Increased Intracranial Pressure

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Increased Intracranial Pressure

• Mary Ann Reilly
• BSN, MS, CRRN
• Santa Clara Valley Medical Center, Rehab Nurse
  Manager

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• In 2004 the SJ Mercury wrote "As he was giving
  his speech he stumbled slightly and then he
  started to perspire a bit. I thought almost
  immediately that something is not right.
• His repeated vomiting prompted paramedics to
  treat him with oxygen and monitor his heart for
  half an hour -- routine care for a sudden
  food-borne illness

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• The initial suspicion that Mayor Ron Gonzales had
  food poisoning Wednesday night shows just how
  difficult some strokes are to detect -- and
  experts say it offers a warning to people who
  might find themselves with similar symptoms.

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• Gonzales' type of stroke is called an
  intraventricular hemorrhage.
• This means that a blood vessel had broken and was
  leaking into the ventricle, which carries spinal
  fluid.

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So whats the big deal?

• Skull

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• Components of Cranial Vault
• Meninges
• Dura
• Arachnoid
• Pia
• Brain
• Brain tissue 80-88
• Blood
• Blood 2-11
• CSF
• CSF 9-10

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http//learntech.uwe.ac.uk/neuroanatomy/neuro4_1.h
tm
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• Blood
• 15-20 of the cardiac output
• 20-25 of all oxygen inspired
• 750cc/min
• 80 from carotid arteries
• 20 from vertebral
• Circle of Willis is collateral circulation
• No sugar/fat/oxygen storage

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Autoregulation

• When intra-cranial pressure begins to rise, the
  bodys own compensatory mechanisms include
  decreasing the production of CSF and restricting
  the blood flow to the brain(by vasoconstriction).

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Autoregulation

• Self Regulated
• PCO2 (carbon dioxide) vasodilator
• For every 1mmHg change in PCO2 there is a 1-2cc
  change in blood flow per 100 GMs of brain
• (1300-1400Gms avg. wt.) s 750 65 or 750
  130
• Diameter of vessels
• Hypercapnia Increases CBF
• Hypocapnia Decreases CBF

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Intercrainial Pressure Regulation

• When BP increases, cerebral arterioles constrict
  to keep blood entering brain at steady rate.
• When BP falls, cerebral arterioles dilate to
  increase blood flow to brain

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Intercrainial Pressure Regulation

• Metabolic regulationchanges in O2 and CO2 Low
  O2 and increased CO2 cause vasodilation CSF
  regulationdecreased production or increased
  reabsorption decreases ICP.

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Factors Affecting CBF

• Viscosity of the blood
• Seizures
• Anemia
• Drugs

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CSF

• 125-150 cc clear fluid
• 500cc produced per day
• 20cc per hour
• Replaced 4-7 times per day
• Function
• Protection, cushions
• Waster disposal
• Nutritional support (2/3 bodies BS)

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CSF Pressure

• Norm
• 1-15 mmHg or lt200mm H2O
• Low pressure
• Dehydration
• Increased pressure
• Val Salva,Tumor, Subdural Hematoma, Subarachnoid
  Hemorrhage, Infections, Hydrocephalus

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Symptoms of Increasing ICP

• Headache
• Visual changes
• Nausea
• Vomiting
• Behavior changes
• Changes in LOC
• Seizures

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Symptoms

• Aniscoria
• Hemiparesis
• Vital sign changes
• Cushing Triad

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Pulse Cardiac center is located in the medulla compression may affect heart rate
Temperature Raised indicates infection Hypothermia seen in drug overdose
Blood Pressure Increase associated with sympathetic stimulation. Decrease rarely attributed to brain injury
Respiration Increase may indicate damage to the midbrain. Decrease may indicate damage to lower pons and upper medulla
Pupils One reacting the other not may indicate pressure on the to the 3rd cranial nerve caused by I-ICP or a lesion
http//learntech.uwe.ac.uk/neuroanatomy/neuro4_4.h
tm
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Cushings Triad

• Vital Sign Changes in ICP
• Systolic pressure increases (widened pulse
  pressure results).
• Slowing of heart occursbradycardia (occurs as
  result of reflexive slowing in response to
  increased systolic pressure)
• Respiration changesbecomes slowed

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Could it be?

• Difficulty speaking
• Blurred vision
• Hypertension
• Shallow rapid breathing
• Visual disturbances
• Paresthesia
• Hypoglycemia

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OR?

