Endocrine/Neuro Exam #3

Papilledema

"Choked disc," swelling of optic nerve head Increase in intracranial pressure

Pancreas

**Normal insulin produced by B cells in Pancreas - Helps move glucose from blood into cell for fuel Abnormal Issues: - Hypoglycemia - Hyperglycemia - Dawn Phenomenon - Somoygi Effect - Type 1 and Type 2 Diabetes

Increased Intracranial Pressure : Clinical Mnifestations

- Change in level of consciousness (LOC) - Change in vital signs= cushing triad, change in body temp=increased ICP on hypothalamus - A change in vital signs may be a late sign of increased intracranial pressure. Trends include increasing temperature and blood pressure and decreasing pulse and respirations. Respiratory irregularities also may occur. - ocular signs: pupil dilation, sluggish response, inability to move eye upward, blurred vision, diplopia, etc.) - Decreased in motor function: (hemiparesis, hemiplegia, decorticate or decerebrate posturing) - Headache- continuous , but worse in morning - Vomiting - w/out nausea Depends on the cause , location and rate of pressure increases

Neurogenic Shock Diagnositc test

- H& P (History of recent trauma - 12 lead EKG - X-ray - Pulse Ox (Continous) - Hemodynamic monitoring

Increased Intracranial Pressure: Diagnostic findings

- History - Physical examination - X - ray - MRI & CT= used to detect the cause of increased ICP. - PET- also used to diagnose the cause Other test: - Cerebral angiography, EEG, CP measurement, brain tissue oxygenation measurement via the LICOX ca transcranial doppler studies, Lab: CBC, coagulation , electrolytes, creatinine, ABG's CSF, ammonia, glucose. drugs, toxicology, etc.)

Neurogenic Shock Risk factors

- Spinal cord injury - Spinal Anesthesia - Drugs (Opioids & Benzodiazepines) depress vasomotor center of medulla - Dilation of peripheral blood vessels = pooling of blood * Any pt who sustains surgical accidental trauma is @ high risk for shock .

Thyroid gland produces

- Thyroxine (T4), one of three hormones secreted by the thyroid gland, is responsible for a number of functions, including maintenance of metabolic rate and normal metabolism, normal growth and development, and protein, fat, and carbohydrate catabolism. Hyperthyroidism due to Graves' disease is generally characterized by a high T4. - Triiodothyronine (T3), the most active of three hormones secreted by the thyroid gland, is responsible for a number of functions, including maintenance of metabolic rate and normal metabolism, normal growth and development, and protein, fat, and carbohydrate catabolism. Hyperthyroidism due to Graves' disease may be characterized by a high T3 level. - Calcitonin (thyrocalcitonin), one of three hormones secreted by the thyroid gland, helps regulate serum calcium (Ca) levels.

Oral antidiabetics

...

1/2 Normal Saline

.45% NaCl in water - Crystalloid solution - Hypotonic - Raises total fluid volume - Hypotonic saline fluids such as 0.45% sodium chloride solution, which expand the intracellular compartment, are indicated for hypertonic dehydration, gastirc fluid loss, and cellular dehydration from excessive diuresis . Monitor closely.

Normal Saline

0.9% NaCl in water crystalloid solution - Isotonic - Increases circulating plasma volume when RBCs are adequate. - Replaces loss without altering fluid concentrations helpful for Na+replacement.

Brain Abscess

Pathology Accumulation of pus within brain tissue that can result from a local or systemic infection Clinical Manifestations Headache Fever N&V Signs of ICP Focal symptoms Diagnostics History and physical CT scan Treatment Antibiotics Symptomatic treatment Complications Subdural empyema Osteomyelitis of cranial bones Epidural abscess Death

Hypoglycemia-

Pathology: - Occurs when there is too much insulin in proportion to avaliable glucose in blood. - Causes blood glucose to drop to < 70mg/dL - Once blood glucose is < 70 (Text book) mg/dL.neuroendocrine hormones are released and the autonomic nervous system is activated. - Those with kidney issues can cause perosn to hold on to medication longer - can lead to hypoglycemia. Clinical Manifestations: - When blood sugar is low (<70) the patient may be (confused, cool, clammy, irritable) - Begin treatment STAT - Poorly controlled diabetics may not realize they are hypoglycemic: they are usually on betablockers. - If a pts BG is high all the time they may have hypoglycemic symptoms even if there BG are a little higher than 70. - Hypoglycemia can affect mental functioning; Can mimic alcohol intoxication. - Sugar feeds brain- lose brain cells every episode Signs and symptoms: - difficulty speaking - Visual distrubances - Shaking/tremors - Diaphoresis (sweating) - Irritable/mentation changes (church lady cuss you out) - Headache - dizziness - Weakness/fatigue - ↑HR - Polyphagia (Hunger) - Stuppor - Confusion - Coma Late S&S - loss of consciousness - Seizures - Coma - Death Risk Factors: - pts w/ very high blood glucose that falls too rapidly. - administering too much insulin/medication - ingesting too little food - delaying time of eating - unusual amount of exercise - Loss of weight without changing medication - Use of Beta Blockers (can mask signs of hypoglycemia) - Those with hypoglycemia unawareness (Autonomic Neuropathy) drops to critical levels and the patient may not be aware of it. - The elderly - its okay for the blood sugar to be a little higher due to this. Diagnostic Tests - History (if possible) and physical examination - Blood glucose - STAT Treatment: Nursing Care Goal: Raise blood glucose level - some source of carbs (simple sugars) (sweets) (Fast acting) - Are they alert and Oriented: give OJ, coke, 10-15g of carbs. Check sugar in 15mins, continue to check every 15 minis until blood sugar is above 65. You may have to give them another 4oz of juice check it again if they are getting better greater than 65 then give them protein. - If they are a Renal patient (NO OJ) **Stay away from milk products. Give turkey, peanut butter - Make sure they are eating their meals - If the patient is Non responsive, can't swallow and have an IV site (50% Dextrose in 50 mL) gonna give an amp or half of an amp 25 mL. Recheck in 15 mins. If it is above then give protein snack once awake. **Non-responsive and no IV, give them glucagon: IM injection. Glucagon raises blood sugar. Causes you to release glycogen stores in the liver. Check sugar in 15 mins and if it is good and the patient is awake give protein snack. - Recheck patients blood glucose 45 mins after snack to ensure hypoglycemia isn't recurring. ** With effective treatment, hypoglycemia can be quickly reversed Medications: - If no significant improvement in pts condition after 2-3 dose of 15 g of simple carbs, call physician Admin. - 1mg of glucagon IM or SQ (nausea is normal) - May also treat w/ 20-50mL of 50% dextrose IV push.

Concussion

A concussion is a closed head injury, and is usually a result of blunt impact to the head. Damage occurs to brain tissue as it bounces, twists, and/or turns within the skull. Depending on the severity of impact, damage may be mild and symptoms may be temporary, or damage may be severe and symptoms may be persistent. A transient loss of unconsciousness or "dazed" appearance typically follows. Memory loss of events preceding the injury (retrograde amnesia) and following the injury (anterograde amnesia) is common. If concussion is from a blunt head injury monitor for: Bloody or clear drainage from either the nasal or the auditory canal after head trauma could indicate a cerebrospinal fluid leak. The appropriate nursing action is to notify the HCP, because this finding requires immediate intervention. Complications from a head injury can arise 2 to 3 days later, and the discharged patient must have a responsible adult who can stay with or check on the patient.

Semi-comatose state

A semi-comatose state is characterized by the absence of verbal responses and inappropriate responses to painful stimuli.

Subdural hematoma

A subdural hematoma, is a collection of blood in the subdural space between the dura mater and the arachnoid layer of the meningeal covering of the brain. A subdural hematoma can be a consequence of a closed head injury or a penetrating head injury. It is usually a result of a venous bleed and therefore is slow to develop into a large mass. Injury resulting in subdural hematoma can be life-threatening because of mass effect on brain tissue and rise in intracranial pressure. With subdural hematoma, bleeding is a result of rupture of blood vessels between the brain and the dura (veins, but can also include small arteries). A subdural hematoma resulting from traumatic brain injury is usually a result of a venous bleed and therefore is slow to develop into a large mass. The patient usually develops a decreased level of consciousness and headache within 48 hours of head injury. An acute subdural hematoma manifests within 24 to 48 hours of the injury. The signs and symptoms are similar to those associated with brain tissue compression by increased intracranial pressure (ICP) and include decreasing LOC and headache. With subdural hematoma, the "mass" effect of blood on brain tissue injures the brain and causes an increase in intracranial pressure (ICP), both of which can be life-threatening.

Antidiabetic agents/Insulins

Action: - Reduces blood glucose levels by increasing glucose transport across cell membranes; enhances conversion of glucose to glycogen Indications: - Type 1 diabetes; type 2 diabetes not responding to oral hypoglycemic agents; gestational diabetes not responding to diet Side effects - Hypoglycemia Nursing Considerations - Teach patient to rotate sites to prevent lipohypertrophy, fibrofatty masses at injection sites; do not inject into these masses - Only regular insulin can be given IV; all can be given SQ Herbal interactions - Bee pollen, ginkgo biloba, glucosamine may increase blood glucose - Basil, bay leaf, chromium, echinacea, garlic, ginseng may decrease blood glucose. Nutrition The recommendation for carbohydrate intake is a minimum of 130 g/day. Low-carbohydrate diets are not recommended for diabetes management.

Craniotomy

After craniotomy the goal is to keep the serum osmolality on the high side of normal to minimize excess body water and control cerebral edema. The normal serum osmolality is 285 to 295 mOsm/kg H2O. A higher value indicates dehydration; a lower value indicates overhydration. The postcraniotomy client typically is sensitive to loud noises and can find them excessively irritating. Control of environmental noise by others will be helpful for this client. Seizures are a potential complication that may occur for up to 1 year after surgery. For this reason, the client must diligently take anticonvulsant medications. The client and family are encouraged to keep track of the doses administered. The family should learn seizure precautions and should accompany the client during ambulation if dizziness or seizures tend to occur. The suture line is kept dry until sutures are removed to prevent infection. After craniotomy, clients may experience difficulty with altered personal appearance. The nurse can help by listening to the client's concerns and by clarifying any misconceptions about facial edema, periorbital bruising, and hair loss (all of which are temporary). The nurse can encourage the client to participate in self-grooming and use personal articles of clothing. Finally, the nurse can suggest the use of a turban, followed by a hairpiece, to help the client adapt to the temporary change in appearance.

Epidural hematoma

An epidural hematoma, is a collection of blood between the dura mater and the skull. An epidural hematoma can be a consequence of a closed head injury or a penetrating head injury. Bleeding is usually arterial, but can be venous. If arterial, the hematoma develops rapidly. Patients often present unconscious, although a brief "lucid interval" often occurs after the head injury and lasts about a minute. This is followed by a decrease in level of consciousness and progression to coma. Injury resulting in epidural hematoma can be life-threatening because of mass effect on brain tissue and rise in intracranial pressure. Prompt surgical intervention is needed. Epidural hematoma often results from a linear fracture crossing a major artery in the dura. The classic sign is an initial period of unconsciousness at the scene and a brief lucid interval followed by a decrease in LOC. Bleeding after a traumatic head injury can also result in epidural hematoma. An epidural hematoma is a collection of blood between the dura mater and the skull. Epidural hematomas develop rapidly, often are arterial bleeds, and patients often present unconscious. Prompt surgical intervention is needed. Traumatic head injury can also result in intracerebral bleeding (bleeding directly into brain tissue).

Skull fracture after blunt head trauma

An indication of a basal fracture is cerebrospinal fluid (CSF) leakage from the ear, which confirms that the fracture has traversed the dura. Periorbital ecchymosis can indicate a skull fracture as well. Complications from a head injury can arise 2 to 3 days later, and the discharged patient must have a responsible adult who can stay with or check on the patient.

