Endocrine disorders, ICP, SCI/tumors, aneurysms

Traumatic Brain Injury (TBI): Scalp Injury

- Bleed profusely; trauma may result in abrasion (Brush wound), contusion, laceration, or hematoma beneath the layers of tissue of the scalp (subgaleal hematoma) - Large avulsions (tearing away) of the scalp - life threatening - *Physical exam, inspection, and palpation - High risk for intracranial infections (area is irrigated before laceration is sutured) - Hemorrhage and hypovolemic shock

syndrome of inappropriate ADH (SIADH): excessive ADH from pituitary gland even in subnormal serum osmolality; INCREASED ADH from posterior Pit gland

- CONCENTRATED urine; water retention -> dilutional hyponatremia Risk factors for SIADH: -damaged hypothalamus - nonendocrine origin: bronchogenic carcinoma; severe pneumonia, pneumothorax, and other disorders of the lungs -sepsis infection of brain (meningitis) - disorders of CNS - head injury, brain surgery or tumor, and infection - medications (e.g., vincristine [Oncovin], phenothiazines, tricyclic antidepressants, thiazide diuretics) and nicotine

Brain Tumor Pharmacology therapy

- Corticosteroids-> to decreased inflammation & cerebral edema ex. Dexamethasone -taper and blood glucose checks adverse effects: hyperglycemia, electrolyte abnormalities, and muscle weakness *Decreasing ICP -Osmotic diuretic- Mannitol [Osmitrol] & Hypertonic 3% NS to decrease fluid content of the brain. -Anticonvulsants to treat/control seizures, benzos, phenytoin ( check serum levels 10-20mcg & meticulous mouth care) -Stool softeners- decrease straining and chances of IICP -Pain Meds- Opioids NO NSAIDS

Brain Tumor Clinical manifestations

- Increased ICP S/S: headache, nausea with or without vomiting, and papilledema (swelling of the optic nerve), Personality changes, and a variety of focal deficits, including motor, sensory, and cranial nerve dysfunction - early morning headache and worse by coughing, straining, or sudden movement (deep, expanding, dull, but unrelenting) -vomiting (not related to food intake) - irritation of vagal centers in the medulla -forceful vomiting (projectile vomiting) -visual disturbances: compression of the third cranial nerve (optic disc swelling or papilledema); diplopia or hemianopsia New onset of seizures in 60% of patients in temporal, frontal, parietal - greatest risk; (upper brain regions- supraentorial); rarely if cerebellar/brain stem seizure control: levetiracetam, carbamazepine, phenytoin, and zonisamide

Spinal Cord Injury (SCI): damage to the spinal cord with resulting functional loss of mobility and/or sensation

- Injury can involve contusion, laceration, and compression of the cord - Spinal cord edema develops; necrosis of the spinal cord can develop - Loss of motor function, sensation, reflex activity, and bowel and bladder control may result Causes: Automobile accidents, falls, violence (gun shots) or sports. Risk Factors: younger age, male gender, alcohol, and drug use Pathophysiology: - complete transection (severing) of the spinal cord (which renders the patient paralyzed below the level of the injury - Partial transection of the cord: spinal cord is damaged or severed partially; symptoms depend on the extent and location of the damage; early treatment is. Needed to prevent further damage Most frequently involved: most susceptible bc there is greater range of mobility in the vertebral column in these areas - Cervical - C5-C7: inability to breathe and quadriplegia - Thoracic - T12: paraplegia and poor trunk control - Lumbar - L1: decrease control of legs, bowel and bladder and sacral function Sacral: decrease control of legs, bowel and bladder and sacral function Primary injuries: result of the initial insult or trauma and are usually permanent. Secondary injuries: resulting from SCI include edema and hemorrhage; early treatment is essential to prevent damage

Abdominal Aortic Aneurysm (AAA):happens in the abdomen; Blood vessel weakening causing a balloon like dilation that is most often seen in the abdominal aorta, an essential blood vessel that supplies blood to your legs.

- Most common cause: atherosclerosis; affects men 2-6 x more than women; 2-3 x more in Caucasian vs. black men and most prevalent in pt. > 65 years of age - Most occur below the renal arteries (infrarenal aneurysms); untreated -> rupture and death Damaged media layer of the vessel -> caused by congenital weakness, trauma, or disease; RF: genetic predisposition, tobacco use, and HTN Only 40% symptoms; - "Feel their heart beating in their abdomen when lying down or feel abdominal mass or throbbing - Associated w/ thrombus -> major vessels occlusion or smaller distal occlusions - Cyanosis and mottling of the toes -> small cholesterol, platelet, or fibrin emboli can be lodged in the interosseous or digital arteries - Prominent, pulsating mass in the abdomen, at or above the umbilicus S/S: - Systolic bruit over the aorta - Tenderness on deep palpation - Abdominal or lower back pain - Approximately 40% of these patients are symptomatic: - Pulsations in the abdomen when lying down - Palpable abdominal mass or throbbing - Cyanosis and mottling of the toes due to lack of circulation to the lower extremities

pituitary adenoma

- account for 16% of all primary brain tumors -pressure from this exerts on optic nerve, optic chiasm, or optic tracts on the hypothalamus. -BENIGN Pressure effects-> HA, Visual dysfunction, hypothalamic disorders (disorders of sleep, appetite, temperature, & emotions) -Increased ICP & enlargement of sella turcica -Hypersecretion of GH-> acromegaly- enlargement of hands & feet Hypersecretion of prolactin-> amenorrhea or galactorrhea (excessive milk production); impotence and hypogonadism) Hypersecretions of ACTH-> Cushing's syndrome feat. assoc. w/ prolonged overproduction of cortisol & ADH (urine retention)

cerebral aneurysm: dilation of the walls of a cerebral artery that develops because of weakness in the arterial wall.

- could be due to atherosclerosis other causes: congenital defect of the vessel wall, hypertensive vascular disease, head trauma, and advancing age. - may cause focal deficits, due to compression of adjacent structures common areas of cerebral aneurysms: - bifurcations of the large arteries at the Circle of Willis are the most common areas. most affected cerebral arteries: - internal carotid artery, anterior cerebral artery, anterior communicating artery, posterior communicating artery, posterior cerebral artery, and middle cerebral artery. most significant complication of ruptured cerebral aneurysm -> subarachnoid hemorrhage

Hypoparathyroidism management and treatment

- increase serum calcium level to 9 to 10 mg/dL (2.2 to 2.5 mmol/L) - combinations of calcitriol, calcium, magnesium, and vitamin D2 (ergocalciferol) or vitamin D3 (calcitriol), the latter being preferred. -thiazide diuretic (e.g., hydrochlorothiazide [HydroDIURIL]) may be given to help decrease urinary calcium excretion - hypocalcemia + tetany occurs after thyroidectomy -> IV calcium gluconate -> no decrease in neuromuscular irritability and seizure activity -> sedative agents (pentobarbital) - provide environment free of noise, drafts, lights, sudden movement - bc of tetany, tracheostomy or vents, O2 suction @ bedside, bronchodilator medications - diet high in calcium and low in phosphorus (RESTRICT milk, milk products, and egg yolk); avoid spinach - administer oral tablets of calcium salts, calcium gluconate - Aluminum hydroxide gel or aluminum carbonate (Gelusil, Amphojel) - given after meals and to decrease phosphate through excretion of phosphate in stool; Nursing Management - signs of tetany, seizures, respiratory difficulties - calcium gluconate IV for emergency; give slowly and cautiously if pt. has a cardiac disorder or is on digoxin - cardiac monitoring - high calcium and vitamin D + low phosphate diet ( avoid soft drinks, meats, eggs) - activity and rest periods - watch out for seizure, cardiac dysrhythmias, cardiac arrest - monitor calcium levels ( 8.6 - 10) + phosphate levels (2.7 - 4.5)

Thyroid gland: produces thyroxine (T4), triiodothyronine (T3), and calcitonin.

- thyroid cannot make T3 + T4 without iodine (must come from food) - controls cellular metabolic activity - cell replication, brain development, normal growth,, basal metabolic rate, tissue thermogenesis, increased temp + HR, alertness, responses, reflexes, serum cholesterol levels, and vascular resistance, TSH regulation - calcitonin: secreted in response to high plasma levels of calcium, and it reduces the plasma level of calcium by increasing its deposition in bone. Negative feedback loop Hypothalamus -> TRH (thyrotropin releasing hormone) -> Anterior pituitary gland -> TSH (thyroid stimulating hormone) -> thyroid -> T3+T4 Types primary - thyroid gland itself central - pituitary gland, hypothalamus, or both secondary - pituitary disorder Tertiary - disorder of the hypothalamus resulting in inadequate secretion of TSH due to decreased stimulation of TRH

Acoustic

- tumor of the cranial nerve VII- responsible for hearing & balance arises within auditory meatus -pt experiences loss of hearing, tinnitus & episodes of vertigo & staggering gait - as tumor becomes larger-> painful sensation of face as a result of the compression of the tumor on the 5th cranial nerve - Many of these are benign- managed conservatively Tx- w/ stereotactic radiotherapy rather than open craniotomy

brain death: irreversible loss of all functions of the entire brain and absence of brainstem reflexes.

-Avoid conflict of interest -DO NOT INITIATE THE DISCUSSION OF ORGAN DONATION ÷ What if the family asks about donation? Organ Procurement Organization (OPOs) have organ procurement coordinators (OPCs) and trained designated requesters (TDRs) available to engage in discussions with the patient's families or agents. - they enter the donor into the UNOs -Neither the physician who attends the patient at the time of death nor the physician who determines the time of death may participate in procuring the patient's organs. **Role is to act for the benefit of the patient and put the patient's need first - role of the designated requester is to act for the benefit of potential donors If the patient is not "signed-up" as a donor: Consent must be obtained in the following order of priority: a) Agent of the deceased (holder of power of attorney for health care or expressly authorized to make an anatomical gift by a signed record). b) Spouse or state registered domestic partner of the deceased. c) adult child of the deceased. d) Parents of the deceased. e) adult siblings of the deceased. f) adult grandchildren of the deceased. g) Grandparents of the deceased. h) Any person acting as the guardian of the deceased at the time of death. i) Any other person having authority under applicable law to dispose of the deceased's remains. Organ Donation Organ/tissue donation and procurement services: Specialized/trained staff approach the family about donation ¡ Washington Regional Transplant Community ¡ www.beadonor.org Dead donor rule Uniform Anatomical Gift Act Organ Donation Research Consortium (ODRC) ¡ Advance organ donation through scientific research in order to improve outcomes for donors, their families, recipients, and society as a whole

Brain Tumor Nurse Management

-Frequent Neuro Checks , VS, Prevent IICP, HOB 30-45, reorient pt (personal possessions, photographs, lists, a clock), assist w/ self-care, prevent injury, strict I/O (DI/SIADH), DVT prevention -change in LOC: most sensitive indicator of IICP (d/t intracranial bleeding or cerebral edema) -Motor strength: subtle changes @ one side of body compared to the other are significant when they occur during the recovery period after craniotomy. -CN Assessment: to monitor pt's response to craniotomy (compare pre-op & post-op) -PERRLA- changes indicate damage/compression to CN III( Oculomotor nerve) Action: Reorient patient, assist w/ self-care; main concern-prevent injury esp w/ seizures -Monitor Serum electrolytes- serum Na+ WNL; possibly high of of normal to prevent fluid moving into cells or interstitium potential raising ICP -Admin stool softeners -Upright position & pain meds administered. -Education about possibility of seizures & adhere to prophylactic anticonvulsants -Risk for aspiration d/t CN dysfunction -Assess gag reflex & ability to swallow; -Pt to direct food to unaffected side -sit up straight to eat- offer soft diet. -Apply mechanical VTE devices and administer pharm prophylaxis of VTE as rx'ed-

encephalitis: inflammation of the brain tissue; caused by viruses, parasites, and fungi (infectious)

-Herpes simplex virus (HSV-1) is the most common cause: Cold sores - Arthropod-borne (or Arboviral) Encephalitis—Hinkle lists FIVE main ones. . .West Nile Virus perhaps most common and Eastern Equine the deadliest. -Viral replication occurs at the mosquito bite site -If immune response is inadequate viremia develops and virus progresses to CNS -Occurs in less than 1% of cases of bites from infected mosquitos. -Fungal Encephalitis typically afflict immunocompromised individuals -Rabies, Lyme Disease, Measles can also progress to encephalitis

Increased ICP complications (uncontrolled ICP)

-Inadequate cerebral perfusion -Cerebral herniation (abnormal shifting of brain tissue from its normal position) -Brain Herniation - sustained increases in ICP result in brainstem compression and herniation of the brain from one compartment to another; *Any brain herniation is catastrophic*! -Diabetes Insipidus (DI) due to the pressure in the cranium; decreased secretion of ADH * lookout for any ICP or neurological patients* - excessive urine output, decreased urine osmolality, and serum hyperosmolarity; Therapy: administration of fluids, electrolyte replacement, and synthetic vasopressin (desmopressin) -Syndrome of Inappropriate Antidiuretic Hormone (SIADH) due to the pressure in the cranium * lookout for any ICP or neurological patients* - increased secretion of ADH -> volume overloaded, urine output diminishes, sodium concentration becomes dilute Tx: fluid restrictions (< 800 mL/day w no free water to correct hyponatremia); severe cases -> 3% hypertonic saline solution!

brain tumor diagnosis

-Neuro exam indicates involved area of CNS CT Scan enhanced by contrast agent, lesion #,size, & identity; provides information about ventricular system & extent of secondary cerebral edema MRI most helpful diagnostic tool for detecting brain tumors (particularly small lesions or tumors in the brain when bone is thick. -Useful when monitoring treatment PET- Measure brain activity; supplement MRI scanning to decide on Tx: -low grade tumors are associated w/ hypometabolism -high-grade tumors show hypermetabolism EEG- detect abnormal brain waves (area w/ or adjacent to tumor) -evaluates temporal lobe seizures- to assist in r/o other disorders CSF Cytology- lumbar puncture detects malignant cells as CNS tumors can shed cells into the CSF but not for all cancers & can increase ICP & herniation

Brain death criteria

-Rule out hypothermia and drug and alcohol overdose before diagnosing brain death American Academy of Neurology: Coma or unresponsiveness, Absence of brainstem reflexes, Apnea Clinical Determination of Brain Death—loss of brainstem reflexes and failed apnea test. Testing of brainstem reflexes includes: 1) Pupillary response to light - no response at all 2) Corneal reflex - no blinking when using q tip or 2x2 Vestibulo-ocular reflex ("Doll's eyes") - eyes are not floating when turned Doll's eyes and cold caloric test for brainstem reflexes (eyes do not deviate to the side of the cold application, that means no brainstem reflexes) 3) Motor response to pain - flaccidity; no reactions to pain at all 4) Gag or cough reflex (suctioning through endotracheal tube or tracheotomy) *After two negative tests for brainstem function (at least 6 hours apart) -> APNEA test is generally Performed* Apnea - No spontaneous respirations despite a rise in PaCO2; disconnect ventilator -> watch for a min to see breathing Brain Death Confirmation: Following the inability to elicit brainstem reflexes and a failed Apnea Test - two electroencephalograms (12-24 hours apart) showing the absence of electrical activity confirms brain death. - Verified and documented by two physicians. -Provide realistic information about the prognosis -Keep in mind cultural differences Provide information about end-of-life care -Provide emotional support through the grief cycle: Kubler - Ross Grief Cycle (Denial, anger, depression, bargaining, acceptance) Patient and Family Advocate Promote compassionate communication Promote collaboration: Be the bridge that links the health care team to patients and their families

Hypoparathyroidism (hypocalcemia + hyperphosphatemia)

-Tetany is general muscle hypertonia, with tremor and spasmodic or uncoordinated contractions occurring with or without efforts to make voluntary movements. - numbness, tingling, and cramps in the extremities - stiffness in the hands and feet. - bronchospasm, laryngeal spasm, carpopedal spasm (flexion of the elbows and wrists and extension of the carpophalangeal joints and dorsiflexion of the feet) -dysphagia, photophobia, cardiac dysrhythmias, and seizures. - anxiety, irritability, depression, and even delirium. - ECG changes and hypotension - paresthesia (tingling on mouth, face, fingers/toes) Assessment and Diagnostic Findings - Chvostek sign - cheek twitch when touched is positive when a sharp tapping over the facial nerve just in front of the parotid gland and anterior to the ear causes spasm or twitching of the mouth, nose, and eye - Trousseau sign is positive when carpopedal spasm is induced by occluding the blood flow to the arm for 3 minutes with a blood pressure cuff Dx: - tetany @ very low calcium levels - phosphate levels are increased, - x-rays of bone show increased density -Calcification is detected on x-rays of the subcutaneous or paraspinal basal ganglia of the brain

Hyperthyroidism nursing interventions:

-avoid highly seasoned foods, stimulants (coffee, tea, cola, alcohol, high fiber, spicy food, caffeine) -high calorie, high protein + carbs -weight, and dietary intake recorded; six meals - 8 small-sized well balanced; - coping measures: reassurance, calm unhurried approach, quiet, uncluttered environment - activity w/ rest - less stimulation room - improving self-esteem - promote coping strategies, eye care, smoking cessation, nutritious food - cool, comfortable temperature, bedding/clothes change as needed, cool baths -cool or cold fluid administered monitoring and managing complications - thyroid storm (severe hypothyroidism) Thyroid storm is characterized by: -High fever (hyperpyrexia), >38.5°C (>101.3°F) -Extreme tachycardia (>130 bpm) -gastrointestinal (weight loss, diarrhea, abdominal pain) or cardiovascular (edema, chest pain, dyspnea, palpitations) -delirium psychosis, somnolence, or coma Management -hypothermia mattress or blanket, ice packs, a cool environment, hydrocortisone, and acetaminophen (Tylenol). - DO NOT USE NSAIDs - humidified oxygen - ABG monitored - dextrose IV fluids - PTU or methimazole - iodine - beta-blockers

Hyperthyroidism: excessing synthesis and secretions of endogenous or exogenous thyroid hormones by the thyroid

-common causes are Graves disease, toxic multi nodular goiter, and toxic adenoma other causes - thyroiditis (inflammation of the thyroid gland) and excessive ingestion of thyroid hormone. - Graves disease: autoimmune disorder that results from an excessive output of thyroid hormones caused by abnormal stimulation of the thyroid gland by circulating immunoglobulins; affects women eight times more frequently than men, with onset usually between the second and fourth decades; may appear after an emotional shock, stress, or an infection - result of inflammation after irradiation of the thyroid or destruction of thyroid tissue by tumor. - excessive administration of thyroid hormone for the treatment of hypothyroidism. -also likely to result in premature osteoporosis, particularly in women.