• - Confusion
• Lethargy
• Nausea Vomiting
• Coma
• Seizures
• Syndrome of Inappropriate ADH

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OR?

• Changes in LOC
• Nausea Vomiting
• Irritability
• Disorientation
• Personality changes
• Seizures
• Fluid Overload

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OR?

• Street drug
• Alcohol withdrawal
• Over dose
• Diabetic ketoacidosis
• Hypervitiaminosis A
• Drug
• www.merck.com/mrkshared/mmanual/section1/chapter3/
  3c.jsp

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Diagnosis of Increased Intracranial Pressure

• Overt symptoms
• Papilledema
• Nuchal rigidity
• Lumbar Puncture

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Lumbar Puncture

• Contraindicated
• Focal signs
• Intracranial mass
• Papilledema
• Cardiorespiratory compromise
• Infection of skin

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Rational for Contraindication

• A simple analogy

Performing a LP in the presence of I-ICP, may
result in herniation
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Herniation

• Tentorium
• Midbrain and diencephalon through the
  tentorium
• Uncal
• Tonsillar
• Cerebellar tonsils
  through the foramen magnum

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Diencephalic Stage

• Confused and drowsy
• Constricted pupils
• Gaze palsies

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Mesencephalic Stage

• Unconscious
• Decerebrate posturing
• Dilated pupils
• Hyperventilation

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Pontine Stage

• Unconscious
• Decerebrate posturing
• Constricted pupils
• Irregular breathing

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Decorticate posture

• Indicated by rigidity, flexion of the arms,
  clenched fists, and extended legs. The arms are
  bent inward toward the body with the wrists and
  fingers bent and held on the chest. Presence of
  this type of posturing implies severe damage to
  the brain with immediate need for medical
  attention.

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Decerebrate Posturing

• Internal rotation and extension of the arms
  lower limb extension
• Due to midbrain compression as the brainstem is
  further compressed

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Medullary Stage

• Unconscious
• Flaccid
• Loss of homeostatic control
• Increase heart rate
• Decrease blood pressure
• Hyperthermia
• Cheyne-Stokes breathing

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Cheyne-Stokes

• Breathing describes a waxing and waning
  ventilation, sometimes with periods of apnea,
  that occur in cycles.
• It is due to a delay in the medullary
  chemoreceptor response to blood gas changes

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http//thediagram.com/3_6/
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Common Causes of I-ICP

• Vascular abnormalities
• AV malformations, aneurisms, stroke
• Diffuse cerebral ischemia
• Closed head trauma, shaken baby, vasospasm
• CNS infections
• Tumors
• Trauma
• Obstruction of CSF flow

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Hydrochepalus
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Intra Cerebral Hemorrhage
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AV Malformation
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Crainal Defect
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Crainial defect with midline shift
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• The Monroe-Kelle Hypothesis states that an
  increase in the volume of one component (blood,
  brain tissue, CSF) must be accompanied by a
  decrease in another component if intracranial
  pressure is to remain constant. The CSF and blood
  volume are the compartments that most easily
  change to accommodate changes in pressure. 
  Interventions to prevent secondary brain injury
  follows these principles and focuses primarily on
  cerebral blood flow and drainage. 

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Management / Trauma

• Rapid transportation
• Early intubation
• Aggressive resuscitation
• Immediate CT
• ICP monitoring

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CAT Scans

• Sensitivity for visualizing blood approximately
  96
• Visualizes
• Fractures
• Hematomas

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Operative Management

• Burr holes
• Intra-operative ultra sound
• Surgical evacuation of mass lesion
• Craniotomy
• Craniectomy
• Ventricular drainage

http//www.trauma.org/neuro/neuromonitor.html
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Medical Management

• Adequate cerebral perfusion
• Dehydration
• Hypovolemia
• Hypoxia
• Hyperventilation
• Sepsis
• Normal or hypothermia
• Hyperthermia causes increased cellular metabolism
  (10-13), increased lactic acid production,
  increased CO2 (vasodilatation)

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Osmotic DiureticsMannitol

• Reduces ICP in 5-10 min. trough osmotic gradient
• BBB must be intact
• Removes H2O not Na
• Caution with
• Hypotension
• Coagulopathy
• CHF

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Duiretics

• Furosemide (lasix)
• Loop of Henle, blocks transport of Cl Na
• Reduced CSF production 40-70
• Postssium depletion

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Other Medications

• Corticosteroids
• H2 Blockers
• Sedation to control agitation, reduces metabolic
  needs
• Analgesia
• Barbiturates to suppress seizures, decreases
  metabolic needs, vasoactive effects