Insulin pump

An insulin pump provides optimal flexibility and control of blood glucose level. An insulin pump includes an infusion set that administers insulin subcutaneously into the abdomen. Usually, a rapid-acting insulin, such as insulin lispro (Humalog) is used. Insulin doses are preprogrammed to infuse insulin continually over a 24-hour period (basal dose), at varying rates dependent on anticipated blood glucose levels (lower rate at night, higher rate before breakfast). Bolus doses are also administered, before meals.

Intracranial laceration

An intracranial laceration, involves tearing of brain tissue. It usually is a result of a penetrating head injury, such as from a bullet. It often leads to intracerebral bleeding.

Anterior cord syndrome

Anterior cord syndrome is characterized by complete motor loss and loss of pain and temperature sensations below the level of injury. Preserved are the senses of vibration, deep touch (pressure), and position. This syndrome is often the result of a hyperextension injury that causes a compression fracture. A wedge of bone impinges on the anterior spinal cord and the anterior spinal artery.

A patient with DKA and a history of renal disease

Assess Change in the level of conciousness when administering IV fluids Too rapid fluid replacement can lead to hyponatremia and cerebral edema. .

Pentobarbital (Nembutal)

Barbiturate for pain

INFLAMMATORY BRAIN CONDITIONS

Brain Abscess Meningitis Encephalitis

Central cord syndrome

Central cord syndrome is characterized by motor loss that is greater in the upper extremities than in the lower extremities and variable sensory loss. This syndrome is the result of injury that caused bleeding or hematoma in the center of the cervical spinal cord.

transsphenoidal resection of the pituitary gland

Cerebrospinal fluid (CSF) leakage after cranial surgery may be detected by noting drainage that is serosanguineous (containing blood) surrounded by an area of straw-colored or pale drainage. The physical appearance of CSF drainage is that of a halo. If the nurse notes the presence of this type of drainage, the HCP needs to be notified.

Babinski's sign

Checking for Babinski's sign is done by stroking the lateral aspect of the sole of the foot with a moderately sharp object from the heel to the ball of the foot. A normal response is plantar flexion of all toes (absence of Babinski's sign). Babinski's sign is present if there is dorsiflexion of the great toe, which may be accompanied by fanning of the other toes. This pathological reflex may be present with a very high intracranial pressure.

Type 1 Diabetes

Chronic disease of absolute insulin deficiency (Type 1) DKA (most of the time they have been sick or it came on 1st time in hospital) - Cortisol goes up (stress) causes sugar to raise. Can be as low as 240, but usually is much higher 700, Nausea vomiting. pH is low, temp, ketones in their blood and urine. - Can happen quick if not taking their insulin. - No insulin production; B cell destruction Metabolic acidosis. Will go on a insulin drip Will need fluids (Isotonic solutions) (Normal Saline) look for underlying cause Teaching about diet Always need an insulin from the outside Thin, young

Lacerations

Clinical Manifestations - Open wound with bleeding Due to vascular which lack restrictive properties, relatively small wounds can bleed profusely Diagnostics - Direct examination - X - ray or CT scan to assess if other injuries may be present Monitoring - Frequent neurologic assessment - Monitor VS Treatment and Nursing Care -Control external bleeding - Assess incision site for wound approximation / healing - Monitor site S&S of infection - Local wound care per order - Complications - blood loss, infection

Skull Fractures

Clinical Manifestations -Frequently occur with head trauma -May occur in 3 forms - linear, depressed; simple, comminuted or compound; closed or open See Table 57 - 6, p8 1439 - Location of fracture alters the presentation - cranial nerve deficits; Battle's sign; periorbital ecchymosis, CSG leakage; See Table 57 - 7 pg 1439 Diagnostics - Direct examination - Neurologic assessment - X - ray - CT Scan - MRI Monitoring - Frequent neurologic assessment - Monitor VS - Observe for S&S of increased intracranial pressure - Assess for CSF leaks Treatment and Nursing Care - Treatment is usually conservative - Control external bleeding - Early recognition of possible complications - Relieve pain without oversedation - If large fragments are present or depressed fractures are present, surgical intervention may occur - If a large portion of bone is destroyed, craniectomy may be performed - Complications - intracranial infections, hematomas, meningeal and brain tissue damage

Methylpredinsolone (Solu-Medrol)

Corticosteroids

Cranial Nerves II, III, IV

Cranial Nerve II : Optic Sensory nerve for vision and visual fields Cranial Nerve III: Oculomotor nerve for EOM, lens & Pupil movement Cranial Nerve IV: Trochlear motor nerve for EOM

Cushing's triad

Cushing's triad is systolic hypertension with a widening pulse pressure, bradycardia with a full and bounding pulse, and irregular respirations. The rise in blood pressure is an attempt to maintain cerebral perfusion, and it is a neurologic emergency because decompensation is imminent.

Two types of Hyperglycemia that occurs in Diabetes type 1 and type 2

DKA occurs in Type 1 diabetics (there is no magic number to say they are DKA) can happen as low as 200 HHNS occurs in Type 2 diabetics with an elevated serum glucose of 800-2000)

Posterior cord syndrome

Damage to the posterior cord causes posterior cord syndrome. Posterior cord syndrome is characterized by loss of vibration, deep touch (pressure), and position senses below the level of injury. Preserved are pain and temperature sensations and motor function.

D5W

Dextrose 5% in water - Isotonic in bag - Physiological IV is hypotonic 260 - Raises total fluid volume - Helpful in rehydrating and excretory purposes. - Physiologically hypotonic - the dextrose is metabolized quickly and only water remains

Diabetic retinopathy

Diabetic retinopathy, particularly proliferative retinopathy, can cause retinal detachment, which has the classic new symptom of a veil coming across the field of vision. This requires emergency treatment. The earliest and most treatable stages of diabetic retinopathy often produce no changes in the vision. Because of this, the patient with type 2 diabetes should have a dilated eye examination by an ophthalmologist at the time of diagnosis and annually thereafter for early detection and treatment.

Head Trauma

Diffuse Clinical Manifestations - Generalized injury; damage to the brain cannot be localized to one particular area of the brain Examples - concussion, diffuse axonal injury (DAI) Focal - Localized injury; damage to the brain can be localized to a specific area in the brain Examples - contusion, hematoma Diagnostics - CT - MRI - PET Monitoring Evoked potentials Transcranial doppler Frequent neurologic assessment Monitor VS Observe for S&S of increased intracranial pressure Assess for CSF leaks Treatment and Nursing Care - Emergency management of head trauma - see Table 57 - 9 on page 1442 - Family and patient teaching - see table 57 - 11 page 1444 - Early recognition of and treatment of complications - Surgical repair - Surgical evacuation of hematomas - Controlling temperature and seizures - Complication - hematomas (epidural, subdural, intracerebral); post concussion syndrome; seizures;

Neurogenic shock Nursing Care and Meds

Early recognition and treatment of shock state. - Interventions to control or eliminate the cause of decreased perfusion - Protection of target and distal organs form dysfunction - oxygen & ventilation - Fluid Resuscitation - Minimize spinal damage w/ stabilization (cervical stabilization w/ collar) Meds - Sympathomimetic : Cause peripheral vasoconstriction AKA - vasopressor drugs Ie: norepinephrine & dopamine - Atropine for bradycardia

Encephalitis

Encephalitis Patho Acute inflammation of the brain Usually viral Clinical Manifestations Fever Headache N&V Any CNS abnormality can occur including hemiparesis, tremors, seizures, cranial nerve palsies, personality changes, memory impairment, amnesia and dysphagia Diagnostic: History and physical CT scan EEG MRI PET PCR testing IgM antibodies to virus in serum or CSF Treatment Symptomatic and supportive Antiretrovirals for HSV infection (Acyclovir, Vidarabine) Anticonvulsants when seizure present or prophylactically for severe cases Prevention - Mosquito control measures, use of insect repellent Residual neurologic dysfunction Complications: Cognitive dysfunction Seizures Death

Aneurysm

Heart rate ↑ or ↓ Establish IV access with normal saline. Subarachnoid hemorrhage is usually caused by a ruptured aneurysm Treatment of an aneurysm involves clipping or coiling the aneurysm to prevent rebleeding (Figs. 58-9 and 58-10). A surgical procedure frequently used to prevent rebleeding is clipping of the aneurysm (see Fig. 58-9), but endovascular techniques are becoming more popular. In the procedure known as coiling, a metal coil is inserted into the lumen of the aneurysm via interventional neuroradiology (see Fig. 58-10). Guglielmi detachable coils (GDCs) provide immediate protection against hemorrhage by reducing the blood pulsations within the aneurysm. Eventually, a thrombus forms within the aneurysm and the aneurysm becomes sealed off from the parent vessel by the formation of an endothelialized layer of connective tissue. GDCs provide an alternative therapy to traditional surgical clipping of aneurysms. (Lewis 1470) - Aneurysm precautions include placing the client on bed rest (as prescribed) in a quiet setting. Stimulants such as caffeine and nicotine are prohibited; decaffeinated coffee or tea may be used. Lights are kept dim to minimize environmental stimulation. Any activity that increases the blood pressure or impedes venous return from the brain is prohibited, such as pushing, pulling, sneezing, coughing, or straining. The nurse provides physical care to minimize increases in blood pressure. For the same reason, visitors, radio, television, and reading materials are prohibited or limited.

Thyroid Surgery

Hemorrhage is always a possible complication of surgery. It is a particular concern after thyroidectomy because hematoma formation can externally compress the airway. Stimulation of the thyroid gland during surgery in conjunction with the stress of surgery can precipitate thyrotoxic crisis. This extreme hyperthyroid condition is characterized by high fever, delirium, tachycardia, and dehydration. This complication is serious, but rare. Since thyroidectomy is performed at the neck area, adjacent to the trachea, postoperative swelling and/or bleeding increases risk of external compression of the trachea and airway obstruction. Inadvertent damage to the laryngeal nerve during thyroidectomy can cause voice changes. The problem is generally self-limited, but permanent vocal cord paralysis can occur. A patient should be asked to speak as soon as possible after thyroidectomy, generally in the Post Anesthesia Care Unit (PACU). After thyroidectomy, external compression of the trachea from postoperative hemorrhage can cause a patient to have difficulty swallowing or coughing and/or a choking sensation. Also, external compression of the trachea can cause airway obstruction that can cause respiratory distress. After thyroid surgery, if bleeding occurs, it is likely that bleeding would be observed and corrected before enough blood was lost to cause blood pressure to drop or pulse rate to increase. After thyroidectomy, bleeding would likely be visible on the patient's anterior neck dressing. After thyroidectomy, the posterior of the patient's neck dressing should be checked for bleeding. Blood drips posteriorly when a patient reclines. A tracheotomy set is bedside, just in case a respiratory emergency develops. After subtotal thyroidectomy, postoperative hypocalcemia, low serum calcium (Ca), can occur secondary to inadvertent damage to or removal of the parathyroid gland(s) during surgery. The parathyroid glands are anatomically located adjacent to or embedded in the thyroid gland. The parathyroid gland(s) secrete parathormone, which helps maintain a normal serum calcium level. Lack of parathormone can precipitate hypocalcemia. Because hypocalcemia is a possible postoperative complication, calcium gluconate is kept at bedside. Calcium gluconate is a calcium salt that can reverse hypocalcemia. - Early symptoms of hypocalcemia include numbness and tingling of the mouth, nose, ears, fingertips, and toes. - Severe hypocalcemia is characterized by painful muscle spasms, tremors and twitching, and convulsions. - Hypocalcemia causes signs and symptoms of tetany, which is a neurological disorder. Hypocalcemia is characterized by numbness and tingling as early symptoms of tetany, and muscle spasms, tremors and twitching, and convulsions as late signs / symptoms of tetany. - tap one side of the patient's face over the area of the facial nerve and observe for local spasm. This is the technique to use when checking for Chvostek's sign. -Trousseau's sign is checked by inflating a blood pressure cuff on the patient's upper arm and observing for muscle spasm in the hand. After thyroidectomy, patients are often fearful about moving their heads. Head and neck should be supported when resting in bed or in a chair. Support with proper alignment can be provided with a folded towel, for example. Support should help feel more secure and comfortable. Head and neck should be manually supported when pt turns or moves in bed or moves into a chair. This should help pt feel more secure. It can also be taught to provide manual head support when pt moves and turns.