Signs of rupturing AAA

-constant, intense back pain; severe hypotension, decreasing hematocrit - Rupture into the peritoneal cavity (fatal) S/S -> hematomas in the scrotum, perineum, flank, or penis - Signs of HF or a loud bruit - suggest a rupture in the vena cava; if aneurysm adheres to the adjacent vena cava -> vena cava may become damaged - Rupture into the vena cava -> higher pressure arterial blood entering the lower pressure venous system (causes turbulence (BRUIT) - High blood pressure and increased blood volume returning to the right side of the heart - > right-sided heart failure (dependent edema (legs and sacrum), JVD, abdominal distention, hepatomegaly, splenomegaly, anorexia and nausea, weight gain, nocturnal diuresis, swelling of the fingers and hand, increased BP, or decreased BP) - severe abdominal or back pain; lumbar pain radiating to the flank and groin - increased pulse rate - signs of shock and hematoma @ flank area Diagnostic testing: Abdominal Aortic Aneurysm (AAA). - Pulsatile mass to mid and upper abdomen (most important indication and most clinically significant; palpable during exams); Take into consideration size of patient - Systolic bruit over the mass - Duplex ultrasonography or CTA - used to determine the size, length, and location of an aneurysm If an aneurysm is small -> 6 moth interval exams until it reaches a size abdominal aortic aneurysms *AAA occur in patients between 60 and 90 years of age. Rupture is likely with coexisting hypertension and with aneurysms more than 6 cm wide*

Diabetes Insipidus S/S (DECREASED ADH)

-dilute urine; Specific gravity b/w 1.001 - 1.005) -polyuria (urine output >250 ml/hour) -Polydipsia: 2 to 20 L of fluids daily; excessive thirst for water and ice - cant be controlled by limiting fluid intake; if you restrict fluid -> craving for fluid and develop hypernatremia and severe dehydration (dry mucous membranes, poor skin turgor, dry skin, hypotension) Dx: -fluid deprivation test (withholding fluids for 8-12 hours) or until 3% - 5% of body weight is lost; weight pt. frequently - if you have DI -> you still continue to pee +for DI -LOW specific gravity d/t diluted urine -weight loss -INCREASED serum osmolality (thick blood) -INCREASED sodium (hypernatremia) - low urine osmolality (<200) - measurement of ADH and plasma and urine osmolality -trial of desmopressin and IV hypertonic solution Pharmacologic Therapy - Desmopressin (DDAVP), synthetic vasopressin: -intranasally; sprays the solution into the nose through a flexible calibrated plastic tube. - 1 or 2 administrations daily (i.e., every 12 to 24 hours) - causes vasoconstriction -use cautiously in patients with CAD -watch out for decreased UO and death by headache (Low Na+) -Chlorpropamide (Diabinese) and thiazide diuretics (mild forms; potentiate the action of vasopressin); hyperglycemia possible Renal origin: Thiazide diuretics, mild salt depletion, and prostaglandin inhibitors (ibuprofen [Advil, Motrin], indomethacin [Indocin], and aspirin) are used to treat the nephrogenic form of DI. Nursing Management: - physical assessment; S/S of dehydration - adequate fluid replacement - strict I/Os; daily weight - monitor serum osmolality - safety/fall risks (hypotensive bc o floss of fluids) -Restrict food (watermelon, grapes, caffeine, lemons) - S/S of hyponatremia w/ meds (desmopressin); observe return demonstration of medication administration; knowledge of medicine - medication compliant/medical bracelet

increased ICP: pressure in the cranium and thus it reflects the pressure of the brain tissue, blood/blood vessels and cerebrospinal fluid (CSF)

Common causes: • Head injury • Brain tumors, subarachnoid hemorrhage, toxic and viral encaphalopathies • Mass lesion (tumors, hematomas) - takes up space in cranium; blocks blood from exiting cranium, normal circulation of blood and CSF • Cerebral edema from head injury • Brain inflammation - swelling • Vascular insult (anoxia, stroke, hemiparesis etc.) - brain does not profuse the blood well • any CNS condition -> consider the risk of IICP. • ↑ CO2 relaxes smooth muscles = vasodilation (too much CoO2) • O2 tension below 50mm Hg results in vasodilatation (not enough O2) • ↓pH Acidosis = vasodilation (too little pH) Cerebral vasodilation leads to an increase in cerebral blood flow and ↑ ICP -> **IMPEDES BLOOD FLOW IN THE BRAIN** brain uses 20% of O2 and 25% glucose available in body. CPP: pressure available to perfuse the blood cells WHEN THE CPP FALLS, BODY WILL ATTEMPT TO RAISE THE B/P IN ORDER TO RAISE THE CPP (AND MAINTAIN BRAIN CELL PERFUSION!)

IICP clinical manifestations earliest sign: changes in LOC; agitation, slowing of speech, delay in response to verbal suggestions vital signs changes - late sign of IICP

Early signs (subtle): Restless, Agitation, Slowing of speech, Anxious, Disorientation, Confusion, increasing drowsiness, like s/s of hypoxia Progressing signs: increased respiratory effort, stuporous, reacting to only loud or painful stimuli, pupillary changes (changes in reactivity to light), *OVAL pupillary* Papilledema (edema of the optic disc, region where the optic nerve forms; often due to increased intracranial pressure), constant headache aggravated by movement, decreasing state of alertness or LOC, decreased or erratic RR rate, increased BP and temperature, HR fluctuates between Brady and tachycardia Late Signs: Altered respiratory patterns (including Cheyne-Stokes and apnea), projectile vomiting * (VOMITING WITHOUT NAUSEA), seizures, limited or no pupillary response, eye opening response, verbal, and motor responses, hemiplegia, abnormal posturing (decerebrate: 4 extremities; extension of elbows, external rotation, decorticate: flexing their wrist, bilateral flaccidity - no movement at all; not even posturing) Decortication (abnormal flexion of upper extremities and extension of the lower extremities): Decorticate posturing and flexion of the upper extremities, internal rotation of the lower extremities, and plantar flexion of the feet. Decerebration (extreme extension of the upper and lower extremities): WORST extension and outward rotation of upper extremities and plantar flexion of the feet. Flaccidity: no movement at all; no motor response in any extremity loss of brainstem reflexes (pupillary, corneal, gag, and swallowing reflexes) coma, death (coma is profound and irreversible -> brainstem reflexes are absent, respirations are impaired or absent, pt. may be evaluated for brain death) ↑ ICP Clinical Manifestations In Infants/Children: ex: hydrocephalus, trauma, • Irritability • Bulging fontanel • Wide sutures b/w bone plates • Increased head circumference • Dilated scalp veins • Sun-setting eyes • High pitched cry

Increased ICP: Monitoring and Managing Potential Complications

Early signs: -Disorientation, restlessness, increased respiratory effort, purposeless movements, and mental confusion -Pupillary changes and impaired extraocular movements - occur as the increasing pressure displaces the brain against the oculomotor and optic nerves (cranial nerves II, III, IV, and VI) -Weakness in one extremity or on one side of the body -Headache that is constant, increasing in intensity, and aggravated by movement or straining. Later S/S of increasing ICP: -level of consciousness continues to deteriorate until the patient is comatose (Glasgow Coma Scale score ≤8). -Increased HR and decreased RR or becomes erratic, BP increases, and pulse pressure widens -Cheyne-Stokes breathing (rhythmic waxing and waning of rate and depth of respirations alternating with brief periods of apnea) and ataxic breathing (irregular breathing with a random sequence of deep and shallow breaths). -Projectile vomiting *VOMITING w/o NAUSEA* -Hemiplegia or decorticate or decerebrate posturing (pressure on the brainstem increases) bilateral flaccidity occurs before death. -Loss of brainstem reflexes, including pupillary, corneal, gag, and swallowing reflexes, is an ominous sign of approaching death Monitoring ICP: - Aseptic technique; insertion site for signs of infection (check temperature, pulse, respirations) - Check all connections and stopcocks for leaks - Transducer in supine position; head should be in the same position relative to the transducer - Repeated neurologic checks and clinical examination Monitoring for secondary complications: DI and SIADH; monitor urine output; DI - fluid and electrolyte replacement, administration of vasopressin; SIADH - fluid restriction and monitor electrolytes

encephalitis types/ TX:

HSV-1 = acyclovir or ganciclovir (anti-herpes agents); continue tx up to 3 weeks -Slow IV administration over 1 hour prevents crystallization of meds in the urine -decrease dose if renal insufficiency Fungal = antifungal agents. . . fluconazole (nausea, vomiting, transient increase in Liver enzymes) or flucytosine (bone marrow depression -> monitor leukocyte and platelet) plus amphotericin B; AE: fever, nausea and vomiting, anemia, uremia, and electrolyte abnormalities (especially potassium and magnesium). -Toxicities may occur, and renal insufficiency is a serious reaction to amphotericin B that can occur Arthropod-borne = "No specific medication for arboviral encephalitis exists; therefore, symptom management is key"

Traumatic Brain Injury (TBI)

Head injury: an injury due to an external force; not always a brain injury. - Can lead to mild concussions to coma and death, injury to: - Scalp - skin covering of head, *bleeding, and infection* (external opening) risk; w/ scalp -> DO NOT apply the pressure (there could be underlying conditions under the scalp); cover with clean loose dressing and take pt. quickly as possible. - Skull - Brain Pathophysiology of Head injury: Primary injuries: consequence of direct contact to the head/brain during the instant of initial injury, causing extracranial focal injuries (e.g., contusions, lacerations, external hematomas, and skull fractures), as well as possible focal brain injuries from sudden movement of the brain within the cranial vault (e.g., subdural hematomas (SDHs), concussion, diffuse axonal injury [DAI]) Secondary injuries: Evolves after hours or days due to inadequate delivery of oxygen or nutrients to cells. Ex: Intracranial hemorrhage (Epidural, Subdural, Intra-cerebral hematomas), cerebral edema, seizures and vasospasm; etc., increase in ICP Alert: preventing secondary injury by aggressive management Monro-Kellie hypothesis: Explains the dynamic equilibrium of cranial contents (cranium cannot expand or constrict) - the cranial vault is a closed system, and if one of the three components (brain, blood, or cerebrospinal fluid) increases in volume, at least one of the other two must decrease in volume or the pressure will increase. - Any bleeding or swelling within the skull increases the volume of contents within the skull -> increased intracranial pressure (ICP). - Herniation of brain stem -> RR, cardiac center (compressed) -> can lead to death; pt. stops breathing *severe* Brain suffers traumatic injury -> brain swelling, or bleeding increases intracranial volume -> rigid cranium allows no room for expansion of contents, so ICP increases -> pressure of blood vessels within the brain causes blood flow to the brain to slow -> cerebral hypoxia and ischemia occur -> ICP continues to rise and brain herniation -> cerebral blood flow ceases

Intracranial Hemorrhage: Collections of blood that develop within the cranial vault, the most serious type of brain injury.

Hematomas: collections of blood in the brain that may be epidural (above the dura), subdural (below the dura), and intracerebral (within the brain); can result of a subarachnoid hemorrhage or an intracerebral hemorrhage Assessment: depends on injury/ clinical manifestations usually result from increased ICP - symptoms are delayed until large hematoma causes distortion of brain and increased ICP - change in neurological signs - changes in LOC - airway and breathing pattern changes - VS signs change - Headache, nausea, vomiting - Visual disturbances, pupillary changes, and papilledema - Nuchal rigidity (not tested until spinal cord injury is ruled out) - CSF drainage from ears or nose (presence of concentric rings (bloody fluid surrounded by yellowish stain; halo sign) when fluid is placed on a white sterile background, such as a gauze pad; CSF - test positive for glucose) - Weakness and paralysis - Posturing - Decrease sensation or absence of feeling - Reflex activity changes - Seizure activity

Cushing's triad: Hypertension, bradycardia, bradypnea (or erratic RR)

Increased B/P (rise in SBP is greater compared to rise in DBP -> widened pulse pressure), decreased pulse, decreased respirations No interventions -> herniation of the brainstem and occlusion of the cerebral blood flow occurs; herniation: shifting of brain tissue from an area of high pressure to an area of lower pressure; Herniated tissue interferes w/ the blood supply in that area -> can result in cerebral ischemia, infarction, and brain death

Hypoparathyroidism - low production of PTH (hypocalcemia + hyperphosphatemia)

PTH stimulated by low Ca+ (<8.6) -> release PTH to get Ca+ levels up -> PTH acts on kidneys + bones to increase Ca+ levels Kidneys - reabsorb ca+, excrete phosphate, activates vitamin D -> in small intestine -> absorption of Ca+ through food; Bones - stimulates osteoclasts (breaks down bones) -> bone resorption -> Ca+ release -> increased level of calcium caused by: abnormal parathyroid development, destruction of the parathyroid glands (surgical removal or autoimmune response), and vitamin D deficiency. - treatment of cancer of neck/throat - hypomagnesemia - > inhibits PTH secretion most common cause: total removal of thyroid gland -> inadequate secretion of parathormone

Hypothyroidism medications and management

Pharmacologic Therapy - Synthetic levothyroxine (Synthroid or Levothroid); dosage-based pt. TSH levels; take in the morning 30-1 hour before breakfast, alone, on an empty stomach! don't withhold thyroid pulls unless ordered; THEY NEED IT. - don't stop abruptly toxicity Signs ( increased heart rate, heat intolerance, chest pain) - don't take within 4 hours of GI meds (Carafate, aluminum hydroxide, simethicone) decreases absorption - long onset; takes 3-4 weeks - if myxedema coma -> IV administration of T4 and T3 pt. also have adrenal insufficiency -> high-dose glucocorticoids (hydrocortisone) every 8 to 12 hours for 24 hours followed by low-dose therapy is recommended until coexisting adrenal insufficiency is ruled out - obtain T4, TSH, and Cortisol before and after administration of ACTH and before administration of glucocorticoid and thyroid hormone therapies - infection, GI bleeding, hyponatremia, hypotension, bradycardia, hypoglycemia, and hypothermia will also require appropriate pharmacologic management 1) prevention of cardiac dysfunction: - be alert for angina and acute coronary syndrome - oxygen needs of myocardium - discontinue hormone administration if angina or dysrhythmias occur - decrease in thyroid hormone absorption when patients are also taking magnesium-containing antacids. - Thyroid hormones may also decrease the pharmacologic effects of digitalis glycosides -> decrease anticoagulant dose in the beginning ( inc risk of bleeding) Supportive Therapy - ABGs - oxygen saturation levels - cautious fluid administration -use extra blankets or clothes instead of external heating pads (PASSIVE REWARMING) -NO heating pads, heating blanket, electric blankets - AVOID painkillers (Vicodin, morphine, Dilaudid, fentanyl) - sedatives ( benzos = Lorazepam) - provide rest, assistance w/ daily activities, prevent exposure to cold, foods high in fiber, increased mobility, -education about meds/ S/S of hyperthyroidism -do not use hypnotic, sedative, and analgesic agents - take levothyroxine first thing in the morning with a full glass of water on an empty stomach! -continue to take meds even after symptoms improve