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Hypothermia

• Decreased cellular metabolism
• Brain temp is 2.0o F higher than body
• Reduces inflammatory process
• Reduces cerebral metabolism
• Limits secondary brain injury

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Nutrition

• Energy requirement 125-200 ABOVE normal
• Early feeding has a favorable effect on survival
• TPN PPN

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Nursing Care

• Assessment
• Touch
• Oxygen
• Control pain
• Medicate prior to administering care
• Break up activities

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Care

• Decrease stimulation
• Positioning
• Bowel
• Bladder

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Glascow Coma Scale
Verbal Eye opening Motor
Score Finding Score Finding Score Finding
Normal fluent appropriate Confused but fluent Mumbling occasional word recognizable Vocalizations but no words No vocalizations or verbalizations Eyes open without stimulation Eyes open to loud noise Eyes open to pain only 1 No eye opening Follows commands Locates pain stimulus Pulls away from pain Flexion posture to pain Extension posture to pain 1 No motor response
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• www.rad.usuhs.mil/rad/herniation
• www.thridage.com/health/adam/ency/article
• www.homestead.com/emguidemaps/files/coma.html
• www.classes.kuma.edu/sm/nurs420
• www.emguidemaps.homestead.com/files/anisocoria.htm
  l
• 6. www.annals.org/cgi/content/full/130
  /5/427/F1
• www.med.harvard.edu/AANLIB/home.html
• http//thediagram.com/3_6/

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http//www.sophysa.com/patient/hydrocephalus/hydro
cephalus3.htm
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Lumbo-Peritoneal Shunt                           
                                                  
                                                  
              
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LEONARDO DA VINCI - Drawing of the cerebral
ventricles after they have been injected with a
dye
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Speech arrest
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Fluent Aphasia
This large cerebral infarct occurred in the
setting of atrial fibrillation and caused a dense
fluent aphasia. The CT scan shown here was
obtained 5 days after the onset of stroke
symptoms. View the temporal movie of this slice
to see the evolution of the lesion over the 5 day
period. Significant swelling in the infarcted
area produces obvious shift of the midline by day
5. This corresponded clinically to a diminished
level of arousal, which resolved after 2 days.
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Cant read
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Hesitating Speech
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Loss of sensation
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Chronic Subdural
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Cavenous angioma
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AV Malformation with MRA
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Acute Stroke
sudden onset of right body weakness and trouble
speaking
Diffusion-weighted MR showed a large area of
abnormal signal in the region clinically
suspected the portion of left hemisphere
supplied by the middle cerebral artery.
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Normal aging brain
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Normal aging
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Normal Aging coronal plane
http//www.med.harvard.edu/AANLIB/home.html
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Cerebral Hemorrhage
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MS
Look at the large round white spot in the right
frontal region. This is a relatively new lesion,
and you can see how it enlarges very rapidly over
the next weeks. Look at the timeline cine. With
time, the lesion enlarges, there is a "halo" of
white (high) signal which surrounds the lesion.
This probably represents the edema which forms in
reaction to the acute damage. At the end of the
movie, you can see that the lesion has nearly
disappeared, with another lesions appearing
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http//www.neuroland.com/default_old.htm
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http//www.neuroland.com/nm/neuropathic_pain.htm
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Burst arteries cause Increased ICP by
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• Increased Intracrainal PressureNormal
  intracrainal pressureless than 15mm Hg or 180mm
  H20. ICP considered when pressure than this.
  When ICP ischemia and hypoxia results and
  damages neural tissue. If ICP continuescan
  cause herniation syndrome.

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• Causes of ICPBrain tumors, abscesses, cerebral
  edema from injuries. CSF obstructionproduces
  hydrocephalus Communicating vs. non-communicating
  Cerebral vasodilationcompensatory mechanism for
  conditions of hypoxia (when pCO2 , cerebral
  vasodilation will occur).