Hemorrhagic Stroke

Hemorrhagic stroke result from bleeding into the brain tissue itself (intracerebral or intraparenchymal hemorrhage) or into the subarachnoid space or ventricles (subarachnoid hemorrhage or intraventricular hemorrhage).1 (Lewis 1463) Subarachnoid Hemorrhage Subarachnoid hemorrhage occurs when there is intracranial bleeding into the cerebrospinal fluid-filled space between the arachnoid and pia mater membranes on the surface of the brain. Subarachnoid hemorrhage is commonly caused by rupture of a cerebral aneurysm (congenital or acquired weakness and ballooning of vessels). Aneurysms may be saccular or berry aneurysms, ranging from a few millimeters to 20 to 30 mm in size, or fusiform atherosclerotic aneurysms. The majority of aneurysms are in the circle of Willis. Other causes of subarachnoid hemorrhage include trauma and illicit drug (cocaine) abuse. About 40% of people who have a hemorrhagic stroke due to a ruptured aneurysm die during the first episode. Fifteen percent die from subsequent bleeding. The incidence increases with age and is higher in women than men. The patient may have warning symptoms if the ballooning artery applies pressure to brain tissue, or minor warning symptoms may result from leaking of an aneurysm before major rupture. Overall, cerebral aneurysms are viewed as a "silent killer" as individuals do not have warning signs of an aneurysm until rupture has occurred. (Lewis 1464) SAFETY ALERT • Sudden onset of a severe headache that is different from a previous headache and typically the "worst headache of one's life" is a characteristic symptom of a ruptured aneurysm. (Lewis 1464) Loss of consciousness may or may not occur. The patient's level of consciousness may range from alert to comatose, depending on the severity of the bleed. Other symptoms include focal neurologic deficits (including cranial nerve deficits), nausea, vomiting, seizures, and stiff neck. Despite improvements in surgical techniques and management, many patients with subarachnoid hemorrhage die. Many are left with significant morbidity, including cognitive difficulties. Complications of aneurysmal subarachnoid hemorrhage include rebleeding before surgery or other therapy is initiated and cerebral vasospasm (narrowing of the blood vessels), which can result in cerebral infarction. Cerebral vasospasm is most likely due to an interaction between the metabolites of blood and the vascular smooth muscle. During the lysis of subarachnoid blood clots, metabolites are released. These metabolites can cause endothelial damage and vasoconstriction. In addition, release of endothelin (a potent vasoconstrictor) may play a major role in the induction of cerebral vasospasm after subarachnoid hemorrhage. Patients with subarachnoid hemorrhage who are at risk for vasospasm are often kept in the intensive care unit for 14 days until the threat of vasospasm is reduced. Peak time for vasospasm occurs on day 6 to 10 after the initial bleed. (Lewis 1464) Increased ICP is more likely to occur with hemorrhagic strokes. Increased ICP from cerebral edema usually peaks in 72 hours and may cause brain herniation. Management of increased ICP includes practices that improve venous drainage, such as elevating the head of the bed, maintaining head and neck in alignment, and avoiding hip flexion. Hyperthermia, which is seen commonly following stroke and may be associated with poorer outcome, needs to be avoided. Increased temperature contributes to increased cerebral metabolism. Drug therapies to treat hyperthermia include aspirin or acetaminophen (Tylenol). A temperature elevation of even 1° C can increase brain metabolism by 10% and contribute to further brain damage. Cooling blankets may be used cautiously to lower temperature. Closely monitor the patient's temperature. Aggressive management of temperature during the first 24 hours after a stroke is most effective in preventing detrimental outcomes. Temperature should ideally be 36° to 37° C with aggressive cooling occurring for temperatures greater than 38° C.17 Seizures occur in 5% to 7% of stroke patients in the first 24 hours. Antiseizure drugs, such as phenytoin (Dilantin) or levetiracetam (Keppra), are given if a seizure occurs. Prophylactic use of antiseizure drugs is not recommended for patients who have not had a seizure. Other measures include pain management, avoidance of hypervolemia, and management of constipation. Cerebrospinal fluid drainage may be used in some patients to reduce ICP. Diuretic drugs, such as mannitol (Osmitrol) and furosemide (Lasix), may be used to decrease cerebral edema. The use of mannitol is being reexamined and compared with hypertonic saline and dextran (HSD) solution infusions for therapeutic treatment of increased ICP. Preliminary findings indicate that HSD solution is as effective as mannitol in lowering ICP.18 As a last resort in the management of ICP, a bone flap may be removed to allow for cerebral edema without increases in ICP. Additional strategies for managing ICP are found in Chapter 57. (Lewis 1469) Diagnostic - CT scan - CT angiography - MRI Prevention - Control of hypertension - Control of diabetes mellitus - Treatment of underlying cardiac problem - No smoking - Limiting alcohol intake Drug Therapy - Platelet inhibitors (e.g., aspirin) - Anticoagulation therapy for patients with atrial fibrillation Surgical Therapy - Carotid endarterectomy - Stenting of carotid artery - Transluminal angioplasty - Extracranial-intracranial bypass - Surgical interventions for aneurysms at risk of bleeding Acute Care - Maintenance of airway - Fluid therapy - Treatment of cerebral edema - Prevention of secondary injury Hemorrhagic Stroke - Surgical decompression if indicated - Clipping or coiling of aneurysm (Lewis 1467)

Hyperkalemia

Hyperkalemia, if left untreated, can cause widening of the QRS complex, followed by cardiac arrest. Emergency treatment for hyperkalemia may include the administration of IV calcium gluconate, sodium bicarbonate, and/or the combination of IV glucose/insulin. These measures decrease serum potassium (K) by forcing potassium molecules back into the cells. Treatments aimed at reversing hyperglycemia and acidosis should also result in correction of hyperkalemia.

Thyroid

Hyperthyroidism

Increased intracranial pressure : Meds

IV mannitol (osmitrol) - osmotic diuretic. Causes fluid to move from the tissue into the the blood vessels, resulting in ↓ of total brain fluid content. Goal is to improve level of consciousness. - Corticosteroids (dexamethasone (decadrom) improves cerebral blood flow and restores auto-regulation * Not recommended fro had injured pts. - Dilantin to prevent seizures * - Fever, agitation shiver, pain can also ↑ICP. Need to avoid. - High dose Barbiturates: pentobarbital (Nembutal) ↓cerebral metabolism and a subsequent decreased in ICP

Osmitrol (mannitol)

IV solution of 15% An inline filter must be used when Osmitrol (mannitol) is prepared. Crystals may be present in an ampule containing Osmitrol (mannitol). If crystals are present, the ampule of Osmitrol (mannitol) should be warmed under warm water and shaken, to eliminate the obvious crystals. There is no need to discard the ampule. In response to the administration of Osmitrol (mannitol), intracranial pressure (ICP) should decrease. Osmitrol (mannitol) is an osmotic diuretic. It has a hypertonic effect that results in fluid shift from tissues (such as the brain) into the intravascular space, for elimination by the kidneys. In Mickey's case, the drug is used to minimize brain swelling and correct increased ICP. In response to the administration of Osmitrol (mannitol), cerebral edema should decrease. Osmitrol (mannitol) is an osmotic diuretic. It has a hypertonic effect that results in fluid shift from tissues (such as the brain) into the intravascular space, for elimination by the kidneys. In Mickey's case, the drug is used to minimize cerebral edema and correct increased ICP. In response to the administration of Osmitrol (mannitol), assuming Mickey has normal kidneys, urine output should increase. Osmitrol (mannitol) is an osmotic diuretic. It has a hypertonic effect that results in fluid shift from tissues (such as the brain) into the intravascular space, for elimination by the kidneys. When prescribed, Osmitrol (mannitol) is used cautiously in small doses. It can result in electrolyte disturbances, severe dehydration, and hypotension that could compromise cerebral tissue perfusion. Also, when head injury is present, Osmitrol (mannitol) can leak through a disrupted blood-brain barrier and cause pressure on the brain to increase. Osmitrol (mannitol) is a drug of choice when brain herniation is impending, but its use in the initial treatment of head injury has been questioned and is controversial.

Kussmaul's Breathing

In compensating for a metabolic acidosis, the lungs can eliminate carbon dioxide (CO2), leaving less available to make acid (carbonic acid, H2CO3). Subsequently, the acidotic state can be reversed. This is accomplished with rapid, deep breathing (Kussmaul's breathing).

Incomplete spinal cord injuries

Incomplete spinal cord injuries are those in which some degree of motor and/or sensory function below the level of cord injury is evident, after the resolution of spinal shock. The term "incomplete injury" has also been defined as preservation of motor and sensory function in the last sacral segment (S4-S5). With incomplete injuries, the amount of function that returns as spinal shock resolves is not necessarily indicative of the amount of function that ultimately will be present. Improvement in function can occur over time. Functional level of injury may descend two levels.

Increased Intracranial Pressure: Pathology

Intracranial pressure is a reflection of the 3 elements within the skull (brain, CSF and blood) remaining at a relatively constant level with the closed structure of the skull (Monro - Kellie doctrine). Normal compensatory mechanisms are to increase absorption or decrease production or flow of either CSF or blood in order to maintain this constant pressure level. Normal ICP ranges from 5 to 15 mm Hg. A sustained pressure above the upper limit is considered abnormal. Increased Intracranial Pressure: A life threatening situation that results from an increase in any or all of the 3 components of the skull: brain tissue, blood, cerebral spinal fluid (CSF) Cerebral edema is an important factor contributing to increased ICP. The extent and severity of the original insult are factors that determine the degree of cerebral edema. Tissue injury causes inflammation, with increased capillary permeability and movement of fluid into the affected area. The skull is a non-compliant cavity filled to capacity with brain, blood, and cerebrospinal fluid. Anything that increases volume or mass within the cavity can cause intracranial pressure (ICP) to increase. Increased intracranial pressure (ICP) results from an increase in any of the three components inside the skull (brain, CSF or blood). Anoxia and cell death are the end result of prolonged pressure increases. Early recognition and reversal of offending process are key to improving patient outcomes. - With an elevated intracranial pressure (ICP), cerebral perfusion is initially increased. As ICP increases, cerebral perfusion decreases. The LOC is the most sensitive and reliable indicator of the patient's neurologic status. Changes in LOC are a result of impaired cerebral brain flow. Papilledema and Cushing's triad are late signs. Tachycardia and a rising systolic blood pressure occur as compensatory mechanisms aimed at maintaining cerebral perfusion. If increased intracranial pressure persists, compensatory mechanisms will begin to fail. As the intracranial pressure increases, the client will exhibit irregular respirations (Cheyne-Stokes), bradycardia and a widening pulse pressure (Cushing's triad). The widening pulse pressure usually occurs because the systolic pressure elevates, while the diastolic is unaffected.

Rapid acting Insulin

Lispro (Humalog) aspart (NovoLog) glulisine (Apidra) Onset: 15 min Peak: 60-90 min Duration: 3-4 hours - Log: Rapid onset (<15 mins); pt needs to have food source available Immediately when given Time of adverse reaction - Midmorning: Trembling, weakness Characteristics: Patient should eat with 5-15 min after injection; also used in insulin pumps.