Medical Management of SCI (Acute phase)

Pharmacologic therapy: - Pharmacological and fluid management: maintain blood pressure and cardiac output -> give vasopressors - Vasopressors, inotropes and IV fluids - Corticosteroids no longer recommended*for spinal management Respiratory Therapy: - Maintain high PaO2 - Avoid flexing extending the patient's neck if intubated - Diaphragmatic pacing (electrical stimulation of the phrenic nerve) Skeletal Fracture Reduction and Traction: immobilization and stabilization: head and neck alignment - Cervical aligned with skeletal traction (skeletal tongs (Gardner Wells Tongs) or halo device): to immobilize the cervical spine and reduce fracture and dislocation - Skeletal traction: traction is increased gradually by adding more weights; once alignment has been restored, reduction occurs (verified by cervical spine x-rays, neuro examination) - Halo device - halo ring fixed to the skull by four pins (inserted into the outer table of the skull); ring is attached to a halo vest (suspends the weight of the unit circumferentially around the chest) - Halo devices - immobilization of the cervical spine while allowing early ambulation - Thoracic and lumbar injuries (w/ surgical intervention followed by immobilization with a fitted brace Surgical Management of SCI: The goals of surgical treatment are to preserve neurologic function by removing pressure from the spinal cord and to provide stability. Decompression laminectomy, spinal fusion using bone grafts SCI assessment: Breathing pattern and strength of cough, auscultation of lungs Reduced excursion occurs Motor ability: Ability to squeeze hands, spread the fingers, move the toes, and turn the feet Sensation: pinching the skin or touching it lightly with an object such as a tongue blade, starting at shoulder level and working down both sides of the extremities. The patient should have both eyes closed so that the examination reveals true findings, not what the patient hopes to feel. The patient is asked where the sensation is felt. pinching the skin or pricking it with a pin, starting at the shoulders and working down the extremities Palpate lower abdomen (retention or overdistention) Monitor temperature Body temperature becomes dependent on surroundings (poikilothermic)

Cushing's disease: hyper-secretion of cortisol!

S/S: - central type obesity ( truncal obesity big belly) - moon face -increased oiliness of skin and acne - fatty buffalo hump in the neck and supraclavicular areas - heavy trunk w/ thin extremities - GI distress - increased acid - thin, fragile, and easily traumatized skin - ecchymoses (bruises) and purple striae - c/o of weakness and lassitude - sleep disruption - excessive protein catabolism -> muscle wasting and osteoporosis; increase risk for fractures, brittle bones - kyphosis, backache, and compression fractures of the vertebrae may result - retention of sodium and water -> HTN and HF - hyperglycemic; hypernatremia, hypokalemia, weight gain; slow healing of minor cuts, and bruises - women b/w age of 20 - 40 5x to develop than men - excessive growth of hair on face (hirsutism) -breast atrophy, menses cease, enlarged clit, deep voice - distress and depression - visual disturbances if a pituitary tumor exists. - decreased inflammatory response, impaired wound healing, increased susceptibility to infections, mood alterations, psychoses Assessment and Diagnostic: - serum cortisol - urinary cortisol (24-hour collection) low dose dexamethasone (Decadron) suppression test (overnight); 1 mg or 8 mg orally late @ night or bedtime -> obtain plasma levels @ 8 am in the morning; *Two of these three tests need to be abnormal to diagnose* - no variation of serum cortisol in these patients ( normally, serum cortisol are higher @ 6-8 am and 4-6 pm) * Suppression of cortisol to less than 5 mg/dL - normal* - stress, obesity, depression, and medications ( anticonvulsants, estrogen, rifampin (Rifadin) can falsely elevate cortisol) - increase in sodium, blood glucose levels (high), and decrease in potassium - reduction in blood eosinophils and disappearance of lymphoid tissue

SIADH - increased ADH = increased water retention

S/S: - fluid overload (edema, weight gain) - HTN (extra fluid in vascular system) - HYPOnatremia ( increased water in the body but sodium stays same - watered down) <135; headache first sign - seizures: (low sodium <135 -> death)/ seizures precaution; ( headache, confusion) - Tachycardia ( compensate for increased fluid) - confusion (brain tissue swelling) -LOW urine output - CONCENTRATED urine -HIGH specific gravity (>1.030) -LOW serum osmolality (thin blood; hemodilution due to fluid overload) - high urine osmolality (>850) -anorexia (feel full) Management: - restrict fluid intake + give salt (to prevent seizures) + diuretics (watch for K+) - No IV/drinking - IV hypertonic solution (3% NS + eat salt) - Lasix + fluid restriction if severe HYPOnatremia present - closely monitor intake and output, daily weight, urine, blood chemistries - neurologic status - safety (seizures) - watch out for headaches, confusion, and agitation

Addison's disease (decreased cortisol and decreased aldosterone); low steroid hormones

S/S: - muscle weakness, anorexia; GI symptoms ( pain, N/V), fatigue - emaciation (thin or weak) -dark pigmentation of the mucous membranes and the skin, especially of the knuckles, knees, and elbows -hypotension - @ risk for vascular collapse, postural hypotension - salt cravings - low blood glucose - cold intolerance - decreased BP - low serum sodium (hyponatremia) -high serum potassium levels (hyperkalemia) - Depression, emotional lability, apathy, and confusion, decreased weight, alopecia - electrolyte imbalances (increased K+ >5.0, Ca+, decreased Na+) - dehydration - diarrhea, nausea, reproductive changes (irregular period, ED males) Addisonian crisis: circulatory collapse -hypotension, cyanosis, fever, nausea, vomiting, and signs of shock) develops. - pallor; c/o headache, abdominal pain, and diarrhea, confusion, and restlessness; - slight overexertion, exposure to cold, acute infection, or decrease in salt -> circulatory collapse, shock, and death if untreated - stress of surgery or dehydration may precipitate an Addisonian or hypotensive crisis Assessment and Diagnostic Findings: - early-morning serum cortisol and plasma ACTH ( patients w. primary insufficiency have greatly increased plasma ACTH level but DECREASED serum cortisol) -hypoglycemia hyponatremia increased WBC (leukocytosis) hyperkalemia

Hypothyrodism: Decreased thyroid function

S/S: low energy, fatigue, weakness, muscle pains, aches, low metabolism (weight gain/water gain), low digestion, constipation, alopecia - extreme fatigue, hair loss, brittle nails, dry skin -paresthesias - numbness, tingling sensation of fingers - husky voice, coarseness, -menorrhagia or amenorrhea -heavy or irregular periods; loss of libido - weight gain w/o increase in food intake - dry skin - subnormal body temperature and pulse rate (slow HR, cold intolerance) - c/o being cold in warm environments; DO NOT GIVE electric blankets - thin hair, hair loss (alopecia), expressionless and masklike - fatigue + irritable -> then becomes apathetic, slow speech, dull; flat, boring, dull personality - slow speech, enlarged tongue, hands, and feet increase in size - deafness may occur - frequent constipation - possible dementia; inadequate ventilation and sleep apnea - Pleural effusion, pericardial effusion, and respiratory muscle weakness may also occur. Severe hypothyroidism - -elevated serum cholesterol level, atherosclerosis, coronary artery disease -poor left ventricular function. -hypothermic, sensitive to sedatives, opioid, and anesthetic agents Myxedema coma: life-threatening; hypothermic and unconscious; can occur in undx, infection or systemic disease, use of sedatives or opioid analgesic agents; forget to take thyroid replacement medications; occurs among older women in the winter months and appears to be precipitated by cold. - signs of depression, diminished cognitive status, lethargy, and somnolence; S/S of myxedema coma - hyponatremia, hypoglycemia, hypoventilation, hypotension, bradycardia, and hypothermia. @ risk: older adults, individuals with cardiac complications, reduced consciousness, persistent hypothermia, and sepsis - abruptly stopping levothyroxine, post thyroidectomy priority: have tracheostomy kit by the bedside; endo intubation set up;

Meningitis Types *septic - medical emergency!

Septic (Bacterial) Meningitis: Caused by bacteria (more common in winter & spring): -Streptococcus pneumoniae - 34% + mortality rate -Neisseria meningitidis - 10% mortality rate -outbreaks in dense community groups ex: college campuses and militarily installation, prisons. Characteristic rash occurs in about 50% of cases Increased risk: tobacco use and viral upper respiratory infection, otitis media and mastoiditis, immune system deficiencies -Haemophiles influenzae - most common cause in children; Rare in the U. S. except for those not immunized for H. Influenza -In pt. who are immunocompromised: -AIDS - cryptococcal Meningitis - headache, nausea, vomiting, seizure, confusion, lethargy; Tx: IV amphotericin B -> fluconazole -Onset of fever, headache, nausea, malaise over few weeks -Only 25% will present w/ stiff neck and photophobia Meningitis in pt. with Lyme disease: - Neurologic deficits are seen in 2 or 3 Stage 2 - occurs w/ the start of a characteristic rash or 1-6 months after rash has disappeared - Cranial nerve inflammation - bell palsy and peripheral neuropathies are common Stage 3 (chronic form); arthritis, skin lesions, and neurologic abnormalities Stage 2 and 3 Tx: IV antibiotics (ceftriaxone or penicillin G) Aseptic (Viral) Meningitis: Often less severe ;occurs more frequently in summer and early autumn). Caused by Viruses -Enterovirus - most common -Mumps virus, Herpes viruses -Herpes simplex, varicella-zoster (which causes chicken pox and shingles) - Measles virus, Influenza virus, West Nile virus Tx: keep them calm, hydrate, treat headache and fever, goes away, not w/ antiviral agents

Traumatic Brain Injury (TBI): Skull Fracture: Pathophysiology: Break in skull from forceful trauma

Types: linear (break in the continuity of bone), comminuted (splintered or multiple fracture line) - might need crainoplasty depressed skull fractures (bones of the skull are forceful displaced downward, and can vary from a slight depression to bones of the skull being splintered and embedded within brain tissue (increased ICP + swelling, damages dura mater -> CSF leaks from dura mater infection risk) Location: frontal, temporal, and basal skull fracture Open (scalp laceration or tear in the dura (e.g from a bullet or an ice pick) Closed - dura is intact; fractures but fragments are not seperated - Non-displaced - Basilar (at base of skull) - edges of the fracture bones can tear the dura, blood vessels, cranial nerves, and venous sinuses. - Patient at risk for infection and herniation syndrome Clinical Manifestations: - Persistent, localized pain - Fractures of cranial vault - may or may not produce swelling in the region of the fracture

encephalitis manifestations:

an early phase of flu-like symptoms (headache, fever, malaise, photophobia, nuchal rigidity). -Signs/symptoms of IICP can occur. -progressive neurological dysfunction and neuropsychiatric complications [behavioral changes, emotional outbursts, focal seizures (+/or generalized seizures), dysphasia, hemiparesis, Parkinson-like movements, altered LOC, auditory and visual hallucinations] Medical and Nursing Management Encephalitis -MRI (shows inflammation) and CSF evaluation -Polymerase Chain Reaction (PCR for herpes encephalitis). -EEG - shows diffuse showing or focal changes in the temporal lobe -Lumbar puncture - reveals a high opening pressure, glucose within normal limits, and high protein levels in CSF Early administration of antiviral medications -Acyclovir or ganciclovir for HSV-1, antifungal - No specific meds for arboviral encephalitis-manage symptoms -Administering Benadryl or Tylenol 30 mins before giving amphotericin B -Increasing levels of creatinine and BUN (development of renal insufficiency) -Monitor neuro status--control seizures (anticonvulsants) -IICP (Lumbar punctures or shunting of CSF) -altered LOC (safety precautions) -Injury prevention -Clothing that provides coverage and DEET - arthropod borne -Monitor labs (BUN, Creatinine), blood chemistry, urine output; Liver function tests (due to use of antivirals) Comfort measures for headache: -Dim lights, limited noise, and visitors, grouping nursing interventions, and analgesic agents -Watch for and manage neuropsychiatric complications (emotional outbursts, erratic or violent behavior, etc.) -Patient and family support

Thoracic Aortic Aneurysm (TAA):

bulging of the wall of the aorta, the main vessel that feeds blood from the heart to tissues and organs throughout the body. When an aneurysm occurs in a portion of the aorta within the chest, it is called thoracic (chest) aortic aneurysm or TAA. If TAA ruptures -> 50-80% do not survive. 70% caused by atherosclerosis; occur most frequently in men b/w ages of 50 and 70 years **thoracic area most common site for dissecting aneurysm; high morbidity and mortality! - endovascular aortic repair

non-traumatic brain injury

can have stroke, LOC, needs CT scan - Systemic hypertension - Rupture of an aneurysm - Vascular anomalies - Intracranial tumors - Bleeding disorders

Addison's Disease: adrenal glands are damaged and cannot produce sufficient amounts of cortical hormones ( ADRENOCORTICAL INSUFFICIENCY)

causes: - Autoimmune or idiopathic atrophy of the adrenal glands -surgical removal of both adrenal glands -infection of the adrenal glands. - Tuberculosis and histoplasmosis - use of multiple pharmacologic therapies such as anticoagulants (resulting in adrenal hemorrhage), anticonvulsants (e.g., phenytoin [Dilantin] and phenobarbital), and antibiotics (e.g., rifampicin) for chronic and severe illnesses - treatment w/ daily administration of corticosteroids for 2-4 weeks

Cushing's disease - an increased secretion of cortisol; oversecretion of glucocorticoids and androgens; excessive adrenocortical activity

causes: - use of corticosteroid medications ( ex: prednisone therapy) -hyperplasia of adrenal cortex -overproduction of endogenous corticosteroids -pituitary, adrenal tumors -ectopic production of ACTH by malignancies; bronchogenic carcinoma (small cell lung cancers)

Diabetes insipidus (common disorder of the posterior lobe of the pit. gland and deficiency of ADH (vasopressin) ( decreased ADH -> losing too much water)

causes: - secondary to head trauma, brain tumor, or surgical ablation or irradiation of the pituitary gland - infections of the central nervous system (meningitis, encephalitis, tuberculosis) or with tumors (e.g., metastatic disease, lymphoma of the breast or lung). - ; this nephrogenic form may be related to hypokalemia, hypercalcemia, and a variety of medications (e.g., lithium, demeclocycline [Declomycin]).