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• Head InjuriesSkull fractureslinear, comminuted,
  depressed or basilar Basilar (occurs at base of
  skull)produces hemorrhage from nose, pharynx,
  ears Bruising over mastoid boneBattles sign May
  cause CSF leaking from ears, nose Brain
  Injuries--Concussion vs. Contusion Intracranial
  HemorrhageEpidural vs. Subdural Hematoma

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• Epidural HematomaBlood collects in the epidural
  space Expanding hematoma causes rapid symptoms of
  I.C.P. and is considered medical emergency
  Treatmentsurgical openings through skull (burr
  holes) to decrease I.C.P., craniotomy may be
  necessary to remove clot and control bleeding

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• Subdural HematomaCollection of blood between dura
  and the brain May be venous in origin, may be
  acute, subacute, or chronic depending on size of
  vessel and amount of bleeding Acutecause is
  major head injury, symptoms develop over 24-48
  hrs. Subacuteless severe trauma, symptoms
  develop over 48 hrs. to 2 weeks Chroniccause is
  minor trauma, seen in elderly, symptoms develop
  over 3 weeks to 3 months

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• Treatment of ICPHyperventilationblow off CO2.
  Osmotic diuretics--serum osmolarity Mannitol
  (Osmitrol) Hypertonic Glucose Loop diuretics
  SteroidsIV or p.o. Dexamethosone (Decadron)
  Methylprednisolone (Solu-Medrol)

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• Treatment of ICP cont.Anticonvulsantsprevent
  seizures IV fluidskeep moderately dehydrated
  GIVE 0.45 to 0.9 NaCl AVOID 5 Dextrose
  Barbiturates may be used in extreme cases in
  order to induce coma and decrease metabolic
  demands on brain.

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• Brain tumors Classified by site, histologic cell
  type, degree of malignancy Gliomasarise from
  neuroglia tissue Medulloblastomamalignant tumor
  of cerebellum Menigiomasarise from meniges, slow
  growing Acoustic neuromasarise from 8th cranial
  nerve Pituitaryarise from pituitary gland, slow
  growing Location of tumors (in cerebral lobes)
  account for specific symptoms

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• Symptoms of Brain Tumors Classic symptoms of
  I.C.P. Headache may be worse in A.M. Seizures are
  common with all types of brain tumors Other
  symptoms depends on location of tumor within the
  cerebral lobes (occipital, frontal, parietal,
  temporal, cerebellar)

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• Treatment of brain tumorsTumor reductionsurgery,
  radiation, chemotherapy Manage and prevent
  symptoms of I.C.P. Crainotomy Supratentorial
  approachabove the tentorium (fold of dura
  separating cerebral cortex from cerebellum and
  brainstem Infratentorial approach---below the
  tentorium

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• Pre-op Nursing CareShaving headpermit needed,
  save hair, provide cap Teach deep breathing and
  leg exercises (no coughing) Pre-op enema is
  controversial Excellent baseline assessments
  necessary pre-op

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• Post-op Nursing CareSupratentorial
  ApproachH.O.B. 30-45 degrees Pillow under head
  and shoulder, align neck Avoid positioning on
  operative side Monitor for cranial nerve
  dysfunction II-visual deficits III-ptosis IV,
  Vdeficits in extraocular movements

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• Post-op Nursing Care for Infratentorial
  ApproachH.O.B. flat, keep client off back Small
  pillow under head, neck alignment Monitor for
  cranial nerve dysfunction III, IV, VIocular
  movements VIIabsent corneal reflex, paralysis of
  facial muscles VIIIdecreased hearing, nystagmus
  IX, Xgag and swallowing reflex decreased

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• Nursing Care Common to both surgical
  approachesContinuous neuro assessments,
  especially for I.C.P. Anticonvulsants, seizure
  precautions Body temperature regulation, prevent
  hyperthermia Turn, deep breath q. 2 hrs.
  Reinforce dressingscheck for CSF on drainage
  Pain managementuse of Codeine

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• S.I.A.D.H. Posterior pituitary secretes ADH to
  regulate water balance Too much ADH causes
  S.I.A.D.H. where kidneys will retain H2O and
  blood serum will be hypotonic Signs and symptoms
  Changes in L.O.C., headache, nausea and vomiting
  Decreased urinary output

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• Treatment of S.I.A.D.H.Fluid restriction 500cc or
  less in 24 hrs. IV fluids 3 or 5 saline with
  appropriate electrolyte replacements (K, Mg)
  Diuretics (Lasix) Lithium Carbonate

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• Diabetes InsipidusFailure of ADH secretion and
  failure of kidneys to store H2O. Signs and
  symptoms Urinary output increased with specific
  gravity of urine decreased Client will have
  dehydration Treatment Use of Vasopressin
  (Pitressin), given I.M. or s.c.

http//academic.luzerne.edu/aisaacs/webversion/nur
204-2003/03increasedintracrainalpressure_files/fra
me.htm