Meningitis

Meningitis Patho: - Acute inflammation of the meningeal tissues surrounding the brain and spinal cord (specifically refers to the infection of the arachnoid mater and the CSF) - Can be bacterial (medical emergency), viral, fungal or associated with chemicals Clinical Manifestations: Fever Headache N&V Nunchal rigidity Photophobia Decreased LOC Increased ICP Coma Seizures Diagnositcs History and physical Culture and sensitivity (C&S) and gram stain (GS) of blood and CSF CT scan PCR testing Lumbar puncture Xpert EV test (viral) Antibiotics Corticosteroids Symptomatic treatment Treatment: Collaborative care Table 57 - 17 page 1453 Care Plan page 1454 Prevention - vaccine Increased ICP Complications: Residual neurologic dysfunction (CN III, IV, VI, VII, VIII) - CN II - papilledema, blindness; CN III, IV, VI - eye movements, ptosis, diplopia; CN V - sensory loss in the trigeminal nerve, loss of corneal reflex; CN VII - facial paresis; CN VIII - tinnitus, vertigo, deafness Hemiparesis Dysphagia Hemianopsia Chronic headache Waterhouse -Friderichsen syndrome (meningococcal) - petechiae, DIC, adrenal hemorrhage and circulatory collapse Death

Metformin (Glucophage)

Metformin (Glucophage) is held 24 to 48 hours before and after a procedure with contrast medium to minimize the risk of acute renal failure and lactic acidosis. Alcohol consumption must be carefully managed and depends on amount, timing, and type of medication. Medication should be continued during illness, with close glucose and ketone monitoring.

Increased intracranial Pressure: Nursing Care

Monitor for Cushing's Triad (indicates brainstem compression & impending death) - systolic HTN w/ widening pulse pressure, bradycardia w/full, bounding pulse & altered respiratory pattern - Pressure monitoring device - ventricular catheter, - fiberoptic catheter or - Subarachnoid bolt / screw - Assess Level of consciousness Frequent neurologic assessments - Measures to avoid increases in ICP are critical. Assessments for early detection of increasing ICP are also critical. Increased pressure on delicate cerebral cells, and cerebral ischemia, can interfere with cerebral function and result in neurologic deficits that can be observed. neurologic checks / Glasgow Coma Scale (GCS) -The head of his bed should be elevated to promote venous outflow from the brain and help minimize ICP. Head of bed elevation at 30-45 degrees is generally recommended. - Neck flexion can cause jugular vein compression, which can impede cerebral venous outflow and increase intracranial pressure (ICP). The neck should be kept in a neutral position. Extreme hip flexion should also be avoided, as this movement increases intraabdominal pressure and ICP. - Physical movement, including turning, can increase intracranial pressure (ICP). Spacing physical activities allows time for ICP to return to "normal" after activity. Mickey is maintained on bed rest. - Activities that increase intrathoracic and intraabdominal pressures cause an indirect elevation of the intracranial pressure. Some of these activities include isometric exercises, Valsalva's maneuver, coughing, sneezing, and blowing the nose. - Exhaling during activities such as repositioning or pulling up in bed, opens the glottis, which prevents intrathoracic pressure from rising. - Anything that causes physical or emotional stress can increase intracranial pressure (ICP). Patients with potential for elevated ICP should be cared for gently. Stressful conversation should be avoided. Dimming the lights in the room minimizes environmental stimuli and can also help prevent an elevated ICP. Fluid and electrolyte disturbances can have an adverse effect on ICP and must be vigilantly monitored. Monitor for CSF drainage: - Leakage of cerebrospinal fluid (CSF) from the ears or nose may accompany basilar skull fracture. CSF can be distinguished from other body fluids because the drainage will separate into bloody and yellow concentric rings on dressing material, called a halo sign. The fluid also tests positive for glucose. Osmitrol and Lasix Serum osmolality will be closely monitored. Serum osmolality between 300-320 mOsm/kg H2O is desired. This level generally provides a sufficient intravascular hyperosmolar effect that avoids increased intracranial pressure (ICP) but does not cause intracellular dehydration H2-blockers are given when corticosteroids are administered to help prevent gastrointestinal bleeding Cerebral Oxygenation Monitoring: Low concentration of oxygen ions and high concentration of hydrogen ions cause vasodilation, which can result in increased ICP if autoregulation has failed LICOX brain oxygenation catheter Jugular venous bulb Goals - to identify and treat the underlying cause of ICP and to support brain function Adequate oxygenation (artificial airway as indicated) Treatment - Surgical interventions for mass related ICP Mannitol to treat cerebral edema - Corticosteroids may be used to decrease vasogenic cerebral edema, which occurs mainly in the white matter and is caused by changes in the endothelial lining of cerebral capillaries associated with tumors and abscesses. - Monitor for fever, seizures; if found treat accordingly Adequate nutrition Care Plan pages 1436 & 1437 Complications - inadequate cerebral perfusion, cerebral herniation, death

Injury to a Spinal Nerve C4-C5

Muscle group - Shoulder abduction Assess - Respiratory assessment - Shrugs shoulder against downward pressure of examiners hands With a C4-C5 spine fracture, respiratory function is variably affected. Spinal cord injuries at the C4-C5 level affect function of the muscles of breathing - the intercostal and abdominal muscles, and the diaphragm. The diaphragm is a major muscle of respiration. The phrenic nerve, which innervates the diaphragm, arises from cervical segments C3-C5 (chiefly cervical segment C4). After cervical spine injury, immediate post-injury edema can affect respiratory function controlled from higher cervical spine levels than the site of injury. This effect is usually temporary. A spinal injury at the C2 level or above results in total loss of respiratory muscle function. If not immediately ventilated, a patient with a high cervical spine injury may die or suffer irreversible hypoxic brain damage.

Intermediate acting insulin

NPH (Humulin N Novolin N ReliOn N) Onset: 2-4 hours Peak: 4-10 hours Duration: 10-16 hours NPH: intermediate acting (used in combination with Log; first % in combo) Time of adverse reaction: - Early evening: weakness, fatigue Characteristics - White and cloudy solution; can be given after meals

Normal lungs

Normal lungs regulate the level of hydrogen ions (H+) in the body (and acid-base status) by increasing or decreasing the rate of breathing (and subsequent elimination of carbon dioxide, CO2). This process is called compensation. Carbon dioxide (C02) potentially exists as carbonic acid (CO2 + H20 = H2CO3). When acid is needed, breathing decreases, and carbon dioxide (CO2) is retained. When acid is in excess, breathing increases, and carbon dioxide (CO2) is eliminated. Respiratory compensation for metabolic acidosis occurs quickly, when pulmonary function is normal.

Dawn Phenomenon

Nursing Consideration: Patient will have hyperglycemia in the morning. Monitor - Check sugar at bedtime: normal/low blood sugar at bed time, but when they wake up in the morning sugar is high - Accucheck: between 2-4am is when you do the finger stick to figure out what is happening (blood sugar will be high) |at 6 am still high or higher Treatment: **Change the time you give the insulin

Somoygi Effect

Nursing Considerations: - Morning hyperglycemia Monitor: - Blood sugar is normal/low between 2-4am (blood glucose is low) (do a finger stick) 6 am BG high (body excrete glycogen from the liver to increase blood sugar) Treatment: - Treat this by giving them a snack at bedtime: protein, Give them insulin coverage at bedtime or change the dosage (do they respond appropriately) The books says: Somogyi effect is rebound caused by too much insulin at bedtime. The hypoglycemia produces counter regulatory hormones, causing rebound hyperglycemia. It is treated with less insulin at night.

Ophthalmopathy associated with thyrotoxicosis

Ophthalmopathy associated with thyrotoxicosis involves lid retraction, which is due to excess sympathetic stimulation. With lid retraction, the lids do not close completely and excessive drying of the cornea and conjunctiva occurs. Ophthalmopathy associated with Graves' disease may also involve a staring appearance, eye grittiness / discomfort / tearing, and proptosis (the eye is forced forward). When proptosis is severe, the condition can threaten vision. Lid retraction may resolve as hyperthyroidism goes into remission, although other aspects of ophthalmopathy may not be reversible. In persons diagnosed with Graves' disease who have signs of ophthalmopathy, treatment with radioactive iodine may be avoided since it can exacerbate the problem. Cigarette smokers may be at increased risk for ophthalmopathy. Many persons with Graves' disease do not develop clinically-apparent ophthalmopathy.

Orientation

Orientation is assessed by evaluating a person's ability to respond appropriately to questions about who he is (orientation to person), where he is (orientation to place), and what time it is (orientation to time). When orientation is documented, the status of each should be noted, although often only negative findings are mentioned, and positive findings are inferred. Often, with deteriorating mental function, orientation to time is lost first, followed by orientation to place, and finally, disorientation to person occurs.

Neurogenic shock Clinical Manifestations

The most important clinical manifestations in neurogenic shock are hypotension (from the massive vasodilation) and bradycardia (from unopposed parasympathetic stimulation).7 The patient in neurogenic shock may not be able to regulate temperature. The inability to regulate temperature, combined with massive vasodilation, promotes heat loss. Initially, the patient's skin will be warm due to the massive dilation. As the heat disperses, the patient is at risk for hypothermia. Later, the patient's skin may be cool or warm depending on the ambient temperature (poikilothermia—taking on the temperature of the environment). In either case, the skin will usually be dry. Tables 67-2, 67-3, and 67-4 further describe the clinical presentation of a patient with neurogenic shock. (Lewis 1722)

Type 2 Diabetes

Patho: - Relative insulin deficiency or resistance (Type 2) - Insulin resistance (low insulin production); B cell exhaustion; 90-95% of diabetics Complications - HHNS (Hyperglycemic hyperosmolar Nonketonic) blood is concentrated and sugar is high 2,000, no ketones in labs (usually comes on over time from not staying hydrated) Main problem is fluid ***Why is this happening*** Fluid resuscitation (main problem is dehydration) Treatment - (hypotonic solution) moves stuff faster. Can use normal saline but hypotonic solution moves quicker 200-250 hour. Do not give IV insulin: only insulin injections in the abdomen Risk factors - older person, issue taking in fluids, sick for a while, problems with the thirst center of their brain. (possible strokes) - over weight If they have Hypoglyemia they can have a hard time because their meds may still be effecting them so you have to check back with them to correct the hypoglycemia. Will have to monitor for longer periods of time. Risk factors: - Obesity - Family history - Ethnicity- Blacks, hispanics and Native Americans - History of gestational diabete Medications: Know them Diagnosis Fasting glucose of 126 or greater Confirming by doing a second test or Random of greater than 200 with symptoms (Polyuria "peeing a lot" (acts as an osmotic diuretic), Polydipsia "fool drink some water", Polyphagia "need to eat") Long term complications: - Retinopathy - Neuropathy - Nephropathy - Peripheral vascular disease Autonomic dysfunction occurs from poorly controled diabetes ominous perstalsis stops working Alcohol should be consumed with food to reduce the risk of hypoglycemia