Common Causes of Secondary injury:

causes: cerebral edema, hypotension, and respiratory depression that may lead to hypoxemia and electrolyte imbalance. Tx to prevent secondary injury: - Stabilization of cardiovascular and respiratory function to maintain adequate cerebral perfusion, control of hemorrhage and hypovolemia, and maintain of optimal ABGs. Treatment of Increased ICP: if ICP remains high, it decreases CPP - Initial management: Preventing secondary injury and maintaining adequate cerebral oxygenation - Surgery - evacuation of blood clots, debridement, and elevation of depressed fractures of the skull, and suture of severe scalp laceration - Monitor ICP closely - Adequate oxygenation, elevating the HOB (30-45 degrees), maintaining normal blood volume - Devices to monitor ICP or drain CSF inserted; maintain aseptic technique; prevention of infection -Positioning (supine w/ head midline, HOB @ 30-45, avoid extreme hip flexion and rotation and flexion of neck) *Follow interventions to prevent increased ICP* · Elevate the head of the bed as prescribed. · Maintain the patient's head and neck in neutral alignment (no twisting or flexing the neck). · Initiate measures to prevent the Valsalva maneuver (e.g., stool softeners). - avoid coughing and sneezing · Maintain body temperature within normal limits. · Administer oxygen (O2) to maintain partial pressure of arterial oxygen (PaO2) >90 mm Hg. · Maintain fluid balance with normal saline solution. · Avoid noxious stimuli (e.g., excessive suctioning, painful procedures). · Administer sedation to reduce agitation. · Maintain cerebral perfusion pressure of 50-70 mm Hg. Supportive Measures: ventilator support, seizure prevention, fluid and electrolyte maintenance, nutritional support, and management of pain and anxiety. Comatose pt. - intubated and mechanically ventilated to ensure adequate oxygenation and protect the airway - Anticonvulsants for seizures - Agitation -> benzodiazepines: Lorazepam (Ativan) and midazolam (Versed); makes it difficult to conduct a neurologic assessment - Propofol IV - sedation (accurate neurologic assessment) - NG tube Brain Death: three cardinal signs of brain death on clinical examination are coma, the absence of brainstem reflexes, and apnea. doing all possible tx and still no improvements --Organ donor? - cerebral blood flow studies, electroencephalogram (EEG), transcranial Doppler, and brainstem auditory-evoked potential, are often used to confirm brain death

Addison's disease Management

combating circulatory shock: restoring blood circulation, administering fluids and corticosteroids, monitoring vital signs -placing the patient in a recumbent position with the legs elevated. -Hydrocortisone (Solu-Cortef) ( IV CORTISOL) + IV Fluids (5% dextrose in normal saline) D5NS -Vasopressors - if hypotension -antibiotics if infection has precipitated adrenal crisis -oral fluids once tolerated -lifelong replacement of corticosteroids and mineral corticosteroids if adrenal gland does not regain function -salt supplement during GI losses of fluids watch for Addison crisis: IV administration of fluid, glucose, electrolytes, and sodium + replacement of missing steroid hormones and vasopressors (IV cortisol stat ( solu cerf) + IV Fluids (D5NS); ( goal: to increase blood sugar, sodium, increase BP) - stressful procedures or significant illnesses -> increase dose of medications; - monitor for lower blood glucose, blood pressure ( sitting, lying, and standing) increased potassium; - H&P, fluid imbalances, watch for skin changes in color and turgor, and daily weight lifelong replacement: replacing cortisol: prednisone, hydrocortisone (if increased stress, surgery, illness -> increase dose) - replacing aldosterone: Florinef - DO NOT stop abruptly; take medications regularly -dietary supplement of salt during GI losses of fluids - select foods high in sodium during GI disturbances and in very hot weather - minimize stress; avoid unnecessary activity and stress - carry medical bracelet, avoid strenuous activity in hot, humid, weather - strategies dealing w/ stress - increase fluid intake and salt w/ excessive perspiration - high carbohydrate, high protein diet w/ adequate sodium intake S/S of adrenal crisis and need for emergency care emergency kit: corticosteroid in prefilled syringes, 100-mg vials of hydrocortisone or 4 mg of dexamethasone, and 0.9% sterile saline to reconstitute the corticosteroid and syringes (entire dose of 100-mg hydrocortisone or 4 mg of dexamethasone should be given and medical attention sought immediately after administering the drug) * add steroids, increase dose when needed, high in protein, carb/sodium, don't abruptly stop -> Addison crisis, not a cure, lifelong hormone replacement)!

Gliomas

develop from glial cells - Originate from cerebellum; develop at curves of brain - frontal cortex susceptible -astrocytoma's- surround neural CT tissue & therefore cannot be totally removed w/o causing considerable damage to vital structures. - Grade IV Glioblastoma- most aggressive lethal Tx: w/ Combo surgery, radiation therapy & chemotherapy

Benign vs. Malignant Brain tumors

doesn't matter for our purpose primary concern is they both increase ICP -Malignant Tumor associated w/ swelling as rapid growth damages brain tissue

Traumatic Brain Injury (TBI): Basilar Skull fractures

fracture of the base of the skull that involves the bony structure at the level of mid face - Fractures @ base of skull - traverse the paranasal sinus of the frontal bone or middle ear located in the temporal bone; produce hemorrhage from the nose, pharynx, ears and blood may appear under conjunctiva - When CSF escapes from the ears (CSF otorrhea) and the nose (CSF rhinorrhea) - Meningeal infection can occur - hallmark sign when dura is ruptured is fluid draining from orifices in ear or nose: risk for infection (clear or blood-tinged fluids) - *Prevent infection* -do not allow the patient to BLOW their nose -Do not plug the nose* -unconscious - do not suction the patient (increases the damage);put loose sterile dressing - Classic symptoms - halo sign - round red blood in the middle but gets lighter and lighter and ring of clear liquid (CSF drainage w/ blood tinged) - Presence of concentric rings (bloody fluid surrounds by yellowish stain; halo sign) - Confirm it to check if its CSF (presence of glucose) + glucose when using a strip test - Bruising over the mastoid (Battles Sign) and around the eyes (periorbital ecchymosis) raccoon eyes and behind the ear - Many blood vessels and cranial nerves can be injured (do neuro exams, assess for CN) Assessment and Diagnostic: CT and MRI Basilar skull fracture Management: - Management of CSF Leakage: Should not stop, collected using loosely applied gauze, patient at risk for infection, drainage may be tested for glucose, avoid nasogastric tube placement, avoid blowing nose, and suctioning - do not clean the drainage but apply a loose, dry sterile dressing - Do not clean the nose, suction, or allow client to blow their nose if there is drainage - Non-depressed fractures: Close observation, generally no surgical treatments - Depressed fractures: Surgical repair with bone or grafts, repair may be delayed due to cerebral edema, debridement; remove the fragmented bones and clean the wound and take care of the pt.; leave the area without any bone and store it in subcutaneous area until the intracranial pressure is maintained then they replace the bone - Positioning: do not position in the area, ask to wear helmet, you can't be restricting activities in kids - 30-45 @ head and neck alignment; if bone fragments are removed (do not position on that side) ◦ Avoid anything that will increase intracranial pressure

Brain Tumor Chemotherapy

in conjunction w/ radiation therapy or sole therapy. -Greatest challenge-> cross blood brain barrier with effective doses w/o causing system toxicity Malignant glioma-> Tx w/ 6 weeks of oral temozolomide (Temodar) during radiation therapy followed by 6 to 12 months of oral temozolomide (1st oral chemotherapy that crosses BBB) Autologous Bone Marrow Transplant- "rescue" pt's from the bone marrow toxicity assoc. w/ high doses of chemotherapy & radiation -aspirated from pts iliac crest & stored-> then reinfused intravenously

Brain Tumor - secondary

metastases Brain tumors develop d/t spread of cancerous cells from the outside brain - 2x as common as primary tumors - Found in Female> Males -Main cancer sites ( lung, breast)-> metastasize to brain

Craniotomy

most common; -skull is removed (bone flap) to biopsy the brain tissue or to excise a tumor Ex: Burr holes: used to remove blood clots in epidural hematoma -Surgeon cuts the skull to create a bony flap-> repositioned after surgery

Epidural hematoma:

mostly arterial (bleeds profusely); Collection of blood in the space between the skull and the dura matter; can result from a skull fracture that causes a rupture or laceration of the middle meningeal artery - Hemorrhage from this artery causes rapid pressure on the brain S/S - brief loss of consciousness, followed by lucid interval in which the patient is awake and conversant; compensation mechanism no longer in pace -> agitation, restlessness, and confusion -> coma Signs of herniation (deterioration of consciousness and signs of focal neurologic deficits - fixation and fixation of a pupil or paralysis of an extremity); common: uncal herniation Hematoma; only a bleeding; no brain structural damage; no CSF infection or injury *CT SCAN* - gold standard; remove the hematoma (surgery) Tx: making openings through the skull (burr holes) to decrease ICP, remove the clot, and control the bleeding; Craniotomy; drain after creation of burr holes or a craniotomy to prevent reaccumulating of blood

subarachnoid hemorrhage *Altered LOC early sign* drowsiness and slight slurring of speech are early signs

occurs because of an AVM, intracranial aneurysm, trauma, or HTN Most common causes: leaking aneurysm in circle of Willis and a congenital AVM of brain S/S: - Conscious pt: severe headache, nausea or vomiting, an early sudden change in LOC, possible seizure - sudden, unusually severe headache, loss of consciousness for a variable period. - pain and rigidity of the back of the neck (nuchal rigidity) and spine due to meningeal irritation - visual disturbances (visual loss, diplopia, ptosis) if aneurysm is adjacent to oculomotor nerve - tinnitus, dizziness, hemiparesis - Severe bleeding may result in cerebral damage followed rapidly by coma and subsequent death. - Ultimately a subarachnoid hemorrhage from an aneurysm is catastrophic even with significant morbidity and mortality. Dx testing: Cerebral Aneurysm: - CT scan or MRI scan - to determine the type of stroke, size and location of the hematoma, presence or absence of ventricular blood and hydrocephalus - * CT scan is usually obtained first* - CTA - confirms the dx. Of intracranial aneurysm or AVM (show the location and size of lesion and provide info about affected arteries, veins, adjoining vessels, and vascular branches - Lumbar puncture - if no evidence of ICP, CT scan are negative - Patients <40 years old - toxicology screen for illicit drug use Prevention of hemorrhaging stroke: control HTN; stroke risk screening and educating about recognition and prevention

Epidural hemorrhage

often characterized by a brief loss of consciousness, followed by a lucid interval in which the patient is awake and conversant and then go into deep coma; -extreme emergency - marked neurologic deficit or even respiratory arrest can occur within minutes. Goal of treatment: Decrease ICP emergently, remove the clot; burr- hole-Surgery, and control the bleeding.

Cushing's Syndrome Management

pituitary tumors -> surgical removal of the tumor by transsphenoidal hypophysectomy - radiation of pituitary gland - Adrenalectomy for pt. w/ unilateral primary adrenal hypertrophy; teach about cortisl replacement therapy after surgery - ectopic ACTH secretion -> Adrenal enzyme inhibitors (e.g., metyrapone [Metopirone], aminoglutethimide [Cytadren], mitotane [Lysodren], and ketoconazole [Nizoral]) may be used to reduce hyperadrenalism - if result of administration of corticosteroids -> attempt to taper the medication to the minimum dose Nursing interventions: -Prevent falls, fractures, injuries - foods high in protein, calcium, and vitamin D -Avoid unnecessary exposure to others w/ infection -Blood glucose monitoring before, during, and after surgery, stools for blood - encourage mobility w/ rest periods - meticulous skin care -assess skin and bony prominences - change positions frequently to prevent skin breakdown -Low carbs, low sodium diet, high protein -> to control weight gain and edema - reassurance/support system Addisonian crisis after surgery or withdrawal of corticosteroids; treat pt. for circulatory collapse and shock -Blood glucose monitoring -Medical bracelet, manage labile emotions, skin care, protective devices and practices to decrease injury/fracture -Foods high in potassium, low in sodium, calories, and carbohydrates, decrease risk of infection -monitoring BP, blood glucose levels, and weight -Balance rest and activity

Cerebral aneurysm: subarachnoid hemorrhage Management

Medical Management: - Bed rest with sedation to prevent agitation and stress - Management of vasospasm, surgical or medical treatment to prevent bleeding - If the bleeding is caused by anticoagulation with warfarin -> INR corrected with fresh-frozen plasma and/or vitamin K. - If seizures occur -> treated with anticonvulsant drugs such as phenytoin (Dilantin); can also be given as a prophylaxis - Treat Hyperglycemia; Avoid hypoglycemia - Intermittent pneumatic compression devices (SCDs) - use starting on the first day of the hospital admission to prevent DVT; they would not be on DVT prophylaxis initially! - If the patient is not mobile after 1 to 4 days from the onset of the hemorrhage and documentation is consistent with resolved bleeding -> Advocate for DVT prophylaxis (low-molecular-weight heparin or unfractionated heparin) - Analgesic agents may be prescribed for head and neck pain - Fever - acetaminophen (Tylenol), iced saline boluses, and devices such as cooling blankets - After discharge: antihypertensive meds Surgical Management: Cerebral Aneurysm - Primary not treated surgically unless patient is showing signs of worsening neurologic examination, increased ICP, brainstem compression, or to prevent rupture. - Surgical evacuation via craniotomy is recommended; surgical intervention as soon as condition is stable - Goal of surgery: to prevent bleeding in an unruptured aneurysm or further bleeding in an already ruptured aneurysm - Done by isolating the aneurysm from its circulation or its strengthening the arterial wall; Ligature or a clip across the neck of the aneurysm; if that's not possible -> aneurysm is wrapped w some substance to provide support and induce scarring - Endovascular techniques to occlude the blood flow from the artery that feeds the aneurysm with coils, liquid embolic agents, or other techniques to occlude the aneurysm itself via Interventional neuroradiology - If aneurysm is very large or very wide at its neck: stent-like device made of a very fine mesh may be used to divert the blood flow away from the aneurysm Post-operative complications: psychological symptoms (disorientation, amnesia, Korsakoff syndrome [disorder characterized by psychosis, disorientation, delirium, insomnia, hallucinations, personality changes]), intraoperative embolization or artery rupture, postoperative artery occlusion, fluid and electrolyte disturbances (from dysfunction of the neurohypophyseal system), and gastrointestinal bleeding. Nursing interventions: - Neurologic flow record (BP, pulse, LOC, pupillary responses, motor function, following commands checked hourly, respiratory status - Non stimulating environment to prevent increase in ICP and further bleeding; bed rest in a quiet, non-stresful environment (activity, pain, and anxiety elevate BP), visitors may be restricted - HOB elevated 30 degrees to promote venous drainage and decrease ICP - AVOID Valsalva maneuver, straining, forceful sneezing, pushing oneself up in bed and acute flexion or rotation of head and neck (compromises Jugular veins) - these prevents ICP - Stool softener and mild laxatives - prevent constipation (constipation increases ICP) - Dim lighting bc photophobia (visual intolerance of light) common - Intermittent pneumatic compression devices to reduce DVT - Observe legs for S/S of DVT (tenderness, redness, swelling, warmth, and edema) and abnormal findings - Keep sensory stimulation to a minimum; reality orientation if needed - Education family - assess for possible vasospasm: intensified headaches, a decrease in level of responsiveness (confusion, disorientation, lethargy), or evidence of aphasia or partial paralysis -> nimodipine -> prevention; fluid volume expanders triple H therapy - Seizures - precautions; maintaining airway and preventing injury are primary goals; Medication: phenytoin - Hydrocephalus - can be acute, subacute, or delayed; acute hydrocephalus: sudden onset of stupor or coma and managed w/ ventriculostomy drain - Subacute and delayed hydrocephalus - gradual onset of drowsiness, behavior changes, and ataxic gait - ventriculoperitoneal shunt to treat chronic hydrocephalus - monitor for symptoms of rebleeding: sudden severe headache, nausea, vomiting, decreased LOC, neurologic deficit; CT scan to confirm; BP maintained w/ meds - Hyponatremia - associated w/ onset of vasospasm; check labs; notify if low serum sodium <135 has persisted more than 24 hours; evaluate for SIADH or cerebral salt wasting syndrome; treatment is use of IV hypertonic 3% saline - Advocate for PT/OT/SLP - Educate about splints or orthotics, proper position, and frequent positioning - Give acetaminophen but not NSAIDS (bleeding risk) or narcotics; distraction/ positioning - Mobilize as soon as possible - Diet: thickened liquids, pureed diet, small meals during recovery - Psychosocial consequences: depression, emotional lability, frustration, fatigue - Prevent blood clots, aspiration, pneumonia, UTI, fecal impaction, skin breakdown, contracture - fall prevention

Meningitis S/S

Pathophysiology of Bacterial Meningitis Transmission (increased in settings where people live in proximity): 1. Direct inoculation: After traumatic injury of facial bones, sinusitis, otitis media, lumbar puncture, skull/spine infection -> penetrates CSF 2. Colonization or local infection (generally via exchange of respiratory and throat secretions Kissing, saliva, mucus, sneezing, water bottles Risk factors: tobacco and URI's due to increased droplet production 3. Through bloodstream Due to infections of heart, lungs, or viscera 4. Retrograde neuronal pathways (olfactory and peripheral nerves). Clinical Manifestations: headache and fever - initial symptoms Early stages: (preliminary and inconclusive) - Severe, throbbing headache, Persistent fever** - Nuchal rigidity (stiff neck and painful neck); attempts at flexion of head is difficult** - Positive Kernig sign: When the patient is lying with the thigh flexed on the abdomen, the leg cannot be **completely extended; bilateral -> + for meningeal irritation; flex the patient's leg at the hip and knee and then straighten the knee.** - Positive Brudzinski's sign - (when the patient's neck is flexed (after ruling out cervical trauma or injury), flexion of the knees and hip is produced; when the lower extremity of one side is passively flexed, a similar movement is seen in the opposite extremity) as the neck is flexed, watch the hips and knees for a reaction *more sensitive indicator than Kernig*** - Photophobia (extreme sensitivity to light) - due to irritation of the meninges** - Rash, skin lesions develop, petechial rash w/ purpuric lesions to large areas of ecchymosis - Disorientation and memory impairment - Seizures can occur; increased ICP (decreases LOC and focal motor deficits), can cause brainstem herniation - Acute fulminant infection -> abrupt onset of high fever, extensive purpuric lesions (over the face and extremities), shock, signs of DIC; death can occur - Cranial nerve involvement Vomiting, seizures, changes in LOC (further disorientation, agitation or decline in responsiveness) can occur early or late Late stages of meningitis = s/s of increasing ICP: -Overwhelming septicemia, shock, DIC -Herniation of brainstem, Coma, death Diagnosis of Meningitis: - CT scan - to detect brain shifts before lumbar puncture in patients w/ altered LOC, papilledema, neurologic defects, new onset of seizure, immunocompromised state, or hx of CNS disease - Bacterial culture and gram staining of CSF and blood *KEY - CSF from lumbar puncture is cloudy, reveals decreased blood glucose (bacteria consumes glucose) ,increased protein, and increased white blood cells. - Positive bacterial cultures of blood & CSF - Eliciting Pain is + Sign - OBTAIN DIAGNOSIS—CSF analysis (MRI/CT scan if evidence of IICP—dangerous to do L/P if pt. has IICP.)

