulating them
Restraining them will make them MORE AGITATED and RAISE THEIR ICP!
Avoid turning, prone position, emotionally disturbing conversation and clustered activities. Other things that may cause IICP are Valsalva’s manuever, REM sleep, restlessness and abnormal posturing.

45. Nursing Interventions
Use minimal stimulation – perhaps one family member that is particularly calming – not the entire neighborhood can stay with client
Use a calm voice when talking to the client
Calmly tell the client what you are going to do when providing care
NO TV IN ROOM
Keep room darkened if needed
Consider the environment. Routines of ICU, monitors, complexity of care can be stressful, may stimulate the patient and affect ICP. Be calm and unhurried. Space activity evenly, speak to unconscious patients. Avoid sudden, loud noises.

46. Nursing Interventions
Keep body temperature within normal limits
Give ordered PRN antipyretics (probably Tylenol)
May need to use cooling blanket
Do not use ice on client
Avoid hyperthermia, increase n metabolic demands on brain tissue will result in increased cerebral blood flow.

47. Nursing Interventions
Hygiene – keep skin clean and dry. Watch for skin breakdown
May need to be on a special bed
Keep mouth clean and moist
May need eye drops to moisten eyes
Families need a lot of support even after client leaves ICU
Client may benefit from rehab to help him adapt and progress

48. Nursing Interventions
Prevent infection
Protect from injury
Avoid factors that increase ICP
Psychological support
Aseptic technique for dressing changes, intact systems for ICP monitoring, CSF sampling.
Lewis p don’t awake suddenly, cluster activities, or allow disturbing conversations at bedside.
Touch and talk- avoid sensory deprivation and sensory overload.

49. Pediatric Considerations
Open fontanels allow expansion of skull
Neuro changes may be harder to detect because child cannot communicate as well
Cushing’s triad rarely seen in children
Compare child’s behavior with their developmental level
Widening of sutures if fontanels open may assist with compensation

50. Pediatric Considerations
Assess for developmental differences and physical anomalies
Is child appropriate for age?
Look for physical injuries such as bites, bruises
Use special Glascow coma scale for child
Allow parents to help elicit responses for assessment.

51. Pediatric Considerations
Allow parent to stay with child as much as possible
Avoid unnecessary stimulation
Crying will increase ICP

52. Head Trauma Usually signifies craniocerebral trauma
Includes alteration in consciousness
High potential for poor outcome
Death at injury
Death within 2 hours after injury
Death 3 weeks after injury
Majority of head injury deaths occur immediately from direct trauma or from massive hemorrhage and shock.
Deaths occurring in a few hours are caused by progressive worsening of head injury or from internal bleeding. Note of changes in neuro status and surgery are critical in prevention of deaths at this point.
Deaths 3 weeks or more after injury result from multisystem failure.

53. Head Trauma statistics
3 million/year in the U.S.
Mortality rate is 19 per 100,000
MVAs and falls have decreased as causes
Firearm-related head injury deaths have increased
Statistics are incomplete because many people die at the scene or because minor conditions are not seen for treatment.
Mortality rate is decreased 21% from 1976/
Other causes: assaults, sports-related, recreational accidents.

54. Head Trauma
Scalp lacerations – scalp has many blood vessels and will bleed profusely. Watch for infection
Skull fracture types
Linear
Depressed
Simple
Comminuted
Compound
Most minor of head traumas. Scalp vessels have poor constrictive abilities.

55. Skull Fracture Locations
Frontal
Orbital fracture
Temporal fracture
Parietal fracture
Posterior fossa fracture
Basilar skull fracture
Occurs at base of the skull
Watch for rhinorrhea and otorrhea
Test fluid leaking from nose or ear for glucose and watch for halo
If the drainage is CSF then the fracture has crossed the dura
Lewis p. 1506
Test fluid for glucose, present in CSF (if blood is present, test is unreliable because blood contains glucose).
Halo sign: allow fluid to drip onto white pad and observe. Blood will be in the center with yellowish ring of CSF around it in a few minutes. Note color, appearance and amount of leaking fluid.

56. Head Trauma
Check head injury client for bruising around eyes called raccoon eyes
Also look at hairline at nape of neck behind ear for bruising called Battle’s sign
Major complications of basilar skull fracture are infection and hematoma
Lewis p 1625

57. Battle’s sign

58. Minor Head Trauma Concussion – client may not lose consciousness
Will be a brief change in LOC, client may not remember the event and will have headache
Post-concussion syndrome is 2 weeks to 2 months after injury
Manifestations usually brief, patient usually discharged to notify if symptoms persist or behavior changes noted. Family should be taught to notify if decreased level of consciousness

59. Post Concussion Syndrome
Persistent headache
Lethargy
Personality changes
Short attention span
Decreased short-term memory
When client is discharged after concussion nurse should instruct family on what to watch for and when to call Dr.
Post-concussion syndrome: 2 weeks to 2 months after concussion. Persistent HA, lethargy, personality and behavior changes, short attention span, decrease short term memory, changes in intellectual ability. May be the beginning of a more serious, progressive problem.

60. Major Head Trauma Contusion – bruising of brain tissue
Has area of necrosis infarction and hemorrhage
Often from coup - contrecoup injury
Seizures are common after contusion
Major trauma includes contusions and lacerations, usually with closed injuries.
Contusion frequently at site of fracture.
Coup-contrecoup occurs because of mass movement of brain inside skull. Injury at site of direct impact of brain on skull and opposite side from injury.