Meningitis

Pathology - Acute inflammation of the meningeal tissues surrounding the brain an spinal cord specifically an infection of the arachnoid matter & CSF. Bacterial - ↑in CSF w/ ↑ in ICP can result in residual neurologic dysfunction. Medical Emergency! Viral - Commonly caused by enterovirus arbovirus, IV & herpes. Risk Factors - Bacterial - Viral respiratory diseases, old age, close quarter living (college dorms & prisons, penetrating wounds of the skull, Fall/winter/spring Viral - Direct contact w/ respiratory secretions Clinical Manifestations/Signs & Symptoms Bacterial - Fever, severe headache nausea, vomiting, neck stiffness, photophobia, ↓LOC, signs of ↑ ICP, skin rash, possible seizures and in rare cases coma. Viral- headache, fever photophobia, stiff neck - Signs of meningeal irritation compatible with meningitis include nuchal rigidity, a positive Brudzinski sign, and positive Kernig sign. Nuchal rigidity is characterized by a stiff neck and soreness, which is especially noticeable when the neck is flexed. Kernig's sign is positive when the client feels pain and spasm of the hamstring muscles when the leg is fully flexed at the knee and hip. Brudzinski's sign is positive when the client flexes the hips and knees in response to the nurse gently flexing the head and neck onto the chest. Diagnostic Test Bacterial - Blood culture & CT scan. Verified by a lumbar puncture: - A client undergoing lumbar puncture is positioned lying on the side, with the legs pulled up to the abdomen and the head bent down onto the chest. This position helps open the spaces between the vertebrae and allows for easier needle insertion by the health care provider. The nurse remains with the client during the procedure to help the client maintain this position. - After the lumbar puncture the client remains flat in bed for at least 2 hours, depending on the health care provider's prescriptions. A liberal fluid intake is encouraged to replace the cerebrospinal fluid removed during the procedure, unless contraindicated by the client's condition. The nurse checks the puncture site for redness and drainage and assesses the client's ability to void and move the extremities. - After the procedure, the client assumes a flat position. If the client is able, a prone position with a pillow under the abdomen is the best position. This position helps reduce cerebrospinal fluid leakage and decreases the likelihood of post-lumbar puncture headache. - analysis of the CSF. - Skull X-Rays. Viral- Xpert EV test of CSF, lumbar puncture, PCR testing of CSF. Nursing Care - Promotion of vaccinations to prevent respiratory infections - Promotion of early treatments of respiratory & ear infections - Assessment of vitals, mental status, I&Os, lung function and skin - Head Of Bed - elevated to decrease ICP - Dark room w/ cool cloth over the eyes. Cool environment - Manage fevers - Safe environment in case pt has seizures Pt Education - Stress adequate nutrition - promote ↑ protein ↑? - Adequate rest and sleep - Progressive range of motion , exercises and warm baths for muscle rigidity. Meds Bacterial- Antibiotics, IV fluids, codeine for headache corticosteroids, antipyretic, mannitol for duresis. Viral - Managed symptomatic as the disease is self limiting

Diabetes insipidus

Pathology - Diabetes insipidus is characterized by polyuria and polydipsia, both a result of inadequate antidiuretic hormone (ADH). Abnormal glucose levels do not occur. - Diabetes insipidus is usually a complication of head injury. Injury to the hypothalamus or posterior pituitary causes a decrease in the secretion of antidiuretic hormone. Subsequently, water reabsorption from the renal tubules decreases, resulting in systemic dehydration (high serum osmolality) and a profound diuresis of extremely dilute urine (low urine osmolality). - Inhibition of ADH Synthesis, transport, and /or release due to organic lesion on hypothalamus, infundibular stem, or posterior pituitary. - Trauma=self-limiting - Surgery= often permanent Risk Factors - Head Trauma - CNS infection - Brain tumor - Brain surgery - Meningitis - Encephalitis - Any organic lesion on hypothalamus, infundibular Clinical Manifestations - 5-20 L/day urine output - low urine osmolality/specific gravity - high serum osmolality (hypernatremia) S&S - Polydipsia, polyuria, fatigue, nocturia, signs of dehydration, generalized weakness, constipation Diagnositc Test - History and physical - low urine specific gravity - imaging - Water restriction test get baseline weight, vital signs, labs - hold fluids for 8-16 hrs - Give vasopressin once urine osmolality stabilizes. - A >9% in osmolality = central D1 - High Serum sodium Nursing Care - Monitor I/O's - Monitor V/S - Monitor urine osmolality/Specific Gravity - skin condition, weight, blood pressure, pulse, temperature, administer pitressin Treatment - Early detection is key! - Fluid/hormone replacement Patient Education: - Long-term management - Follow-up & labs (monitor closely) Meds - hormone/fluid replacement - Desmopression (po/IV/SQ/nasal spray) ↓ diuresis - IV fluids if indicated - maintain hydration

Thyrotoxicosis

Pathology - In Graves' disease, high levels of thyroid hormones are secreted from the thyroid, due to stimulation by an abnormal thyroid-stimulator. High levels of circulating T3 and T4 inhibit secretion of TSH. This process is thought to be an autoimmune, familial disorder. - a condition of excess thyroid hormones. - Thyrotoxicosis is most often due to hyperthyroidism (hyperfunction of the thyroid gland). Hyperthyroidism is frequently caused by Graves' disease. - Excess T4 and or T3 reduced TSH - Physiological effects of hypermetabolism - Other common causes of thyrotoxicosis include toxic goiter (more common in older persons), and thyroiditis (of autoimmune or viral etiology). Risk Factors - over productive thyroid - malfunction of anterior pituitary Clinical Manifestations - Everything is speeded up - ↑HR, ↑BP metabolism - ↑Peristalsis →diarrhea, ↑ metabolism →weight loss, manic - Irritability due to the circulating thyroid hormones - sweating, anxiety, tremors - heat intolerance - May have goiter, exopthalamus - Oligomenorrhea or decreased menstrual flow, or even the absence of menstruation (amenorrhea), decreased libido and impotence in men - muscle fatigue - weakness Diagnositc test - Blood is drawn for TSH (thyroid-stimulating hormone), free T4 (thyroxine), free T3 (triiodothyronine), and thyroid antibodies. A radioactive iodine uptake (RAIU) with thyroid scan is scheduled. - T3 & T4 will be increased and TSH will be decreased - check levels - H&P - ophthalmologic tests - ECG (possible sinus Tachycardia) - Radioactive iodine uptake: (RAIU) with thyroid scan. The tests will be performed at the same time, although different equipment will be used for the tests. You explain that the pt will need to take a capsule containing a radioactive substance the day before the scan. The substance is targeted for absorption by the thyroid gland. - The pt will be exposed to very low levels of radiation for the tests. A small amount of radioactive substance will be ingested. The equipment used the day of testing is not x-ray equipment and does not contribute to radiation exposure. It is appropriate that you give the pt this accurate information. - Since the dose of the radioactive substance required for the procedures is minimal, no special precautions are required afterward. - Pregnancy would contraindicate radioactive iodine uptake (RAIU) with thyroid scan, since the radioactive substance could potentially affect a developing fetus. Breastfeeding is also a contraindication - The radioactive substance taken for these procedures is often radioactive iodine. Generally, allergy to shellfish indicates allergy to iodine. Allergy to shellfish or iodine may be a contraindication for these procedures. - informed consent - Sonogram to look for lesions Nursing Care/Treatments Major goal: get thyroid hormone under control - Goiter can be large enought to push on carotid: can cause syncope when lifting hands above head - PTU - treatment of symptoms (monitor BP, I & O, electrolytes, weight) - Thyroidectomey - trach tray @bedside, note any hoarseness, observe for signs of tetany due to damage to PTH (chvosteks and trousseau) - - Assess for signs of bleeding - if pt is continuously swallowing or clearing throat this could mean they are bleeding in throat (look for blood) - Comfort measures Surgery - prior to surgery - Lugol's solution is prescribed. It is a strong solution of potassium iodide (SSKI). It shrinks thyroid tissue and makes the gland more firm, decreasing risk associated with surgery. Dilute the solution with water, milk or fruit juice or carbonated beverage and have the client drink it wit a straw to help disguise the strong, bitter taste. It can stain teeth in drinking straight. - The vascularity of the thyroid gland is decreased with administration of Lugol's solution. The risk of perioperative bleeding is therefore reduced. - post surgery - do not hyperextend neck Thyroid surgery: Can cause thyroid storm when hormones are squeezed out - Always have a trach tray at the bedside post op; Too much edema and swelling to intubate - Voice can be damaged (permanently) ask patient to speak in recovery room to check for laryngeal damage. - With removal of thyroid will need synthroid meds for life - Monitor for hypothyroidsim - Monitor cardiac dysrhythmias - Ensure adequate O2 - Replace fluid and electrolyte via IV - Provide a calm, quiet room b/c increased metabolism can cause sleep disturbances - Relieve eye discomfort and prevent corneal ulceration →apply artificial tears Medications - BetaBlocker- lol, BP, anxiety, tremors (Inderal (propranolol) should alleviate some symptoms. The drug which is a beta-blocker, will antagonize of the sympathetic nervous system and should alleviate complaints of tachycardia, diaphoresis, nervousness, and tremors. In addition, the drug may reduce some conversion of T4 to T3, the more active of the thyroid hormones. - A drop in blood pressure could result in dizziness, which should be reported. Drug dosage might need to be decreased. The drug should not be stopped abruptly. - PTU propylthioracil) - blocks thyroid hormone production (started @ high dose) Report: Sore Throat immediately. Surgery - Radioactive iodine - shrinks thyroid in leu to surgery. A Sodium iodide destroys the thyroid follicular cells and thyroid hormones are no longer produced. Commonly recommended for graves disease, especially the elderly. - The client needs to be educated about the need for lifelong thyroid hormone replacement. Permanent hypothyroidism is the major complication of RAI treatment. - meds to ↓ gastric emptying - No narcotics to slow peristalsis Anti-Thyroid drugs - antithyroid drug, PTU (propylthiouracil) -Tapazole (methimazole) - Antithyroid drugs inhibit synthesis of thyroid hormones and reduce thyroid antibody levels. PTU (propylthiouracil) also blocks the conversion of T4 to T3, the more potent thyroid hormone. Antithyroid drugs are usually administered for 12-24 months, with the dose decreased as the hyperthyroid state improves. This length of time is usually required to achieve remission. Symptom control is not immediate with use of antithyroid drugs. - Inderal (propranolol) is often needed for symptom control for a few months after antithyroid drugs like PTU (propylthiouracil) are started. Report to HCP immediately if: - Onset of sore throat, mouth sores or fever, since it may indicate infection and onset of agranulocytosis. Agranulocytosis involves an extreme decrease in or lack of granulocytes (neutrophils, basophils, and eosinophils). Granulocytes are one type of leukocytes (white blood cells). White blood cells are critical in preventing infection. In persons taking antithyroid drugs, onset of agranulocytosis may be abrupt. - report any signs of jaundice, which would occur with hepatitis, another adverse effect of antithyroid drug therapy. - Signs of jaundice include dark urine, light-colored stools, and yellow skin and sclera. - Start at high dose →monitor results/symptoms - Can cause hypothyroidism - Monitor T3, T4, T7 (thyroid hormones ) and TSH (released by pituitary) - Not bioequivalent - pts should stay on drugs that works best for them - Some patients get radioactive iodine (those with big vascular thyroid gland): Works to make thyroid gland produce less hormone. - Radioactive iodine therapy is usually ablative, that is, it eliminates most thyroid tissue. Over time, remaining thyroid tissue may be unable to produce enough hormone to maintain a normal metabolic state, and hypothyroidism occurs. - To reduce risk for thyrotoxic crisis (a severe hyperthyroid state), especially in elderly persons or those with cardiac problems, antithyroid drugs are often given for at least a month before radioactive iodine treatment. - Prevents goiter - periodically return to the clinic for blood tests and examinations. - Complete blood count (CBC) with differential will be followed to detect agranulocytosis. Liver function tests will be monitored, since hepatitis can be an adverse effect of drug therapy. Thyroid function tests will be followed to monitor the effectiveness of therapy. Nutritional needs - High calorie diet/high protein may be order to satisfy hunger and prevent tissue breakdown. - If thyroid is removed - caloric intake must be reduced to below they amt that was required before surgery to prevent wt gain - With hyperthyroidism, metabolic rate is increased. Stimulants such as caffeine (contained in coffee, tea, cola, and chocolate) should be avoided to prevent further increases in metabolic rate. Stimulants also increase peristalsis and can contribute to diarrhea, which may occur with a hyperthyroid state. - Frequent nutritional snacks will provide extra calories to meet high metabolic needs while she continues to be in a hypermetabolic state. - Monitor weight. Weight should increase if drug therapy is effective in treating hyperthyroid condition.