Meningitis Management

Prevention of Meningitis: -Meningococcal conjugated vaccine be given to youth at 11 to 12 years of age, with a booster dose at 16 years of age. -First year college students and military ppl who have not been vaccinated are @ risk -People exposed to others with meningococcal meningitis should be treated with antimicrobial chemoprophylaxis using rifampin, ciprofloxacin hydrochloride, or ceftriaxone within 24 hours after exposure. -Vaccination (meningococcal and Strep. Pneumoniae) for people at risk (such as those in close contact with infected individuals). -Vaccination against Haemophilus influenzae and S. pneumoniae should be encouraged for children and adults who are at-risk Medical Management of Meningitis: - Dexamethasone - give 15 to 20 minutes before the first dose of antibiotic and every 6 hours for the next 4 days -Dexamethasone used prior to antibiotics - potent anti-inflammatory! shrinks the meninges, CSF circulates better, bacterial doses get into the system better; decreases inflammation! -Early antibiotics that cross the blood-brain barrier: Often double or triple antibiotics Penicillin G + cephalosporins (ceftriaxone sodium, cefotaxime sodium) IV w/in 30 minutes of hospital arrival -Respiratory (droplet) isolation precautions: For at least 24 hours after initiation of antibiotic therapy - or facility protocol -Oral and nasal discharge is considered infectious -Treat dehydration and shock: Fluid volume expanders (hypertonic Mannitol) -Prophylactic anticonvulsants (or not prophylactic: Dilantin may be ordered -ET Tube/mechanical ventilation - if in ICU Nursing Management of Meningitis -Frequent Vital Signs (manage fever) -Pain management due to overall body aches and neck pain -Controlled, quiet environment, darkened room -Infection control precautions *RESPIRATORY DROPLET PRECAUTIONS* -Encourage hydration orally or peripherally -Close neurologic monitoring -Blood pressure (usually arterial line) -Seizure Precautions - protecting the patient from injury secondary to seizure activity or altered LOC -Protect patient from injury due to altered mental status -Monitor: daily weight, urine output & specific gravity, electrolytes, osmolality if SIADH is suspected -Prevent complications from immobility ex. Pressure ulcers and pneumonia -Family support and resources - (case management, social work, clergy, support groups)

hyperparathyroidism treatment

Surgical Management - primary hyperparathyroidism - removal of abnormal parathyroid tissue (parathyroidectomy) Surgery is recommended for asymptomatic patients who meet one or more of the following criteria: '(1) younger than 50 years, (2) any patient unable or unlikely to participate in follow up care, (3) serum calcium level more than 1 mg/dL (0.25 mmol/L) above normal reference range, (3) GFR < 60 mL/min, (4) urinary calcium level greater than 400 mg/day (10 mmol/day, (5) bone density at hip, lumbar spine, or distal radius with T score < -2.5 or previous fracture fragility at any site, (6) nephrolethiasis or nephrocalcinosis Hydration Therapy - daily fluid intake of 2,000 mL or more is encouraged to help prevent calculus formation. - watch for abdominal pain and hematuria - AVOID thiazide diuretictics - avoid dehydration and seek help if ( vomiting, diarrhea) occur Mobility - encourage to walk Diet and Medications - prune juice, stool softeners, and physical activity, increased fluid to help constipation - peptic ulcer: antacids and protein feedings - precautions about airway patency, dehydration, immobility, and diet - closely monitors the patient to detect symptoms of tetany - monitor calcium levels; decreased Ca+ ( numbness, tingling, excessive twitching, +T/V) - diet low in ca+ and high in phosphate (watch in renal pt. bc they might already have hyperphosphatemia) - strain urine -> any renal calculi?/ I and Os - semi fowlers position, trach kit, and suction O2 @ bedside Medications: LOWER PTH, LOWER Ca+, keep pt+ hydrated (to prevent calculi) ( loop diuretics, phosphates, calcitonin) 1) calcimimetics "sensipar": prescribed for patients w/ secondary causes of CKDS ( decreases PTH, decreases Ca+, decreases phosphate levels) *for renal patients*; take with food 2) Calcitonin (injection or nasal) - lowers Ca+ (suppresses osteoclasts), increases osteoblasts activities (protects bones) + causes kidney to excrete Ca+ 3) Loop diuretics - Lasix; decreases Ca+ (watch for K+ levels) 4) biphosphonates: helps protect bones from losing ca+; increase osteoblasts - pamidronate or Fosamax - take on empty stomach by itself; full glass H20; sit upright for 30 minutes - wait 30 minutes before taking vitamins/antacids - Managing pain (medication and nonpharmacologic interventions)

Supratentorial

-incision behind hairline on forehead parietal lobe -Maintain HOB at 30 degrees w/ neck in neutral position -avoid positioning pt on operative side if large tumor removed

Hyperparathyroidism: overproduction of PTH by parathyroid gland and characterized by bone decalcification and development of renal calculi (kidney stone) containing calcium

primary hyperparathyroidism: - 2-4 times more often in women than men - most common b/w 60 - 70 years Secondary hyperparathyroidism: - occurs in patients who have chronic kidney failure and so-called renal rickets as a result of phosphorus retention, increased stimulation of the parathyroid glands, and increased parathormone secretion.

AAA signs of impending rupture: *RIPPING AND TEARING PAIN*

severe abdominal pain (persistent or intermittent); pain is localized in the middle or lower abdomen to the left of the midline -low back pain may be present (pressure of the aneurysm on the lumbar nerves) -Specific to impending rupture because otherwise, it'd be asymptomatic

Spinal Cord Tumor Surgery: Monitor and Managing complications

- If tumor in cervical area-respiratory compromise d/t postop edema. -Monitor asymmetric chest movement, abdominal breathing and abnormal breath sounds. -ET Tube remain in place until adequate respiratory function is ensure -Maintain suction equipment at bedside-> ineffective cough. - Maintain immobilization & stabilization-> prevent further damage. -Bladder scan for urinary retention- also monitor for incontinence -urinary dysfunction usually-> decompensation of spinal cord function -.I/Os -Auscultate for bowel sounds -Passive ROM to prevent contractures/loss of muscle tone -Staining of the dressing may indicate leakage of CSF at surgical site -Bulging at the incision may indicate contained CSF leak. -monitor for increasing bulging known as pseudo meningocele requires surgical repair

Coping W/ sensory deprivation

- Periorbital edema->fluid drains into periorbital areas when patient has been positioned prone during surgery -Hematoma under scalp or down the orbit producing ecchymosis on one or both eyes may be edematous and temp black eye after surgery -elevate HOB (if not contraindicated) -apply cold compress over eyes to reduce edema -announce you are entering the room so as not to startle the patient

transphenoidal hypophysectomy

- endoscopic procedure to remove a pituitary tumor -incision of the sphenoid sinus beneath the upper lip to gain access to nasal cavity -maintain nasal packing in place and reinforce as needed -Instruct patient NOT to blow nose -prep oral care according to policy -Keep HOB elevated to promote venous drainage

Monitor for increased ICP & bleeding

- increase in BP, decrease in pulse and respirations->IICP -accumulation of blood under bone flap- life threatening clot must be suspected in any patient when they do not awaken as expected or whose condition deteriorates. -Intracranial hematoma-> dilated pupil on the operative side

Spinal Cord Tumor Assessment and Diagnostic findings

-Reveals pain, loss of reflexes below the tumor level, loss of sensation or motor function, weakness, paralysis -Initial LBP (low back pain) may radiate down to leg or arms MRI- Gold Standard; mostly commonly used diagnostic tool - f primary mass found- then do biopsy to diagnose tumor type + CT of chest & abdomen

FLuid and electrolyte imbalance

-can contribute to development of cerebral edema; -daily serum lab values collected -I/Os -Fluids may need to be restricted in pts w/ cerebral edema. -Oral fluids-> resumed after first 24 hrs post-op -check gag & swallowing reflexes -Observe patients for s/sx of N/V as diet is progressed -Corticosteroids-> risk for hyperglycemia- serum glucose levels Q4-6 hrs- insulin sliding scale; -For patients prone to stress ulcers-> H2Blockers to suppress the secretion of gastric acid Surgical sites near the hypothalamus & pituitary gland DI- excessive UOP, increased serum osmolality, decreased urine osmolality, HyperNa+ & low specific urine gravityF -Fluid replacement must compensate for UOP & serum K+ levels must be monitored SIADH-> water retention w/ HypoNa+ & serum hypoosmolality occurs in a wide variety of CNS disorders (brain tumor & head trauma) causing fluid imbalance

Spinal Cord Compression (SCC) from tumor

-is a medical emergency - tumor extends into the epidural space -need immediate Tx to prevent permanent neurological damage surgical removal is preferred

subarachnoid hemorrhage (SAH) Complications

1) Cerebral hypoxia and decreased blood flow Cerebral Hypoxia and Decreased Blood Flow: -Provide adequate oxygen* -Adequate hydration (IV fluids) -Observing for seizure activity and initiating appt. treatment* -Maintain hemoglobin and hematocrit* 2) Vasospasm: development of cerebral vasospasm (narrowing of the lumen of the involved cranial blood vessel); a leading cause of morbidity and mortality in those who survive the initial subarachnoid hemorrhage. - Monitor vasospasm through use of transcranial doppler ultrasonography or follow up cerebral angiography - Watch out for worsening headache, decrease in LOC (confusion, lethargy, disorientation), or new focal neurologic deficit ( aphasia, hemiparesis) Tx: early surgery to clip aneurysm; Nimodipine (CCB) to prevent, euvolemia - to prevent delayed cerebral ischemia and induced arterial HTN (treatment of delayed cerebral ischemia) 3) Increased ICP: almost always follows a subarachnoid hemorrhage, usually because of disturbed circulation of CSF caused by blood in the basal cisterns. - Perform neurologic assessments - Evidence of deterioration from increased ICP (due to cerebral edema, herniation, hydrocephalus, or vasospasm) -> CSF drainage - Mannitol to reduce ICP *watch for dehydration, F/E imbalances (sodium and potassium) * - Monitor fluid balance and asses for signs of dehydration and rebound elevation of ICP - Elevating HOB to 30 degrees, avoidance of hyperglycemia and hypoglycemia, sedation and use of hypertonic saline in variety of concentration (3%, 7.5, or 23%) 4) Hypertension: most common cause of intracerebral hemorrhage - Lowering SBP of 140 mmHg - Nicardipine - continuous IV infusion, Labetalol and hydralazine ( IV boluses), during administration of antihypertensives -> hemodynamic monitoring essential to detect drop in BP -> brain ischemia - Stool softeners to prevent straining (straining can elevate BP)

IICP -Medical Management

1) Monitoring ICP & Cerebral Oxygenation: Monitoring: less invasive, less side effects, easier to manage; -> cannot drain; not therapeutic Drainage: can lower ICP; therapeutic, more invasive, can have damage on brain tissue; catheter -> increases risk of infection! Ventriculostomy (intraventricular catheter) or intraventricular catheter monitoring device -> allows CSF to drain, can be used to drain blood from the ventricle, continuous drainage of CSF under pressure control Complications: infection, meningitis, ventricular collapse, occlusion of the catheter by brain tissue or blood, and problems with monitoring system subarachnoid bolt - does not require ventricular puncture; avoids complications from brain shift and small ventricle size; complications: infection and blockage of screw by clot or brain tissue -> decrease in accuracy at high ICP readings epidural or subdural catheter - uses a pneumatic flow sensor to detect ICP; low incidence of infection complications; you cannot withdraw CSF for analysis Fiberoptic transducer tipped catheter place in the subdural space or in the ventricle - reflects pressure changes -> converted into electrical signals; catheter can be inserted into the ventricle, subarachnoid space, subdural space, or brain parenchyma or bone flap; if inserted into ventricle -> can be used w/ CSF drainage device 2) Decreasing cerebral edema - OSMOTIC DIURETICS: Mannitol and hypertonic saline (3%) - dehydrate the brain tissue; they reduce volume of the brain and extracellular fluid; mannitol draws fluid out of the brain and increases osmolarity of blood and fluid of the brain; CAREFUL MONITORING - Indwelling urinary catheter to monitor urinary output and manage diuresis - Osmotic diuretics (assess serum osmolality and electrolytes to assess hydration status) - IV corticosteroids (dexamethasone) - reduces inflammation and swelling -> decreases ICP - Fluid restriction (leads to dehydration and hemoconcentration which decreases Cerebral edema) - Induced hypothermia: Lowering body temperature (reduces O2 and glucose demands) ; cooling core temperature (80s-98.6) ex: use cooling blankets; AVOID HYPER THERMIA!; USED only in select settings 3) Maintaining cerebral perfusion: CPP to be maintained > 70 mm Hg - Cardiac Output must adequate - 1) Vasopressors/Inotropic agents - dobutamine and norepinephrine)- (raises BP and maintain Cardiac output); - Fluid management is carefully done Surgical intervention: Decompressive hemicraniectomy-removal of a bone flap to relieve pressure; burr holes; temporary complications: infection and increased injury to unprotected underlying brain structure; surgically replace the bone flap after the pt. is no longer @ risk for IICP 1) Reducing Cerebrospinal Fluid and Intracranial Blood Volume Insertion of a ventriculostomy drain: catheter slipped through the skull and the tip is placed in lateral ventricle; use of auricle as the zero line @ the level of ear; black arrow on chamber indicates pressure level set by surgeon -Caution while using CSF - excessive drainage can result in collapse of the ventricle and herniation Serial lumbar punctures: LP's (daily, for example) to remove CSF: If taps are done in presence of IICP, there is a risk of brain shifting (herniation) due to rapid release of pressure; Concerns about infections and excessive removal of fluid. *stop cock on the spinal needle -> SLOWLY open and gently let small amount of fluids come out Hyperventilate to decrease PaCO2 levels to 30-35 mm Hg. (CO2 dilates cerebral blood vessels so lowering it constricts blood vessels): DECREASING BLOOD VOLUME BY lowering PaCo2! -> PaCo2 < 30 - negative outcomes (hypoxia, ischemia, and increase in cerebral lactate levels) *PaCO2 (30-40) * - Maintaining oxygenation and reducing metabolic demands: ABGs: maintain PaO2 > 60 mmHg while keeping PaCo2 low (30-35 mmHg); class - *30-40 - Low O2 causes vasodilation -> increased ICP * keep PaO2 > 60; *> or equal to 70*! *class > or equal 70 2) Controlling Fever -Antipyretic medications: used aggressively; the higher the temperature rises, ICP increases; KEEP TEMPERATURE DOWN! -Environmental controls (cool room, no blanket, sponge bath). -Cooling blanket (induced hypothermia); observe pt. for shivering; avoid shivering -Medications can be given to prevent shivering. 3) Maintaining Oxygenation and Reducing Metabolic Demands -ABG's to adjust ventilator to maintain PaO2 > 60 mm Hg while keeping PaCO2 low (30 - 35 mm Hg if possible). *PaCO2 (30-40) *; paO2 > or equal to 70* -Sedation - pt. can't move, can't respond to or report pain; pentobarbital, thiopental, propofol, and dexmedetomidine; *neurologic assessment can't be performed*; -> assess ICP, BP, HR, RR, and pt. response to ventilator therapy (fighting or bucking the ventilator) complications: hypotension. -Continuous cardiac monitoring, intubation, mechanical ventilation, arterial pressure monitoring, ICP monitoring -Barbiturate-induced Coma - medically induced coma w/ barbiturates, hard to maintain, additional damages/concerns, phenobarbital; not as common