61. Major Head Trauma Lacerations Tearing of brain tissue
Occurs with depressed skull fracture and penetrating injuries
May have bleeding into the brain structures-intracerebral hemorrhage
Very difficult to remove blood
Tissue damage is severe, surgical repair is impossible because of texture of brain tissue.
Hemorrhage manifests with unconsciousness, hemiplegia on opposite site, dilated pupil on same side as injury. With hematoma expansion, symptoms of IICP more severe, prognosis poor if large bleed.

62. Major Head Trauma Epidural hematoma
Comes from bleeding between dura and inner surface of the skull
Will be unconscious, then awake, and then deteriorate
Headache, nausea and vomiting
Needs surgical intervention to prevent brain herniation and death
Neurologic emergency, usually caused by fracture crossing a major artery in the dura. Arterial tear develops rapidly and under high pressure: unconscious at scene, brief lucid interval, decreased LOC. HA, N/V. acute arterial bleeding has these typical signs: unconscious at scene, regains consciousness briefly, then nonresponsive. May have venous or arterial origin.
Subdural hematoma usually venous in origin, much slower to develop mass large enough to produce symptoms, may be acute, subacute, chronic. Chronic develops over weeks or months after minor head injury, peak incidence in 60s and 70s, brain atrophy causes tension on structures, may tear. Head trauma only 60-70% of cases.
Intracerebral hematoma usually from rupture of vessels in frontal and temporal lobes at time of injury.

65. Subdural Hematoma
Usually bleeding is from veins, so bleeding is GENERALLY slower than epidurals
CAN be from arteries and these require IMMEDIATE removal
Administration of anticoagulants is one of the causes of CHRONIC TYPES esp. in the elderly.

67. Diagnostic Studies Skull xrays routine to r/o or identify fracture
CT/MRI are best to determine trauma rapidly

69. Emergency Management-Initial
Airway
Stabilize cervical spine
Oxygen administration
IV access (2 large bore catheters), LR or NS
Control external bleeding with pressure
Assess for rhinorrhea, otorrhea, scalp wounds
Remove clothing

70. Emergency Management-Ongoing
Maintain patient warmth
Monitor VS, LOC, O2 sats, cardiac rhythm, GCS, pupil size and reactivity
Anticipate intubation if absent gag reflex
Assume neck injury with head injury
Administer fluids cautiously to prevent IICP

71. Rehab Most head trauma requires rehab
Some rehab units do coma management
Client may have trouble swallowing and need speech therapy
Client may agitate easily and act out sexually
May be a flight risk and have to be in a locked ward until passes through the agitation phase

72. From Rehabilitation Nursing

73. From
Rehabilitation
Nursing

74. Pediatric Client
Child is vulnerable to acceleration deceleration injuries because their neck is supple and moves around easily and the head is larger in proportion to their bodies
In a very young child the cranium may be able to expand enough to allow for some edema

75. Pediatric Client Epidural hemorrhage is rare in children
Subdural hemorrhage – from shaken baby syndrome, falls
Can result in quadriplegia, hyperthermia, bulging fontanels
Retinal hemorrhages
Dizziness
Unsteady gait

76. Elderly At risk for head trauma from falls
Be alert if client has fallen and is taking anticoagulants

77. Cranial Surgery Brain tumor (benign or malignant) CNS infection
Hydrocephalus
Vascular abnormalities
Intracranial bleeding
Aneurysm repair
Arteriovenous malformation
Craniocerebral trauma
Skull fractures
Epilepsy
Intractable pain
Lewis p Table 55-13

78. Types of Cranial Surgery: Stereotactic
Stereotactic: neurosurgery
Often computer assisted to precisely target area
CT and MRI used to image targeted tissue
Burr hole or bone flap for entry
Can remove small tumors and abscesses, drain hematomas, perform ablative procedures, repair AV malformation
Reduces damage to surrounding tissue

79. Types of Cranial Surgery: Craniotomy
Location varies
Frontal
Parietal
Occipital
Temporal
Combination
Burr holes drilled, saw to remove bone flap
Bone flap wired or sutured after surgery
Drain may be placed to remove blood or fluid

80. Nursing Care: Pre-op Compassion Teaching
Uncertainty and fear about prognosis/complications
Teaching
What can be expected
Hair will be shaved
Client will be in ICU after surgery

81. Nursing Care: Post-op Prevent increased ICP!!!
Maximum swelling occurs within hours
Frequent assessment of neuro status x 48 hrs.
Monitor fluids, electrolytes, osmolality closely
Detects changes in sodium regulation, onset of diabetes insipidus, severe hypovolemia
Positioning varies depending on procedure
Assess dressing, drainage, incision
Care to prevent wound infection

82. Nursing Care: ambulatory and home
Rehab potential depends on reason for surgery, post-op course of recovery, and client’s general health
Nursing considerations
Foster independence for as long as possible to highest degree possible
Positioning, skin and mouth care, ROM exercises, bowel and bladder care, adequate nutrition
Potential recovery cannot be determined until cerebral edema and IICP subside
Maintain as much function as possible while waiting to see how much rehab will be possible.