Spinal Cord Injury - Cervical

Pathology - In most patients with spinal cord injury, the spinal cord is intact, but damaged. Synaptic connections are interrupted, nerve cells are damaged, and peripheral nerve roots may be compressed. Blood flow is impaired, bleeding may occur, and tissue swells. Autonomic control of vital functions is impaired, at least temporarily. Motor and sensory functions that control mobility and feeling are disrupted, in varying degrees. - Causes of SCI include trauma, motor vehicle crashes, falls, violence and sports, injuries account for the majority of causes. SCI can be due to cord compression by bone displacement, interruption of blood supply to the cord, or traction resulting form pulling on the cord. Risk Factors: - young males (16-30 yrs) - Athletes - Motorcyclists Clinical Manifestations - pain, tenderness, deformities, or muscle spasms adjacent to vertebral column. - numbness, paresthesias - Alterations in sensation: temp, light, touch, deep pressure - difficulty breathing - Weakness, paralysis or flaccidity of muscles - lack of feeling sensation below injury. - spinal cord injury at the level of C5 ,Altered breathing pattern indicates that the respiratory rate, depth, rhythm, timing, or chest wall movements are insufficient for optimal ventilation of the client. This is a risk for clients with spinal cord injury in the lower cervical area. Diagnostic test - X-ray of spine - ABG's - CT scan - MRI - Myelography - Venous diplex studies - Urinalysis - EMG to measure evoked potentials Emergency treatment - If spine injury is suspected, the spine should be immobilized as soon as possible with a backboard with straps, a rigid cervical collar, and supportive blocks. Immobilization is designed to prevent hyperflexion, hyperextension, and rotation of the spine, which could cause cord injury if a fracture is present. - Spine immobilization and alignment must be maintained until there is radiological proof that all vertebrae are negative for injury. Three-view spinal x-ray, supplemented by CT scan as needed, is usually used to confirm or rule out spinal injury. Treatment Skeletal traction with weights can be applied with cervical tongs to reduce the fracture and realign the spine. Cervical tongs are two-point tongs attached to the skull by two cranial pins inserted through two burr holes in the skull, one on each side of the head. Tongs are intended to realign the vertebrae in their normal position and prevent further injury to the spinal cord. Skeletal traction with cervical tongs is used when a cervical spine injury is relatively stable. Nursing care - Ensure patient airway (especially w/ cervical injury) - Stabilize C-spine - administer O2 - Establish IV access w/two large bore catheters - Assess for spinal shock and return of DTR's - Administer high dose steroids (w/in 12 hours) - To avoid further damage to the spinal cord after the initial spinal cord injury, systolic blood pressure is maintained above 90 mm Hg. Treatment to increase blood pressure is initiated if systolic blood pressure falls below 90 mm Hg. Spinal cord injury causes immediate damage to the spinal cord. Secondary injury may occur as a result of variety of mechanisms, including hypoperfusion and ischemia of the spinal cord that can lead to cell death. To avoid secondary spinal cord injury, systolic blood pressure is maintained above 90 mm Hg and mean arterial blood pressure is maintained between 85-90 mm Hg for the first seven days after acute spinal cord injury. - A heart rate below 50 beats per minute is generally treated. - Clear fluid drainage from pin sites may be normal (expected as a result of normal inflammation). However, drainage could be cerebrospinal fluid (CSF), which would not be normal. CSF drainage from pin sites is NOT expected -- it would indicate dural tear and require immediate medical intervention. Drainage should be checked to see if it is CSF. CSF creates a "halo" effect when it dries on bed linens or a gauze pad. - If traction weights are left in place with one cranial pin dislodged, the cervical spine could become misaligned. Generally, weights are immediately removed if a pin becomes dislodged. The physician is then notified. - The halo device alters balance and can cause fatigue because of its weight. The client should cleanse the skin daily under the vest to protect the skin from ulceration and should avoid the use of powder or lotions. The liner should be changed if odor becomes a problem. The client should have food cut into small pieces to facilitate chewing and use a straw for drinking. Pin care is done as instructed. The client cannot drive at all because the device impairs the range of vision. Meds - Solu-Medrol (methylprednisolone) Given within eight hours of spinal cord injury IV Solu-Medrol (methylprednisolone) may minimize spinal cord damage from post-injury edema and other effects, and result in greater preservation of motor and sensory function. Possible harmful effects of high-dose steroids include gastrointestinal bleeding and infection. - Steroids with in 12 hours of injury which decreases inflammation. - Vasopressor (Dopamine)- used to maintain MAP above 90 and hypotension. - Dobutrex (dobutamine) could be used to treat hypotension. - Atropine sulfate should be available to treat bradycardia. Atropine is the drug of choice for treatment of symptomatic bradycardia. It enhances both sinus node and AV node conduction. *Pharmacologic properties and drug metabolism are altered in SCI: drug interactions may occur. - Carafate (sucralfate), which coats the stomach and helps prevent ulceration. After the acute phase of spinal cord injury, the Functional Independence Measure (FIM) is used to assess functional disabilities resulting from injury and the need for assistance. Use of this tool allows for standardized measurement and understanding across caregivers.

Closed Head Injury

Pathology - Motor vehicle collisions - Falls - Firearms, assaults, - Sports- related trauma, recreational injuries, War - related injuries - pedestrian event Head injury, the direct result of trauma, damages the brain. Secondary brain injury can occur as a result of increased intracranial pressure (ICP), and problems it can cause, such as cerebral ischemia. Measures to avoid increases in ICP are critical. Assessments for early detection of increasing ICP are also critical. Increased pressure on delicate cerebral cells, and cerebral ischemia, can interfere with cerebral function and result in neurologic deficits that can be observed. Risk factors - Males are twice as likely to sustain a head injury as females Clinical Manifestations - Raccoon eyes - Bruises or cantusansafface CSF leaking from ear or nose Battles's sign (Bruising behind the ears) - disruption in the LOC - Deceberate or decorticate posturing - confusion of the brain Confusion Seizures GCS<12 - Motor function, when impaired, usually occurs contralateral (on the opposite side) to brain injury. Motor function impairment may involve hemiparesis (weakness) or hemiplegia (paralysis). An expanding hematoma, a consequence of right-head trauma, could result in progressive weakness and paralysis on the left side. - Pupil changes that happen as a result of brain injury occur ipsilateral (on the same side) to the site of brain injury. The oculomotor, or third cranial nerve, controls pupil response. - A pupil size of 4 mm is usually normal. Pupil size larger than 5 mm may be abnormal (dilated). Pupil size smaller than 3 mm may be abnormal (constricted). Diagnostic test - CT scan is the best diagnostic tool to confirm the diagnosis and pinpoint the location a hematoma. - MRI, PET may also be used in the diagnosis & differentiation of head injuries Glasgow coma scale Nursing Care: - Ensure patient airway - Stabilize cervical spine - Establish IV access with 2 large bore catheters to infuse normal saline or lactated ringer's solution - Monitor vital signs, O2 saturation, GCS score, pupil size,& reactivity - Assess for Rhinorrhea, otorrhea, scalp wounds Patient Education: - use seat belts - wear helmet Meds - Administer O2 via non rebreather mask - May use phenytoin (Dilatin)prophylactically to prevent seizures - Supportive measure for pain relief.

Pheochromocytoma

Pathology - Rare condition charactered by a tumor on the adrenal medulla that produces excessive catecholamines. - most are non-malignant - epinephrine and norepinephrine are hormones which raise BP and HR. - "Flight or fight" Risk factors - Most commonly seen in young to middle age adults Clinical Manifestations - Severe episodic hypertension (hypertensive crisis type) - Severe pounding headache - generally not cancer issue is mainly episodic high BP - nervousness, headache, tremors - palpitations - Nausea/vomiting and weight loss - Wide pulse pressure (bounding pulse) - Hyperglycemia - Profuse sweating - Renal artery stenosis - Tremors - unexplained abdominal or chest pain transcient for a few minutes, hours or for weeks at a time Diagnostic Test - 24 hr urine collection (check for VMA (metabolite catecholamine), look for the by-products - Normal results 1-5mg (positive for tumor if significantly higher) - Some foods may alter VMA: Coffee, tea, bananas, vanilla, chocolate - All drugs discontinued during test - Urine collected on ice or refrigerated with preservative. - CT and MRI are used for tumor localization - Tumor can also occur anywhere, form neck to pelvis, along course of sympathetic nerve chain. - Xray to see tumor - Retropariteneal - CT scan to confirm - Draw blood during the episode and check for catecholamine during symptomatic period (RARE you catch this time period) Treatment Adrenalectomy surgery (remove of adrenal gland) - remove tumors -70 % will be curied; 30% will still need something to control BP (Betablockers are tried first) Nursing Care - When BP is high draw blood to see if you can catch the levels epinephrine and norepinephrine - 24 hour urine (know what goes on ice and check what the lab wants you to do with the urine) - Best treatment remove tumor - usually in one side of adrenals - 30% will still have hypertension even after removal - Surgery is more commonly done via laparoscopic adrenalectomy. - Complete removal of the adrenal tumor cures the hypertension in the majority of individuals - If surgery is not an option metyrosine (denser) is used to diminish catecholamine production by the tumor & simplify chronic management - Assess the pt for the classic triad of symptoms of (pheocharomocytoma) - Severe pounding headache, tachycardia & profuse sweating. - Monitor the BP immediately if the patient is experiencing a "attack" - Monitor blood glucose levels, try to make the patient as comfortable as possible. Medications: - BP meds : betablockers or any class - BP meds required preoperatively to control BP and prevent hypertensive crisis. - Propranolol to ↓ tachycardia and other dysrhythmias - If metyrosin is used advise the patient to rise slowly. (orthostatic hypotension) Nutrition: Increase caloric, vitamin and mineral intake due to increased metabolic demand. Avoid coffee, tea, cola, and food containing tyramine.

Neurogenic Shock Pathology

Pathology is a hemodynamic phenomenon that can occur within 30 minutes of a spinal cord injury at the fifth thoracic (T5) vertebra or above and last up to 6 weeks. The injury results in a massive vasodilation without compensation due to the loss of SNS vasoconstrictor tone. This massive vasodilation leads to a pooling of blood in the blood vessels, tissue hypoperfusion, and ultimately impaired cellular metabolism (Fig. 67-4). In addition to spinal cord injury, spinal anesthesia can block transmission of impulses from the SNS. Depression of the vasomotor center of the medulla from drugs (e.g., opioids, benzodiazepines) also can result in decreased vasoconstrictor tone of the peripheral blood vessels, resulting in neurogenic shock (see Table 67-1). (Lewis 1722) - Due to spinal cord injury @ T5 level or above - Can occur w/ in 30 mins **Life threatening condition in which there is insufficient blood flow through out the body due to loss of signals from sympathetic nervous system. Blood vessels dilate. Assessment - In neurogenic shock, pulse rate is slow. In other forms of shock, pulse rate becomes rapid. Poor tissue perfusion and poor oxygenation characterize all forms of shock (hypovolemic shock, cardiogenic shock, septic shock, neurogenic shock). For all types of shock except neurogenic shock, heart rate and respiratory rate increase as compensatory efforts to maintain adequate tissue oxygenation. With neurogenic shock, a compensatory increase in heart rate cannot occur because there is loss of nerve impulse transmission and sympathetic vasomotor tone. This results in unopposed parasympathetic control of heart rate, and subsequent bradycardia.