SCI Management of Acute complications of Spinal Cord injury

1) Spinal shock - sudden depression of reflex activity in the spinal cord below the level of injury Loss of motor, sensory, reflex, and autonomic function that occurs immediately after the injury as the cord's response to the injury; usually less than 48 hours but can continue for several days S/S: flaccid paralysis, loss of reflex activity below the level of injury, bradycardia, hypotension, paralytic ileus, and bowel distention (decompress through NG tube) Tx: MAP at 85 mmHg or higher 2) Neurogenic shock: develops because of the loss of autonomic nervous system function below the level of the lesion S/S - decrease in BP, HR, and CO, venous pooling, and peripheral vasodilation *Hypotension and bradycardia*, no perspiration in the paralyzed portions of body; close observation required for early detection of an abrupt onset of fever Decreased vital capacity, retention of secretions, increased PaCo2 levels, and decreased O2 levels, respiratory failure, and pulmonary edema 3) Venous Thromboembolism (VTE) - @ risk for DVT and PE due to immobility, flaccidity, and decreased vasomotor tone PE: pleuritic chest pain, anxiety, SOB, increased PaCO2 and decreased PaO2 - Low dose anticoagulation therapy, SCDs and anti-embolism stockings to prevent DVT and PE - DVT has already developed -> do not use SCDs and keep it without moving - Never massage the calves or thighs of a patient who is immobile 4) Autonomic Dysreflexia (autonomic hyperreflexia) - acute life-threatening emergency that occurs because of exaggerated autonomic responses to stimuli that are harmless in people without SCI Occurs in 80% of patients with injury above T5-T6 level; Occurs only after spinal shock has resolved S/S: Severe, pounding headache with paroxysmal hypertension, profuse diaphoresis above the spinal level of lesion (most often the forehead), nausea, nasal congestion, and bradycardia Sudden onset, severe throbbing headache, severe HTN and bradycardia, flushing above the level of the injury, pale extremities below the level of injury, nasal stuffiness, nausea, dilated pupils, or blurred vision, sweating, piloerection (goose bumps), restlessness and a feeling of apprehension Sudden increase in BP -> retinal hemorrhage, hemorrhagic stroke, MI, seizures Triggers: distended bladder (the most common cause); distention or contraction of the visceral organs, especially the bowel (from constipation, impaction); or stimulation of the skin (tactile, pain, thermal stimuli, pressure ulcer). Interventions: - Place in a sitting position and raise HOB to reduce HTN - priority! - Rapid assessment to identify and alleviate the stimulus: irritation (straps, wrinkles in clothing or sheets), broken skin, examine for fecal mass. - loosen tight clothing on client - bladder is emptied immediately via a urinary catheter. If an indwelling catheter is not patent, it is irrigated or replaced with another catheter. - Fecal mass: a topical anesthetic agent is inserted 10 to 15 minutes before the mass is removed, because visceral distention or contraction can cause autonomic dysreflexia. - skin exam: areas of pressure, irritation, or broken skin. - Any other stimulus that could be the triggering event, such as an object next to the skin or a draft of cold air, must be removed. - If these measures do not relieve the hypertension and excruciating headache -> antihypertensive IV (Hydralazine IV) - patient is instructed about prevention and management measures. - inform that such an episode is possible and may occur even many years after the initial injury Monitoring and managing potential complications: 1) VTE: measure circumferences of thighs and calves daily; anticoagulation within 72 hours of injury and continue at least 3 moths (LMWH (warfarin); ROM, antiembolism stockings, adequate hydration, SCDs; avoid external pressure on the lower extremities (avoid flexion of the knees) 2) Orthostatic hypotension: close VS before and during position changes, fluid status, vasopressor, antiembolism stockings, abdominal binders, slow progression of position changes from recumbent to sitting and upright, tilt tables 3) Contractures and/or spasticity: -careful positioning -hand higher than forearm; forearm higher than .. - maintain joint mobility - passive range of motion

Increased ICP Nursing Management/Interventions

1. Maintaining a Patent airway - suction secretions, pre oxygenate, avoid coughing (increases thoracic pressure -> IICP), auscultate lungs q8 (adventitious sounds or area of congestion); elevate HOB (clearing secretions and improving venous drainage of the brain) - Preoxygenation! Hyperventilate using 100% oxygen; suction should not last longer than 15 seconds; cautious use of PEEP Achieving an Adequate Breathing Pattern: increased pressure on frontal lobes or deep midline -> chyne-stokes respiration; pressure in the midbrain -> cause hyperventilation - If pons and medulla is involved -> respirations becomes irregular and eventually cease - Hyperventilation - maintain PaCO2 *30-40* and PaO2 > or equal to 70 - Neurologic observation record Optimizing Cerebral Tissue Perfusion POSITIONING IS IMPORTANT: drainage out of cranium: -Head at midline (promotes venous drainage); HOB @ 30-45 degrees -Avoid extreme rotation of neck and flexion of neck (compresses or distortion of jugular veins increases ICP) -Avoid extreme hip flexion (increases intraabdominal and intrathoracic pressure; impedes blood flow and blood backs up AVOID STRAINING & VALSALVA MANEUVER (stool softener, pain meds, sedatives to avoid bearing down; exhale while being moved); -Calm and quiet! -Assess abdominal distention avoid enemas and cathartics -When moving or turning in bed -> instruct patient to exhale (opens the glottis) to avoid the Valsalva maneuver DO NOT "CLUSTER" CARE—SPACE the interventions out. *Provide long periods of rest without being interrupted -avoid emotional stress and frequent arousal from sleep -calm atmosphere and environmental stimuli (noise, convo) be minimal) Maintaining Negative Fluid Balance: administration of osmotic and loop diuretics, corticosteroids promote dehydration -> monitor skin turgor, mucous membranes, Urine output, and serum and urine osmolality; AVOIDING over hydration! Mannitol - observe for HF and pulmonary edema. - Monitor VS, indwelling catheter - renal function and fluid status - Urine output monitored hourly; output > 200 mL per hour for 2 consecutive hours - indicates onset of DI - Careful oral hygiene, frequently rinsing the mouth with nondrying solutions, lubricating the lips -removing encrustations relieve dryness and promote comfort -Preventing Infection (aseptic techniques, checking loose connections, observe character of CSF drainage and for cloudiness or blood) -monitor for S/S of meningitis: fever, chills, nuchal (neck) rigidity, and increasing or persistent headache. Nursing Management a few other measures 1) Mouth care 2) Skin/joint and corneal integrity 3) Nutritional needs: peg tube? NG tube? TPN? 4) Prevent urinary retention/promote bowel function Monitoring and Managing Complications · Respiratory failure/pneumonia/aspiration · Prevent urinary retention/promote bowel function · Pressure ulcers · Seizure prevention/safety - seizure prophylaxis (anticonvulsants, bed low, bed padded, side rails up, O2 (Seizure precautions) · DVT; DI (FVD; hypernatremia); SIADH - fluid volume overload

Hypercalcemic crisis

>13 mg/dl calcium result in neurologic, cardiovascular, and kidney symptoms - Rapid rehydration with large volumes of IV isotonic saline fluids to maintain urine output of 100 to 150 mL per hour is combined with administration of calcitonin if edema -> stop saline infusion and loop diuretics - loop diuretics are not first line treatment - Bisphosphonates to decrease calcium : (e.g., etidronate [Didronel], pamidronate [Aredia]) - Cytotoxic agents (e.g., mithramycin), calcitonin, and dialysis may be used in emergency situations to decrease serum calcium levels quickly. *calcitonin + corticosteroids to reduce serum calcium)

anterior pituitary gland Posterior pituitary gland

Anterior pituitary gland: Follicle-stimulating hormone (FSH) Luteinizing Hormone (LH) Prolactin Adrenocorticotropic hormone (ACTH) Thyroid-stimulating hormone (TSH) Growth hormone (somatotropin) Posterior pituitary gland: - Antidiuretic hormone (vasopressin): controls the excretion of water by the kidney; its secretion is stimulated by an increase in the osmolality of the blood or by a decrease in blood pressure - oxytocin

SCI manifestations

Clinical Manifestations of SCI: depends on type and level of injury; Type: extent of injury to the spinal cord itself Classification of SCI: according to the degree of sensory and motor function present after injury Level of SCI injury: lowest spinal cord segment with intact motor and sensory function Below the neurologic level: may be total or partial, sensory and/or motor paralysis (dependent upon affected tracts), loss of bladder and bowel control (retention/distention), loss of sweating and vasomotor tone, and reduction of BP from loss of peripheral vascular resistance S/S Conscious - acute pain in the back or neck -> radiate along the involved nerve Respiratory dysfunction is related to the level of injury. Muscles contributing to respiration: Diaphragm (C4), intercostals (T1-T6), and abdominals (T6-T12) - Injuries at C4 or above (causes paralysis of the diaphragm) - requires ventilator support - Injuries of T12 and above - impacts respiratory function Complete spinal cord lesion: loss of sensory and voluntary motor communication from the brain to the periphery -> paraplegia or tetraplegia (quadriplegia) Incomplete spinal cord lesion: sensory/or motor fibers are preserved below the lesion Assessment and Diagnostic findings: - Neurologic exam - X-rays (lateral cervical spine x-rays) - CT scans - MRI - Continuous EEG (if SCI is suspected bc bradycardia and asystole common in patients w/ acute SCI) - Respiratory status changes, motor, and sensory changes below the level of injury, loss of reflexes below the level of injury, loss of bladder and bowel control, urinary retention and bladder distention, presence of swear, which does not occur on paralyzed areas Cervical injuries: Inability to breathe and quadriplegia/tetraplegia (paralysis of all four extremities) - C2-C3 - fatal - C4 - phrenic nerve; involvement above C4 causes respiratory difficulty and paralysis of all four extremities - Injury at C5-C8 -> movement in the shoulder and may also have decreased respiratory reserve pt. wont be able to deep breathe/ ask to cough and expel secretion -> may not be able to do it @ increased risk for respiratory infections and stagnation of the secretions, atelectasis, and pneumonia *pulmonary toileting important Thoracic level injuries: Paraplegia (paralysis of the lower body) and poor trunk control - Loss of movement of the chest, trunk, bowel, bladder, and legs may occur - Leg paralysis (paraplegia) - Autonomic dysreflexia w/ injuries above T6 - Visceral distention from noxious stimuli such as distended bladder or an impacted rectum -> sweating, bradycardia, HTN, nasal stuffiness, and goose flesh Lumbar and sacral injuries: decrease control of legs, bowel and bladder, and sexual functions - Loss of movement and sensation of lower extremities may occur - S2 and S3: below this level, bladder will contract but does not empty (neurogenic bladder) - Injury above S2 in males: an erection but unable to ejaculate (sympathetic nerve damage) - Injury between S2 and S4: preventing erection or ejaculation) Emergency management of SCI: consider having SCI until injury is ruled out - rapid assessment, immobilization, extrication, and stabilization or control of life-threatening injuries, and transportation @ The scene: immobilized on a spinal (back) board, with the head and neck maintained in a neutral position to prevent an incomplete injury from becoming complete - assess the respiratory pattern and maintain a patent airway - prevent head flexion, rotation, or extension - during immobilization, maintain traction and alignment on the head by placing hands on both sides of the head by the ears - during treatment and x-ray department - pt. is kept on the transfer board, maintain pt. an extended position - no part of the body should be twisted or turned, and pt. not allowed to sit up - rotating specialty bed or in a cervical collar - once extent of injury is determined

spinal cord tumors: abnormal tissue growth in or around the spine

Classification of SC tumors: May be primary or metastatic Intramedullary- within the spinal cord Extramedullary- around the spinal cord Secondary SC Tumor is always:30-70% from bone cancers Area of tumor- cervical, thoracic, lumbar Location of tumor- anterior or posterior of the spine

Spinal Cord Tumor - Medical Management

Depends on type, location, sx & patient's physical status (Hx, PMH) Monitor- for small benign tumors that are not growing or pressing on surrounding tissues. -Do periodic scans are needed to monitor the tumor -Surgical interventions: Primary Tx but not always possible; to debulk or remove to relieve pressure & preserve neuro function -Radiation- To decrease tumor size post-op or if no surgery is possible; 1st line for metastatic tumors -Steroids- Dexamethasone (IV); used initially to decrease edema following radiation or surgery -Chemotherapy- Limited benefit bc of BBB -Complementary/ alternative therapies: music, massage, guided imagery Nerve damage from cord compression is often permanent; usually patients don't have significant functional recovery, even after tumor removal

Increased ICP and brain tumors

Enlarging tumors & it's associated edema disrupts the equilibrium between the brain, blood & CSF -As tumor grows, compensatory adjustment may occur but WHEN they fail-> IICPHA, Nausea w or w/o vomiting & papilledema ( swelling of optic nerve -HA- most common in the AM & made worse by coughing, straining, or sudden movement -Front Tumors- pain between 2 temples (bitemporal) -Cerebellar-> HA in sub occipital region -Vomiting-result of irritation of vagal center in the medulla- forceful projectile. -HA may be alleviated by vomiting. -Visual disturbances-> edema compressing CN III; diplopia, hemianopsia, varying levels of blindness -Seizures- occur in 60% of patients pts initially or throughout disease process -Tumor is parietal, frontal & temporal lobes-> greater risk. Can also be cause by electrolyte imbalances

Focal vs. general Brain tumor

Focal - wherever tumor is, that specific fxn is affected - Sensory or motor loss , change in cognition, change in vision. Ataxia (cerebellar), Aphasia (speech/language changes) General- all r/t ICP Sx of ICP=HA, change LOC, change in VS, Cushing's Triad (increased SBP, widening pulse pressure, decreased HR, alteration in RR)

Abdominal Aortic Aneurysm (AAA) Treatment

Pharmacological and Non-pharmacological Measures: Abdominal Aortic Aneurysm - Stable aneurysm on serial duplex ultrasound scans -> BP monitored closely; (association b/w hypertension and aneurysm rupture) - Antihypertensive agents: Diuretics, ARBs, ACEIs, Calcium channel blockers, Beta-Blockers. - Diet modification - Behavioral Modification: Smoking Cessation if applicable; ETOH Surgical Procedure: Endovascular Aortic Repair (EVAR): tx. Of infrarenal AAA, involved the transluminal placement and attachment of a suture less aortic graft prosthesis across an aneurysm; performed under local or regional anesthesia (TAP block) Contraindications of EVAR: tortuous, small, calcified, or thrombotic abdominal and iliac arteries Complications - bleeding, hematoma, wound infection @ the arterial insertion site, distal ischemia or embolization bowel ischemia, embolization, dissection or perforation of the aorta, graft thrombosis, graft infection, break of the attachment system, graft migration, proximal or distal graft leaks; delayed rupture; AKI, impotence -> gonadal branch affected Pre op EVAR: - Assess hemodynamic stability, monitor for bleeding - Assess Functional capability of all organs - Neuro, CV, Resp, Renal compromise d/t atherosclerosis hx - Medication continuation or hold - Signs of rupture, RP bleed, shock Post op EVAR: - Lie supine (flat) for 6 hours - HOB may be elevated up to 45 degrees after 2 hours; NO MORE than 45! - Use a bedpan or urinal while on bed rest - VS and doppler pulse check q15x4, then 30m x2, then q1h - Assess access site (usually femoral artery) - when VS and pulses are monitored - Assess for bleeding, pulsation, swelling, pain, and hematoma formation - Skin changes of the lower extremity, lumbar area, or buttocks - indicate signs of embolization (extremely tender, irregularly shaped, cyanotic areas, changes in VS, pulse quality, bleeding, swelling, pain, or hematoma) - Temperature every 4 hours - Post implantation syndrome (w/in 24 hours of stent graft placement ; S/S - spontaneously occurring fever, hyperthermia, leukocytosis, and transient thrombocytopenia) ; Management: acetaminophen (tylenol) or anti-inflammatory agent (ibuprofen) and usually subside within a week - Increased risk of hemorrhage: notify provider if persistent coughing, sneezing, vomiting, or SBP > 180 mmHg (these are symptoms that would increase intravascular pressure) administer Antiemetics! -Maintain IV infusion until adequate PO intake; resume pre procedure diet and encourage to drink fluids (fluids assist kidneys to contrast agents, maintain blood flow through the arterial repair site) -SIX hours after the procedure, pt may be able to roll from side to side and ambulate with assistance to the bathroom -Frequent monitoring of pulmonary, cardiovascular, renal, and neurologic status -Complications of surgery: arterial occlusion, hemorrhage, infection, ischemic bowel, kidney injury, and impotence - Pain management pre and post op

Spinal Cord tumor Clinical Manifestations

Progression of Sx d/t increased SCC 1. New onset of severe back pain 2. Numbness, tingling 3. Bladder & bowel dysfunction 4. Motor weakness/sensory deficits 5. Progressing to paralysis) if tumor is in cervical area, pt may notice loss of manual dexterity & clumsiness

craniectomy

excision of a portion of the skull cranioplasty-> repair of cranial defect using a plastic or metal plate

Infratentorial

incision at the nape of neck around the occipital lobe. -Maintain neck straight in alignment - avoid flexion of the neck to prevent possible tearing of the suture line -Position patient L or R

pituitary gland

master gland; controlled by hypothalamus; anterior vs. posterior

Hyperthyroidism treatment/pharmacologic

(1) Radioactive iodine therapy: destroys the thyroid - NPO 2-4 before; 1-2 hours after - contraindicated in pregnancy - take a pregnancy test before; 5-7 days before withhold thyroid meds; - pt. can contaminate household and another person through saliva, urine, or radiation emitting from their body -avoid sexual contact, sleeping in same bed w other ppl, having close contact w/ children and pregnant women and sharing utensils and cups - avoid everyone!; flush 3x in the restroom; urine spills -> call hazmat team! pt. urine is risk for nurse (2) antithyroid medications: - MMI (methimazole, tapazole) - propylthiouracil (PTU) - (baby safe) monitor cardiac parameters, hypothyroidism -watch for rash, nausea, vomiting, agranulocytosis, thrombocytopenia, SLE *take in the morning, empty stomach, 30 minutes before eating to avoid decrease in absorption associated with some foods such as walnuts, soybean flour, cottonseed meal, and dietary fiber. - pharyngitis and fever or the occurrence of mouth ulcers, the patient is advised to stop the medication - discontinue PTU after the first trimester and switch to MMI for the remained Adjunctive therapy: - potassium iodide (KI), Lugol's solution, and saturated solution of potassium iodide (SSKI): shrink thyroid before removal, stains teeth (use straw +juice) or milk - beta-blockers(e.g., propranolol, atenolol, metoprolol): decreasing heart rate, systolic blood pressure, muscle weakness, nervousness, tremor, anxiety, and heat intolerance. Surgical management: return thyroid levels to normal (by giving anti-thyroid medications): - antithyroid meds + beta-blockers given; stop aspirin weeks before surgery; - monitor iodinism(swelling of the buccal mucosa, excessive salivation, cold symptoms, and skin eruptions) Thyroidectomy: 1) airway - laryngeal stridor, noisy breathing, hoarseness, weak voice * endo tube/trach kit bedside) 2) breathing 3) circulation - bleeding on pillow/ surgical site -> neutral head + neck alignment, HOB 30-45 degrees; NOT supine; no flexing or extending neck 4) calcium < 8.6 (hypocalcemia) -> tingling or numbness, circumoral tingling/finger -> - after surgery: Low Ca+) -> look for troussaeu "twerk arm w/ BP x 3 min - look chovestek - cheek twitch when touched

Meningioma

- 15% of all primary tumor -benign- in arachnoid cells on the meninges, slow growing occur - often in middle age adult. - Women> Men Manifestations often result d/t to compression rather than invasion of brain tissue Tx Surgery complete removal or partial dissection-> radiation therapy may be useful in some patient

Hyperparathyroidism clinical manifestations

- Apathy, fatigue, muscle weakness, nausea, vomiting, constipation, hypertension, and cardiac dysrhythmias - irritability and neurosis, psychoses - kidney stones (renal calculi), obstruction, pyelonephritis, and kidney injuries - demineralization of bones - skeletal pain and tenderness ( back and joints) - pain on weight-bearing - pathologic fractures and deformities; shortening of body status - increased risk of fracture - increased incidence of peptic ulcer and pancreatitis ( N+V, epigastric pain = increased acid) - constipation Assessment and Diagnostic findings: - persistent elevation of serum calcium and elevated PTH - radioimmunoassays - bone changes on x rays or bone scans - double-antibody PTH test - distinguish b/w primary hyperparathyroidism and malignancy as a cause of hypercalcium -Ultrasound, MRI, thallium scan, and fine-needle biopsy

TBI assessment

- Assessment and diagnosis of the extent of injury - Physical and neurologic examinations - patient's LOC using the Glasgow Coma Scale (GCS) and assessing the patient's response to tactile stimuli (if unconscious), pupillary response to light, corneal and gag reflexes, and motor function - GCS: eye opening response, verbal response, and motor responses to verbal commands or painful stimuli - CT (one as the pt. comes and one again in 24 hours) and MRI *ALWAYS GOLD STANDARD* - PET scans - Any patient with a head injury - presume to have a cervical spine injury until proven otherwise (transport pt. from the scene of injury on a board w/ head and neck maintained in alignment with axis of the body); DO NOT flex neck and head - Cervical collar applied and maintained until cervical spine x-rays done and absence of cervical SCI - Therapy: preserving brain homeostasis and preventing secondary brain injury (injury to the brain that occurs after the original traumatic event)

Traumatic Brain Injury: Nursing Interventions

- Maintenance of a patent airway; Monitor PaCo2 - 30-35 or 30-40 and O2 > equal to 70 on mechanical ventilator - Unconscious pt. (drainage of oral secretions - HOB 30 degrees) - Effective suctioning (suctioning produces coughing and straining, which increases ICP) - Monitor ABGs - Monitor or ARDS and pneumonia - Provide good oral hygiene - Avoid coughing, vomiting, straining - Decrease stimulants in the environment - Monitor for signs of increased ICP (Crushing's reflex) - Monitoring neurological function: LOC: Glasgow Coma Scale:3-8 indicate severe head injury - GCS: most sensitive indicator of change in neurologic functioning - CPP: Elevate the head of the bed 30 - 45-degree angle - Motor function: squeeze fingers; lower function: place hands on soles of pt. feet and to push down - Possible develop deficits such as anosmia (lack of sense of smell), eye movement abnormalities, aphasia, memory deficits, and post-traumatic seizures or epilepsy. Patients may be left with residual psychological deficits (impulsiveness; emotional lability; or uninhibited, aggressive behaviors) and, because of the impairment, may lack insight into their emotional responses. - Fluid and electrolyte balance -SIADH /DI; monitor electrolytes, blood glucose, and I/Os; test urine for acetone; daily weights -Adequate nutritional status - body is in hyper-metabolic state so needs adequate nutritional supplementation: IV supplementation, NG tube, NJ tube; elevate HOB to prevent distention, regurgitation, and aspiration; enteral or parenteral feedings until swallowing reflex returns -higher concentration of protein if tolerated -Osmotic diuretics (mannitol, 3% hypertonic saline), IV dexamethasone (reduce tissue edema; anti-inflammatory) -Preventing injury: check dressing and casts for constriction; padded side rails -avoiding opioids as a means of controlling restlessness -reducing environmental stimuli by keeping the room quiet, limiting visitors, speaking calmly, and providing frequent orientation information, adequate lighting -lubricating pt. skill with oil or emollient lotion; catheters (intermittent Cath) -Seizure precautions (anticonvulsants), antihypertensives - barbiturates - Morphine sulfate or opioids to decrease agitation and control restless pain caused by pain but caution (respiratory depressant) Maintain Body temperature within normal limits: <100.4 degrees F -monitor every 2-4 hours; using acetaminophen and cooling devices to maintain normothermia but don't induce shivering; cool sponge baths, hypothermia blanket, Removing all bedding over the patient (except for a light sheet, towel, or small drape) -Assessing all body surfaces and skin integrity every 8 hours -Turning and repositioning every 2 hours -Providing skin care every 4 hours -Assisting pt. to get out of bed to a chair 3x a day if conscious Complications: Decreased cerebral perfusion Cerebral edema and herniation Impaired oxygenation and ventilation Impaired fluid, electrolyte, and nutritional balance Risk of post traumatic seizures

SCI nursing interventions

Nursing interventions SCI: Promoting adequate breathing and airway clearance: Clearing bronchial and pharyngeal secretions (preventing atelectasis) Use suctioning with caution Chest physiotherapy and assisted coughing Proper humidification and hydration Assess for respiratory infection (cough, fever, dyspnea) Assess for signs of hemorrhage or bleeding around the bleeding site Assess for signs of shock (hypotension, tachycardia, and a weak and thready pulse) Improving mobility Proper body alignment Use splints to prevent footdrop; removed and reapplied ever 2 hours Trochanter rolls (prevents external rotation of hip joints) Monitor BP Passive ROM to prevent contractures of the tendon and joint capsule Toes, metatarsals, ankles, knees, and hips - full ROM at least four, or five times daily Pt. w/ cervical fracture w/ neurologic deficit - move gradually to an erect position; neck brace or molded collar is applied Preventing injury due to sensory and perceptual alterations: Glasses, hearing aids, emotional support and educating about coping Maintaining skin integrity Pressure ulcers @ sacrum, heels, ischial tuberosity, and occiput is common sites Skin breakdown from the cervical collars @ shoulders and occiput Change position every 2 hours Inspect skin every time turned Assess skin for redness or breaks, perineum for soilage and catheter for adequate drainage Keep skin clean by using mild soap, rinsing well, and botting dry Lubricated and soft with oil or emollient lotion Maintaining Urinary elimination: neurogenic bladder could occur Foley catheter (@ acute) Maintain F/E balance, adequate fluid intake of 2000 mL/ day unless C/I and UTI and calculi Intermittent catheterization Record fluid intake, voiding pattern, amounts of residual urine after voiding, characteristics of urine, and any unusual sensations INTAKE AND OUTPUT Improving bowel function - NG tube to relieve distention and prevent vomiting and aspiration; bowel program; stool softeners, laxatives Providing comfort measures: traction with tongs or halo vest Pins, tongs, or calipers - headache or discomfort; Complaints of being caged in Clean the four pin sites of a halo device at least daily observe for redness, drainage, and pain Observe pins for loosening (can cause infection) If one of the pins become detached -> one person stabilize head in neutral position while other notifies the physician Have torque screwdriver ready in case screws on the frame need tightening Skin under the halo vest - inspect for excessive perspiration, redness, and skin blistering especially on bony prominences Vest opened at the sides to allow the torso to be washed Do not wet the liner of the vest (causes skin excoriation) Do not use powder inside the vest Use normal saline to clean the curst Change the liner periodically to promote hygiene and good skin care Educate the pt about VTE, respiratory impairment, UTI;

Peripheral Aneurysm

affect arteries other than the aorta or the brain; may involve vessels such as subclavian artery, renal artery, femoral artery, most frequently (popliteal artery); between 50% - 60% popliteal aneurysms are bilateral Most common sites: femoral, popliteal, iliac most common complication: formation of blood clots that may block blood flow distal to it. Most often due to atherosclerosis. -silent until critically symptomatic. Symptomatic -> blocks blood flow distal to it! Manifestations: could be asymptomatic - Pulsating mass and disturbs peripheral circulation distal to it - loss of pulses - Pain and swelling develop (pressure on adjacent nerves and veins; pain @ rest or w/ exercise numbness and weakness due to nerve involvement - Gangrene due to tissue death in setting of severe blockage Dx of peripheral aneurysms: - duplex ultrasonography or CTA to determine the size, length, and extent of the aneurysm. - Arteriography: injection of dye; evaluate the level of proximal and distal involvement. -major complication associated with popliteal artery aneurysms: distal embolization Pharmacological and Non-pharmacological Measures: Peripheral aneurysm - Treatment is based on location, size, and condition surrounding blood vessels, and the health of patient - Watchful wait with f/u - Lifestyle changes Surgical management: - Surgical repair is performed with replacement grafts -EVAR (endovascular) repair using a stent-graft or wall graft, which is a Dacron (polyester) or PTFE graft with external structures made from a variety of materials (e.g., nitinol, titanium, stainless steel) Nursing interventions: - Plan of care as previously stated - Frequent NV checks to affected extremities - Pulse presence and strength - Temperature of the extremity - Pain, Pallor, Paresthesia - Post-op care: site monitoring for hematoma and bleeding

Brain Tumor: Radiation

- cornerstone in tx for most brain tumors; it is used alone or in combo w/ surgery brachytherapy (delivers high dose of radiation at a short distance) -allows for treatment of deep, inaccessible tremor in a single session advantage: no surgical incision needed Disadvantage -> lag time b/w tx and the desired result as well as potential for developing radiation process Side effects: fatigue, reddening of skin (sunburn appearance), HA, swelling, visual changes, neuro disturbances, hearing loss, facial numbness

Nursing Management of Intracranial surgery

-Cerebral perfusion- watch for hypoxia or hypercapnia-> vasodilation -ET Tube is left in place until patient shows signs of awakening secondary brain damage from impaired cerebral oxygenation -some cerebral edema peaks @ 24 to 36 hours post op; potentially decreasing responsiveness on 2nd post op day. -Intraventricular drainage is carefully monitored -VS- LOC, responsiveness, motor & pupillary response q15 to 60 min. -HOB 30 degrees - seizure precautions; after seizure MUST GIVE /GOOD amount of oxygen -Infratentorial -lay patient of the side. -Supratentorial- lay pt on back and on unoperated side -LOG ROLL pt to decrease strain on incision & possibly tearing sutures -Reposition q2 - alignment of head and neck in neutral position without flexion will promote venous drainage -control of cerebral edema -regualate temperature

Regulate temperature

-Fever treated vigorously to combat effect of increased temp on brain metabolism -removing blankets -add ice packs & an antipyretics NO SHIVERING

Spinal Cord Tumor: Nursing Management post op

-Pain, ineffective coping, impaired physical immobility -Non-Surgical & Pre-op care: monitor neuro status, pain control, bowel & bladder dysfunction, respiratory status -Keep body in alignment, bed is flat initially -Frequent monitoring of neuro status- check for return of movements, strength or sensation -Monitor- sudden onset of worsening neuro deficits -CSF drainage on the surgical dressing= indicates leakage, inflammatory reaction & can lead to infection. Action-> leakage can lead to infection & increase risk of brain herniation; Notify HCP if excessive drainage! -Managing pain- adequate amounts at regular intervals; More bone pain at night. If need to turn ->LOGROLL side-lying is usually the most comfortable; place pillow between knees

Intracerebral hemorrhage (ICH) and hematoma

Bleeding into the parenchyma of the brain. - common seen in head injuries when force is exerted to the head over a small area (e.g., missile injuries, bullet wound, stab injuries - Can bleed into the brain ventricles -> increased ICP and blood will mix w/ CSF - Can become subarachnoid hemorrhage hemorrhages within the brain may also result from the following: non traumatic - Systemic hypertension, which causes degeneration and rupture of a vessel - Rupture of an aneurysm - Vascular anomalies - Intracranial tumors - Bleeding disorders such as leukemia, hemophilia, aplastic anemia, and thrombocytopenia - Complications of anticoagulant therapy S/S: insidious onset w/ development of neurologic deficits followed by headache Tx: supportive care, control of ICP, careful administration of fluids, electrolytes, and antihypertensive medications; craniotomy or craniectomy (removal of blood clot and control of hemorrhage but areas can be inaccessible) Tx: transport quickly, first assessment - CT scan

Hypothyroidism - under-active thyroid gland; decreased t3 and T4; can range from mild S/S -> myxedema (severe deficiency)

Causes: - autoimmune thyroiditis (Hashimoto disease), in which the immune system attacks the thyroid gland; no T3 + T4 -> goiter; (Hashimoto thyroiditis, post-Graves disease) -Atrophy of thyroid gland with aging - Tx of hyperthyroidism: Radioactive iodine (131I) and antithyroid medications - Thyroidectomy (surgical removal) - Medications - Lithium -Iodine compounds - Radiation to head and neck in treatment for head and neck cancers, lymphoma -Infiltrative diseases of the thyroid (amyloidosis, scleroderma, lymphoma) - Iodine deficiency and iodine excess Medications that cause hypothyroidism: - amiodarone (Cordarone) - aspirin - cimetidine (Tagamet) - diazepam (Valium) - furosemide (Lasix) - heparin - lithium (Lithotabs) - phenytoin (Dilantin) and other anticonvulsants propranolol (Inderal)