Hyperthyroidism:

Pathology: - free circulation hormone TSH elevated causing secretion of T3, T4, - speeds everything up HOT Graves disease is a form (exophthalmus protruding eyes) Wear dark-colored sunglasses to help prevent irritation. Manifestations - Chest pain, increase HR, Raises BP, can cause a stroke - increases perstatlisis , diarrhea - lose a lot of weight (40 lbs a month) - don't get a lot of rest : 2-3 hours of sleep - Skin feels hot - Women lose period, body hair falls out - nervous feeling Treatment Start medicaiton high Anitthyroid medication to bind to the hormone to stop production or Tapazol May have to give a beta blocker for this patient (helps control tremors) Thyrotoxicosis (clinical name for too much thyroid hormone) Thyroid storm (happens by manipulating the thyroid) or removing the thyroid give them inderal to lower BP (temps can be high) Surgery: Parathyroids effect calcium (larygeio stridor, airway at bedside, may have edema and swelling. trach tray at bedside if they tell you they are clearing their throat alot get a pen light and look . They may be swallowing blood and can cause thier stomach to swell. Autoimmune disorders usually happen in clusters: diabetes and thyroid Rheumatoid arrhritisis and Chrons disease

Hyperosmolar Hyperglycemic Nonketotic Syndrome (HHNS) TYPE 2

Pathophysiology - Extreme hyperglycemia that leads to severe osmotic diuresis and fluid volume deficit - is an acute hyperglycemic crisis (BG=800-2000) - Hyperosmolarity - Severe dehydration without ketoacidosis - Person does not drink, which is common in the elderly - Can take some time to develop - Glucose production and release into the blood is ↑ or glucose uptake by the cells is ↓ When the cells don't receive enough fuel (glucose), liver converts glycogen to glucose→ blood stream. When all excess glucose molecules remain in the serum, osmosis causes fluid shifts. The cycle continues until fluid shifts in the brain cause coma and death. Hyperosmolar -Blood concentration, dehydrated Hyperglycemic - Blood sugar is high Nonketotic - Not producing ketones. Risk factors - Patient with type 2 diabetes - UTI - Pneumonia - Sepsis - patient over 60 Clinical Manifestations - Severe dehydration - High glucose levels ↑600 - Impaired thirst sensation - dry mucous membranes - Altered mental status (stupor - coma) - Polyuria, polydipsia, and polyphagia - Hypotension and tachycardia - Diaphoresis - Tachypnea - Lethargy and fatigue - Increased osmolarity Diagnostic Test - History and physical - Blood studies (blood glucose 800-2000mg/dL, CBC, pH, ketones are absent so there is no acidosis (produce just enough insulin), electrolytes, ↑BUN, ABG's) - Urinalysis (glucose positive - Serum osmolality is elevated >95 - BUN level high→dehydration - High K+ Nursing Care/Treatment 1. Immediate IV admin of either Isotonic 0.9% or hypotonic 0.45% NaCl - Record I&O 2. Assess Blood Glucose levels : insulin therapy; less insulin required than with DKA; do finger stick and determine amt of insulin needed (SubQ) - When blood glucose levels fall to approximately 250 mg/dL, IV fluids containing glucose are administered to prevent hypoglycemia. - Q1hr accuchecks - Monitor electrolytes - Assess mental status - Monitor blood/rine for ketones - EKG - Assess V/S - If patient is in a coma : airway support, mechanical ventilation 3. Treat underlying cause Medications - IV fluids - Regular insulin (Humilin R, Novolin R, ReliOn R) - Electrolyte replacement K, Mg, Na be Nutrition The recommendation for carbohydrate intake is a minimum of 130 g/day. Low-carbohydrate diets are not recommended for diabetes management.

Diabetic Ketoacidosis (DKA)/ TYPE 1

Pathophysiology - caused by a deficiency of insulin and is characterized by hyperglycemic ketosis acidosis and dehydration. - Low pH; High K⁺ (hyperkalemia): as acidosis gets worse glucose level increase and hyperkalemia develops - Produces glucose in urine - Produces ketones in urine and blood: Fatty acids develop too rapidly and are converted to ketones→ metabolic acidosis - Insufficient or no insulin in body →body breaks down fat for energy: liver responds to lack of fuel (glucose) in cells and converts glycogen to glucose for release in blood stream - It is most likely to occur in people with type 1 diabetes. - Occurs if the patient has a severe illness or stress. the pancreas can not meet the extra demand for insulin. - Persons with type 1 diabetes have absolute insulin deficiency. Immune-mediated or idiopathic conditions have led to pancreatic beta-cell defect or destruction, and total lack of endogenous insulin. - Patients with untreated diabetic ketoacidosis are typically hyperkalemic. Hyperkalemia occurs secondary to an exchange of potassium (K+) from cells for hydrogen (H+) from the serum. This compensatory shift occurs in an effort to make serum pH normal. With the shift, less H+ is available to potentially combine with H20 and CO2 and contribute to an acid state (H2CO3, carbonic acid). - In DKA, the arterial pH is lower than 7.35, plasma bicarbonate is lower than 15 mEq/L, the blood glucose level is higher than 250 mg/dL, and ketones are present in the blood and urine. The client would be experiencing polyuria, and Kussmaul's respirations (deep and rapid breathing pattern) would be present. - Leukocytosis occurs with infection, inflammation, tissue necrosis, and leukemic neoplasia. Leukocytosis may also occur with trauma or stress, and is commonly seen with ketoacidosis. Infection is a common cause of ketoacidosis. Risk factors: - Illness, infection, an extremely stressful medical condition - Steroid medications - Poor self management (missed or inadequate doses of insulin, or spoiled insulin - Undiagnosed type 1 DM - mismatch between food (too much) and insulin (too little or none) - Blood glucose level also increases in response to physical or emotional stress. Glucagon release from the pancreas occurs in response to epinephrine release from the adrenal medulla. Glucagon promotes glycogenolysis (breakdown of glycogen to glucose). Clinical Manifestations/Signs and symptoms - Poor skin turgor, orthostatic hypotension - Tachycardia, pt will have kussmal respirations) - Rapid deep breathing) - Sweet fruity breath - Dry mucous membrane, lethargy - dehydration - Wt loss - muscle wasting - Polyuria, polydipsia, and polyphagia - Vision changes - Abd cramps, N&V - Coma Diagnostic test - History and physical examination - Blood studies, including Immediate blood glucose ( 200-800), complete blood count, pH, ketones( >3.0), electrolytes (elevated K⁺), blood urea nitrogen - Arterial or venous blood gases (showing metabolic acidosis) - Urinalysis (positive for ketones and glucose), including specific gravity, glucose, acetone - Elevated serum osmolality - Lab results suggest diabetic ketoacidosis (DKA), which is more common in persons with type 1 diabetes. With type 1 diabetes, a normal blood glucose cannot be maintained without use of exogenous insulin, and risk for ketoacidosis is high. Persons with type 1 diabetes who present with an elevated serum glucose (hyperglycemia), urine ketones, deep rapid breathing, and low arterial pH and HCO3 are diagnosed with DKA. DKA is also characterized by a high serum osmolality, secondary to the high glucose load. Nursing Care, Treatment: - Monitor vital signs, level of consciousness, cardia rhythm, O2 sat, urine - Assess breath sounds for fluid over load. - In diabetic ketoacidosis, the lungs try to compensate for the acidosis by blowing off volatile acids and carbon dioxide. This leads to a pattern of Kussmaul respirations, which are deep and not labored - Monitor serum glucose and serum potassium - Even if the patient has normal potassium levels, there can be significant hypokalemia when insulin is administered as it pushes the serum potassium intracellularly. This can lead to life-threatening hypokalemia. - Administer potassium to correct hypokalemia - administer sodium bicarbonate if sever acidosis. 1. Control of glucose levels : Insulin therapy (drip) during acute phase, Q1hr accuchecks, Change to D5W as blood sugar nears 250 md/dL to prevent hypoglycemia, Correction of hyperglycemia can be rapid, and hypoglycemia can occur quickly. As treatment for diabetic ketoacidosis (DKA) continues, to prevent hypoglycemia and starvation ketosis, dextrose is added to IV fluids, usually when blood glucose reaches 250 mg/dL. Restoration of electrolytes and acid base: monitor K+ for hypokalemia 2. Rehydration: non dextrose IV fluids →0.9% NaCl: if patient is in a coma: Support airway, mechanical ventilation 3.Treat underlying cause - a bolus dose of regular insulin IV. This is to be followed by a regular insulin infusion. A hyperglycemic continuous insulin infusion protocol with hourly bedside blood sugars will be followed. Following this protocol, insulin infusion rate will be changed hourly, based on bedside blood glucose results. Medications: - Insulin administration is therapy directed toward correcting hyperglycemia - Regular insulin is the only insulin that can be administered intravenously. Regular insulin is a short-acting insulin that should quickly lower blood glucose. Regular insulin administered IV has an onset/peak action of 10-30 minutes, and a duration of 30-60 minutes. - A sodium chloride solution (generally 0.9% sodium chloride, normal saline) is the fluid choice when preparing an insulin infusion. - The standard insulin infusion is prepared to achieve a concentration of 1 unit/ 1 mL. - Insulin is a high alert drug. If insulin is administered at an incorrect infusion rate, consequences can be life-threatening. An infusion device will help insure correct rate of administration. - And hypokalemia and serum potassium - Vasotec (enalapril maleate) - lower blood pressure monitor: Vasotec (enalapril maleate) decreases peripheral vascular resistance, which in turn causes a decrease in blood pressure. This drop in blood pressure is expected but can be greater than anticipated, especially when a patient is hypovolemic. Careful monitoring of blood pressure is indicated. A person taking an ACE inhibitor should be observed for signs of angioedema, an adverse reaction. Angioedema (swelling of face, tongue, larynx, and extremities) has been reported with use of ACE inhibitors. Subsequent airway obstruction can be life threatening.

Adrenals

Pheochromocytoma

Betablockers

Propranolol (Inderal) Atenolol (Tenormin)

Glycosylated hemoglobin (A1C)

The glycosylated hemoglobin is the amount of glucose bound to hemoglobin, and it remains there for the life of the cell (120 days). This test indicates glycemic control over 2 to 3 months. - blood sample can be taken without fasting - Normal is 4%-6% -Lowering hemoglobin A1Cc (to average of 7%) reduces microvascular and neuropathic complications. Tighter glycemic control (A1C < 6%) may further reduce complications but increases the risk of hypoglycemia.

CRANIAL SURGERY

The indication for surgery can vary greatly. Types of surgery and indications for them can be found in Tables 57 - 14 and 57 - 15 on page 1449

Short acting insulin

Regular (Humilin R,) Novolin R, ReliOn R) Onset: 1/2- 1hour Peak: 2-3 hours Duration: 3-6 hours Regular: 30-45 mins Time of adverse reaction: - Midmorning, mid-afternoon: weakness, fatigue Characteristics: - Clear solution; given 20-30 min before meal; can be alone or with other insulins

Increased Intracranial Pressure: Risk factors

Seizures Fever Risk for ineffective cerebral tissue perfusion Risk for disuse syndrome Death

Checking pupils

The lights in the room should be dimmed to assess pupil response to light. After the lights are dimmed, a bright light should be directed into the eye. The normal response is brisk pupil constriction in response to light. Each eye should be checked separately. Pupils should be equal in size and react to light at the same, quick rate. Mickey's pupils are equal in size and react equally to light with constriction.

Diabetes Mellitus Diagnostic Test

Serum Glucose Fasting Serum Glucose - NPO 8-12 hrs B4 - Normal FG= 70-100 Glucose Tolerance Test - Sample drawn 2 hrs after a 75-gram glucose drink - Less than 140mg/dL=normal glucose tolerance AIC - Used to determine how well diabetes is being controlled - provides an avg of blood sugar control over a 6 to 12 wk pd - normal range bet 4% and 5.6% - 6.5% or higher = diabetes Urine - Glucose - ketones

Broca's motor speech

Slurred speech occurs secondary to Broca's motor speech area of the brain being affected. It can be a sign of increasing intracranial pressure (ICP).

Coma

Some clients who have awakened from an unconscious state have remembered hearing specific voices and conversations. Family and staff should assume that the client's sense of hearing is intact and act accordingly. Additionally, positive outcomes are associated with coma stimulation-that is, speaking to and touching the client.