Subdural Hematoma (SDH): more venous

Collection of blood between the dura matter and brain. Most common cause: trauma but can result of coagulopathies or rupture of an aneurysm - More venous origin (Slow) and caused by rupture of small vessels that bridge the subdural space Acute Subdural Hematoma: Associated with a major head injury involving contusion or laceration. S/S: - changes in LOC, pupillary sings, and hemiparesis - coma, increasing BP, decreasing HR, and slow RR Tx: immediate craniotomy to remove the subdural clot; control of ICP; careful monitoring of respiratory functions; high mortality rate bc of associated brain damage Chronic Subdural hematoma: Can develop from minor head injuries and is seen mostly in older adults who are prone due to brain atrophy bc of aging process; can be mistaken for a stroke - bleeding is less profuse but compression of intracranial pressure - blood within the brain changes in character in 2-4 days (becomes thicker and darker) - few weeks, clot breaks down and has color and consistency of motor oil S/S: headache (comes and goes), alternating focal neurologic signs, personality changes, mental deterioration, and focal seizures Tx: evacuation of the clot; multiple burr holes, or craniotomy may be performed for a mass that cannot be suctioned or drained through burr holes

dissecting aneurysm

Dissecting Aneurysm in setting of arteriosclerosis -> tear develops in the intima or media layer -> dissections - 3 times more common in men that in women, occurs most commonly between the ages of 50-70 -Associated w/ poorly controlled HTN, blunt chest trauma, and cocaine use. Type A @ascending (Acute Medical Emergency): SOB, Sudden severe sharp pain Type B (Chronic) @ descending: HTN, Severe, sharp back pain that can feel like it is extending into the chest or abdomen Clinical Manifestations: - Sudden, acute onset of S/S - Severe and persistent pain (tearing or ripping) - Pain is in anterior chest or back and extends to shoulders, epigastric area, or abdomen - Could be confused w/ MI - Cardiovascular, neurologic, GI symptoms - Pt. may be pale, diaphoretic, tachycardia, hypertensive (elevated BP) and show a difference from one arm to the other if dissection involves the orifice of the subclavian artery on one side Diagnostic testing: Dissecting aneurysm: Arteriography, MDCTA, TEE, Duplex ultrasonography, MRA Pharmacological and Non-pharmacological Measures: Dissecting aneurysm Type A: Valve sparing root replacement (David procedure): take the root off and placing the graft and reattach the root Type B: - Medical management, routine imaging, and HR/BP control (anti-impulse therapy). - EVAR if concerns for reduced or occlusion of blood flow to the organs Nursing Plan of care: Dissecting aneurysm: Same management and intervention as described in previous nursing care slide: Assessing, circulation, wound care, BP control

Tumor Location and manifestations

Frontal Lobe/ Motor Cortex: Hemiparesis, partial seizures on opposite side of body-> generalized seizures. -Change in emotional state & behavior, apathetic attitude, may use obscene language. Parietal: decreased sensation on opposite side of body, sensory or generalized seizures Temporal: Seizures, psychological disorders Occipital: Visual manifestations, Contral lateral; Homonymous hemianopsia (visual loss in half of visual field on opposite side of tumor). Visual Hallucination Cerebellar: Dizziness, ataxic or staggering gait w/ tendency to fall toward side of lesions, muscle incoordination, nystagmus (involuntary rhythmic eye mvmts) Cerebellopontine angle tumor: 1st tinnitus, vertigo, then deafness CN VIII dysfunction, then numbness/tingling of face/tongue-> CN V Then paralysis/weakness of face (CNVII)

Adrenal cortex: aldosterone and cortisol

Fx of adrenal cortex: releases steroid hormones (corticosteroids) , aldosterone (mineralcorticosteroids) + cortisol (glucocorticoids)+ sex hormones Fx of aldosterone: regulates BP through renin-angiotensin aldosterone system; retains sodium; secretes potassium Fx of cortisol: stress hormone; helps body deal with stress; ex: illness, external stress; increases blood glucose (by metabolism of sugar); breaks down fats, protein, + carbs; regulates electrolytes Negative feedback control: Hypothalamus -> releases CRH (corticotropin releasing hormone ) -> pituitary glands -> ACTH (adrenocorticotropic hormone) -> adrenal cortex (cortisol)

Meningitis

Meningitis: inflammation of the meninges, which cover and protect the brain and spinal cord *most often pia mater Major causes: bacterial, viral, and fungal infections 3 types of infections: -Bacterial (septic meningitis): caused by bacteria -Viral (aseptic meningitis): secondary to cancer or having a weakened immune system ex. HIV; enteroviruses; occurs more frequently in the summer and early fall -Fungal meningitis Complications: visual impairment, deafness, seizures, paralysis, hydrocephalus, and septic shock

IICP - Assessment and Diagnostic Findings

Most common Dx: CT scanning and MRI; CT scan Labs Cerebral angiography, PET, SPECT scans Transcranial doppler - provide information about cerebral blood flow Electrophysiologic monitoring Assessments: evaluation of mental status, LOC, cranial nerve function, cerebellar function (balance and coordination), reflexes, and motor and sensory function; pupil checks, assessment of cranial nerves, frequent measurements of S and ICP and using GCS -Subjective data from patient or family members -Vital signs (Rising BP, decreased HR, erratic respiratory changes) - Monitor CO2: CO2 is a potent vasodilator -> you want it to be LOW - Alertness and orientation (remember AVPU) - alert? Verbal stimulation? Pain? Unconscious? -Glasgow Coma Scale * pt. who is comatose or neurologically damaged*; quantify the patients responsiveness! Eye opening, verbal, motor response; best score = 15; worst possible score: 3; for intubated 10 best, 2 worse - Respiratory status - Cranial nerve assessment: Pupillary checks are important - Response to noxious stimuli - Reflexes: indicators of loss of brain stem reflexes -Abnormal posturing -Intracranial Pressure Monitoring Complications of increased ICP - brainstem herniation, diabetes insipidus and SIADH Brainstem herniation - pressure builds in the cranial vault and brain tissue presses down on the brainstem -> cessation of blood flow to the brain -> irreversible brain anoxia and brain death

Brain Tumor: Surgical management

Objective: to remove as much tumor as possible w/o increasing the neuro deficits (paralysis and blindness) or to relieve symptoms by partial removal (decompression) -requires craniotomy (incision into the skull) to biopsy brain tissue or excise a tumor if entire tumor is not able to be removed, the tumor is debulked, removing as much of it as possible, leaves behind fewer cells to become resistant to radiation or chemo. If post op: - Neuro changes -> HCP orders CT imaging to see if a structural change is present to produce new finds -Neuro assessment (LOC, orientation, motor strength, sensation) -compare current assessment to the last one and most current baseline

Impaired gas exchange

Q2hr turns remember immobility-> atelectasis Incentive spirometer, deep breathing & coughing (unless contraindicated) -Increase humidity in the O2 to help loosen secretions RT-> chest physiotherapy

Risk factors/Causes of Arterial Aneurysms

Risk factors and causes of arterial aneurysms: - Age (seen in men 50-70 years old) - Tobacco (causes vasoconstriction) - Atherosclerotic changes in the aorta (can cause ulcer; erode arterial wall) - Congenital: Primary connective tissue disorders (Marfan syndrome, Ehlers-Danlos syndrome) and other diseases (focal medial agenesis, tuberous sclerosis, Turner syndrome, Menkes syndrome) - Mechanical (hemodynamic): Poststenotic and arteriovenous fistula and amputation related - Traumatic (pseudoaneurysms): Penetrating arterial injuries, blunt arterial injuries, pseudoaneurysms - Inflammatory (noninfectious): Associated with arteritis (Takayasu disease, giant cell arteritis, systemic lupus erythematosus, Behçet syndrome, Kawasaki disease) and periarterial inflammation (i.e., pancreatitis) - Infectious (mycotic): Bacterial, fungal, spirochetal infections - Pregnancy-related degenerative: Nonspecific, inflammatory variant - Anastomotic (postarteriotomy) and graft aneurysms: Infection, arterial wall failure, suture failure, graft failure

Hyperthyroidism: high secretion of thyroid hormone

S/S: - nervousness - hyperexcitable, irritable, and apprehensive; they cannot sit quietly; increased BP - smooth skin and soft hair - moody, restless, and insomnia -palpitations - rapid pulse @ rest as well as on exertion - heat intolerance (cant) and perspire but CAN tolerate cold - flushed skin; salmon color in Caucasians; warm, soft, and moist - fine tremor of hands - exophthalmos (abnormal protrusion of one or both eyeballs), which produces a startled facial expression. -increased appetite and dietary intake, weight loss, fatiguability and weakness (difficulty in climbing stairs and rising from a chair) -diarrhea -thyroid gland enlarged, feels soft, and thrill can often be palpated -amenorrhea, and changes in bowel function. - A-Fib; sinus tachycardia or dysrhythmias, increased pulse pressure, and palpitations; - Myocardial hypertrophy and heart failure Assessment and diagnostics: - thyroid gland enlarged, soft, may pulsate, bruit heard over thyroid arteries -DECREASED TSH, INCREASED free T4, increase in radioactive iodine uptake

Traumatic Brain Injury (TBI): Open/Closed:injury to the dura mater or the covering of the brain and meninges

TBI closed (blunt) - occurs when head accelerates and then rapidly decelerates or collides with another object (e.g. a wall, dashboard of a car) and brain tissue is damaged but there is no opening through the skull and dura TBI, open (penetrating) - an object penetrates the skull, enters the brain, and damages the soft brain tissue in its path or when blunt trauma to the head is so severe that it opens the scalp, skull, and dura to expose the brain Concussion (Closed): Blunt trauma; Temporary loss of neurologic function with no apparent structural damage to the brain Frontal lobe affected - bizarre irrational behavior Temporal lobe - temporary amnesia or disorientation Symptoms: headache, N/V, Photophobia, amnesia, blurry vision, last 24 hours (+/-) Treatment: Observation, often discharged in less than 24 hours (after they return to baseline), slowly resume normal activities. - Observe the patient for decreased LOC, worsening headache, dizziness, seizures, abnormal pupil response, vomiting, irritability, slurred speech, numbness, or weakness in arms and legs. - Repeated concussive -> chronic traumatic encephalopathy Contusion (Closed): more severe injury, involving bruising of the brain due to acceleration/deceleration or blunt trauma; can impact intracranial pressure (slight change in ICP) - Most common are in anterior portions of frontal and temporal lobes, around the sylvian fissure, and orbital areas Clinical manifestations of Contusion: - Loss of consciousness associated with stupor and confusion - Hemorrhage and edema peak after about 18-36 hours -> increased ICP and herniation syndromes (common in temporal lobe contusions) - Later, vitals return to normal, headache, vertigo, impaired concentration, change in LOC Treatment: Observation: Keep patient calm, quiet and low light; GCS Diffuse Axonal Injury: Widespread shearing and rotational forces that produce damage throughout the brain; severe massive brain injury; brain substances are completely damage and brain can come out; bleeding occurs; to axons in the cerebral hemisphere, corpus callosum, and brainstem - associated with prolonged traumatic coma; more serious and is associated with a poorer prognosis than a focal lesion. - patients are in severe head trauma experiences no lucid interval, immediate coma, decorticate and decerebrate posturing - decorticate - flexion posturing - decerebrate - extension Dx: CT or MRI; recovery depends on severity of axonal injury

aortic aneurysm: abnormal dilation of arterial wall caused by localized weakness and stretching in the medial layer or wall of the aorta - can be located along the abdominal aorta

Types of aneurysms: 1) False aneurysm—a pulsating hematoma. The clot and connective tissue are outside the arterial wall. One, two, or all three layers of the artery may be involved. 2) Fusiform aneurysm—symmetric, spindle-shaped expansion of entire circumference of involved vessel. 3) Saccular aneurysm—a bulbous protrusion of one side of the arterial wall. 4) Dissecting aneurysm—this usually is a hematoma that splits the layers of the arterial wall. 1) Fusiform: diffuse dilation that involves the entire circumference of the arterial segment 2) Saccular: distinct localized outpouching of the artery wall 3) Dissecting: created when blood separates the layers of the artery wall, forming a cavity between them 4) False (pseudoaneurysm): occurs when the clot and connective tissue are outside the arterial wall because of vessel injury or trauma to all 3 layers of the arterial wall

TAA Manifestations/Treatment

depend on how fast aneurysm dilates and how the pulsating mass affects surround intrathoracic structures; could be asymptomatic - Pain - most prominent symptom; constant, ripping, tearing, piercing, sudden pain -pain may occur when pt. is supine -"wakes them out of their sleep"; pain extends to neck, shoulders, lower back, or abdomen - Dyspnea - by of pressure of the aneurysm sac against the trachea - Syncope, increased pulse - Paroxysmal cough (brassy quality), hoarseness, stridor, or aphonia (loss of voice) from the pressure against the laryngeal nerve -dysphagia (bc of impingement of the esophagus by the aneurysm) - Cyanosis of chest wall and edema of the upper extremities due to large vein compression of the chest by the aneurysm ( Superficial veins of the chest, neck, or arms become dilated and edematous area of the chest wall and cyanosis are often evident - bc the large veins are compressed by the aneurysm) - Unequal pupils - pressure on the cervical sympathetic chain Diagnostic Testing: thoracic Aneurysm: -Chest x-rar -Ct scan with angiography (CTA) - looking at arterial circulation -Magnetic resonance angiography (MRA) -transesophageal echocardiography (TEE) if pt. is stable Med management: BP control and correcting risk factors - Correcting risk factors: ex: smoking cessation - BP control medications: - Beta blockers (atenolol, metoprolol, carvedilol) - ARBS (Losartan, Valsartan, irbesartan) - ACE inhibitors (prils) - Statins - Treat infections if mycotic Surgical management: - Pre op BP control for dissecting aneurysms - SBP maintained @ 90-120 to maintain a mean arterial pressure @ 65-75 mmHG w/ a beta blockers (esmolol) or metoprolol - Hydralazine and nitroprusside (continuous IV drip to lower BP; rapid onset) - vasodilators for MAP Surgery goal: to repair aneurysm and restore vascular continuity with a vascular graft and ICU care will be required - Vascular graft (interventional radiology, cardiac cath lab or combined interventional suite and OR) - endovascular graft (gore-tex or PTFE material w/ nitinol or titanium stents); inserted into the thoracic aorta through brachial or femoral artery; complication: spinal cord ischemia To decrease the chances of spinal cord ischemia and paraplegia -> lumbar spinal drains are placed in pt. undergoing an endovascular repair of TAA; cerebrospinal fluid drainage - to decrease the arterial to cerebral spinal fluid gradient -> improving spinal perfusion Preventing neurologic deficit - maintain the cerebrospinal fluid pressure less than or equal to 10 mmHg and to keep MAP > 90 mmHg for the first 36-48-hour post op Thoracic open repair - chest is opened, using the graft, clamping aorta, cutting aorta, and placing a graft, sutures, putting the graft in place TEVAR (endovascular)- less invasive, entry could be femoral artery! Graft put in and it expands once inserted within the line; post op -> pulses and bleeding Nursing interventions of TAA: - Assess: pulses, perfusion,VS - every 15 min first hour, every 30 for 2nd, and every 1 hour after -post op medication needs - antihypertensives (to control the BP), pain medications, BP goals, follow up imaging, clamp time (how long? EBL (estimated blood loss), Urinary output, kidney function (baseline) BUN/Cr? wound care including drainage, neuro checks, spinal cord ischemia prevention -first dressing change done by surgeon; if anything, wrong -> reinforce the dressing and call the provider - Lumbar drain care if applicable - how much drain in an hour? Positioning? What position? When can they change position? Drains should not be cloudy or bloody; should be clear! - Sternal precautions (don't reach behind the head, no pressure on self when getting out the chair, work closely w/ PT and OT) pt. and family education, discharge planning (starts @ the time of admission); do not lift objects heavier than 15-20 pounds for 6-12 weeks; avoid activities requiring pushing, pulling, or straining

Brain Tumors: glioma neuroma, meningioma, acoustic, pituitary adenoma, angioma

occupies space within the skull, the effects are caused by inflammation, compression & infiltration of tissue. Physiological changes-> IICP & Cerebral edema, seizure activity, focal neuro signs, hydrocephalus, altered pituitary function

Brain tumor - primary

originate from brain (cells w/in the brain) - mostly glial cells that make up brain & spinal cord -are located @ Supraentorial (above cerebellum covering) -Progress locally Risk Factors: Genetic & Ionizing radiation exposure Graded I to IV (aggressive)