Spinal Shock

Spinal shock involves loss of all motor activity (both voluntary and reflex) below the level of spinal injury. It is reflected in a flaccid paralysis. In addition, loss of reflex sympathetic vasomotor tone causes vasodilation and peripheral pooling that results in a neurogenic shock, with hypotension, bradycardia, and warm dry skin. Resolution of spinal shock is highly variable, gradually occurring over a period of days to weeks (often within 24-72 hours, but may be up to six weeks or longer). Clinical Manifestations - Gooseflesh and shivering are sympathetic nervous system responses that are absent when spinal shock is present. Their return would indicate that spinal shock was resolving. - The bulbocavernosus reflex (anal sphincter contraction in response to tugging at the Foley catheter or squeezing of the glans penis) is absent when spinal shock is present. Its return would indicate resolution of spinal shock. With resolution of spinal shock, other reflexes below the level of injury would return as well. - There is also a neurogenic shock, which results in loss of sympathetic vasomotor tone. This results in unopposed parasympathetic control of heart rate, and subsequent bradycardia. Bradycardia associated with spinal shock spontaneously resolves as spinal shock ends. Pulse rate would increase to normal range. Nursing Care - Maintaining temperature within a safe range is a major concern in the immediate post-injury period while spinal shock is present. With spinal shock, absence of sympathetic activity prevents coping mechanisms designed to conserve/create heat (vasoconstriction/shivering) or dissipate heat (perspiration) as necessary. During this period, body temperature is regulated by environmental temperature (poikilothermy). A rise in temperature secondary to infection requires prompt attention to avoid extreme hyperthermia. A cool environment could quickly cause hypothermia, with symptomatic bradyarrhythmias. - Preventing pressure ulcers is an immediate and ongoing concern for the patient with a spinal cord injury. Frequent turning, use of pressure reduction devices, and skin assessment are important. Pressure on bony prominences (heels, elbows, sacrum, back of head) should be avoided. Use of a rotation bed is beneficial in facilitating turning and reducing pressure. Traction weights should not be removed, even with turning. Patient inability to feel pressure or pain makes frequent skin inspection imperative. As recovery progresses, transfer to a chair should be done a few times a day, with shifting of position at least every one-half hour. - Preventing deep vein thrombosis (DVT) is an important immediate and ongoing concern after spinal cord injury. Venous pooling and sluggish blood flow associated with spinal shock, and immobility, increase risk for clot formation. DVT frequently causes pulmonary embolus (PE). Preventative measures include graduated compression stockings and/or pneumatic compression devices and use of a rotation bed to promote blood flow and venous return. Anticoagulation with heparin is commonly instituted as a prophylactic measure. - Preventing infection is a major concern. risk for infection because of the hospital environment and invasive procedures (Foley catheter, cervical tongs, IV catheters etc.) increased risk for nosocomial pneumonia because of assisted ventilation. Prognosis - Because of spinal shock, immediately after injury, patients with spinal cord injury frequently (but not always) are areflexic and have total loss of motor function below the level of injury, and sometimes above the level of injury. As spinal shock resolves, the long-term effects of injury become more evident. In patients with an intact spinal cord, function may return, although this happens in highly variable degrees.

Stupor

Stupor is characterized by confusion in a patient who is responsive only to repeated stimulation and who otherwise remains in a deep sleep.

Autonomic dysreflexia

The most frequent cause of autonomic dysreflexia is a distended bladder. Straight catheterization should be done every 4 to 6 hours (catheterization every 12 hours is too infrequent), and Foley catheters should be checked frequently to prevent kinks in the tubing. Constipation and fecal impaction are other causes, so maintaining bowel regularity is important. Other causes include stimulation of the skin from tactile, thermal, or painful stimuli. The nurse administers care to minimize risk in these areas. Autonomic dysreflexia (hyperreflexia), a complication common in patients with spinal cord injury (T6 and above, more common with cervical injuries), only after spinal shock has resolved. Autonomic dysreflexia is characterized by sudden headache, severe hypertension that can lead to stroke, sweating and flushing above the level of injury, and cool pale skin with gooseflesh (piloerection) below the level of injury. Nursing Care - head elevation should be implemented immediately when autonomic dysreflexia occurs. This measure helps reduce blood pressure by encouraging pooling of blood in the legs. If worn by the patient, graduated compression stockings should be removed to allow venous pooling. - The most common causes of autonomic dysreflexia are bladder distention and fecal impaction. It would be appropriate to check the patency of foley catheter. Meds -Nitropress (nitroprusside) is an antihypertensive drug that has a direct action on blood vessels, causing vasodilation. The drug is administered reconstituted and then diluted in dextrose 5% in water for titrated infusion. The infusion should be protected from light. Onset of drug action is rapid (1-2 minutes) and duration of action is short (1-10 minutes).

Functional Independence Measure (FIM)

The American Spinal Injury Association (ASIA) Impairment Scale is used to classify a spinal cord injury as incomplete or complete, based on motor and sensory function present. Assessment using this scale is done immediately after injury on admission and continued throughout recovery. Ongoing use of this scale is important, since patient status can change. Use of this tool allows for standardized measurement and understanding across caregivers.

The Brown-Sequard (lateral) syndrome

The Brown-Sequard (lateral) syndrome is characterized by ipsilateral motor loss in the upper and lower extremities and contralateral loss of pain and temperature sensation in the upper and lower extremities. This syndrome is a result of damage to one side of the spinal cord.

MRI scanner

The MRI scanner is a hollow tube that gives some clients a feeling of claustrophobia. Metal objects must be removed before the procedure so that they are not drawn into the magnetic field. The client may eat and may take all prescribed medications before the procedure. - If a contrast medium is used, the client may wish to eat lightly if he or she has a tendency to become nauseated easily. The client lies supine on a padded table that moves into the imager. The client must lie still during the procedure. The imager makes tapping noises during the scanning. The client is alone in the imager, but the nurse can reassure the client that the technologist will be in voice communication with the client at all times during the procedure.

cranial nerve VIII

The cochlear division of cranial nerve VIII is responsible for hearing. Clients with hearing difficulty may benefit from the use of a hearing aid. The vestibular portion of this nerve controls equilibrium; difficulty with balance caused by dysfunction of this division could be addressed with use of a walker.

Glasgow Coma Scale

The three dimensions of the Glasgow Coma Scale are eye opening, best verbal response, and best motor response. The Glasgow Coma Scale (GCS) is a quick, practical, and standardized system for assessing the degree of impaired consciousness. The three areas assessed in the GCS correspond to the definition of coma as the inability of a patient to speak, obey commands, or open the eyes when a verbal or painful stimulus is applied. Specific assessments evaluate the patient's response to varying degrees of stimuli. Three indicators of response are evaluated: (1) opening of the eyes, (2) the best verbal response, and (3) the best motor response (see Table 57-5). Scoring with the Glasgow Coma Scale (GCS) is on a scale of 3 to 15. A Glasgow Coma Scale (GCS) score of 15 is normal and suggests that the brain is fully functioning. It indicates that a person's eyes open spontaneously, he is alert and oriented, and is able to physically respond appropriately to verbal commands. The highest GCS score is 15 for a fully alert person, and the lowest possible score is 3. A GCS score of ≤8 is generally indicative of coma. The Glasgow Coma Scale (GCS) should be used in conjunction with other neurological examinations. The Glasgow Coma Scale (GCS) is not sensitive for evaluation of altered sensorium or focal or lateral neurologic deficits. Many patients with a high Glasgow Coma Scale (GCS) score have serious brain damage requiring intervention.

Thyrotoxic crisis (thyroid storm)

Thyrotoxic crisis (thyroid storm), a sudden, severe, increase in signs and symptoms associated with thyrotoxicosis, may occur in some patients with thyrotoxicosis. Thyrotoxic crisis generally occurs in patients who are not adequately treated or who do not comply with therapy. Thyrotoxic crisis can also be triggered by stress or onset of infection. Severe dehydration can occur with thyrotoxic crisis, secondary to severe fluid deficit from losses associated with diaphoresis, diarrhea, and increased metabolic demands. Dehydration can present with fever, nausea and vomiting, and confusion. Extreme tachycardia and other cardiac problems can occur as metabolic rate increases dramatically. With thyrotoxic crisis, delirium and seizures may also occur. Hyperthermia that occurs may be fatal. Atrial irritability can occur in hyperthyroidism, due to increased workload of the heart and increased sympathetic stimulation. Atrial fibrillation and paroxysmal supraventricular tachycardia are the most common dysrhythmias associated with hyperthyroidism. Atrial fibrillation is more common in older patients. Tachycardia associated with hyperthyroidism is an increased workload on the heart and can result in heart failure. This complication is more common in older patients with preexisting heart disease. With thyrotoxic crisis, cardiac failure can occur and result in death.

Arterial line

To ensure accurate pressure readings from an arterial line, the transducer should always be level with the patient's atrium (fourth intercostal space at the midaxillary line). This anatomically consistent site is called the phlebostatic axis. The arterial line transducer may drift and readings can change in response to withdrawal of blood, room temperature changes, and changes in patient position. To insure accuracy of readings, recalibration should be done at least every 4-12 hours, and after withdrawing blood, transporting the patient, or changing the patient's position, and when readings change significantly. Protocols vary.

BRAIN TUMORS

Tumors of the brain can arise anywhere in brain tissue (or in the spinal column). They represent the origin (primary) of abnormal tissue growth or are the manifestation of metastasis (secondary) from another part of the body. Brain tumors are classified by their originating cell types. The most common type is astrocytes (gliomas); accounting for 65% of primary tumors. See types of brain tumors in Table 57 - 12 page 1446. Metastatic brain tumors from a malignant neoplasm elsewhere in the body are the most common type of brain tumors. All brain tumors eventually cause death from increasing tumor volume that leads to increased ICP, and all tumors should be removed. Seizures are common in patients with gliomas and brain metastases. Brain tumors rarely metastasize outside the CNS because they are contained by structural (meninges) and physiologic (blood-brain) barriers. Clinical Manifestations Depend on location and size of tumor See table 57 - 13 pager 1447 Headache, seizures; N&V; cognitive dysfunction; memory problems, mood or personality changes; muscle weakness; sensory losses; aphasia; visual - spatial dysfunction Diagnostics History Extensive physical and neurologic exam X -ray MRI PET SPECT scan Computer - aided sterotactic biopsy Monitoring Same as ICP Treatment and Nursing Care Goals are to: identify type and location of tumor, removing or decreasing tumor mass and preventing or managing ICP. Surgical therapy Ventricular shunts Radiation therapy Stereotactic radiosurgery Chemotherapy Anticonvulsants

Propylthiouracil PTU) Methimazole (Tapazole)

inhibits production of thyroid hormone

Tegretol dilantin

antiseizure

Lioresal

antispasmodic

Long acting insulin

glargine (Lantus) detemir (Levemir) Onset: 1-3 hours Peak: no pronounced peak Duration: 24+ hours Characteristics: - Maintains blood glucose levels regardless of meals; cannot be mixed with other insulins; given at bedtime

lumbar puncture:

lumbar puncture: - A client undergoing lumbar puncture is positioned lying on the side, with the legs pulled up to the abdomen and the head bent down onto the chest. This position helps open the spaces between the vertebrae and allows for easier needle insertion by the health care provider. The nurse remains with the client during the procedure to help the client maintain this position. - After the lumbar puncture the client remains flat in bed for at least 2 hours, depending on the health care provider's prescriptions. A liberal fluid intake is encouraged to replace the cerebrospinal fluid removed during the procedure, unless contraindicated by the client's condition. The nurse checks the puncture site for redness and drainage and assesses the client's ability to void and move the extremities. - After the procedure, the client assumes a flat position. If the client is able, a prone position with a pillow under the abdomen is the best position. This position helps reduce cerebrospinal fluid leakage and decreases the likelihood of post-lumbar puncture headache.