Monday, December 18, 2006

more review

  • More Review
  • Endocarditis--strep, staph. Vegetative lesions. Flu like symptoms. Fever high as 103F Roth spots. Petechiae. Splinter hemorrhages. Numbness tingling. Oslers nodes are small and painful on fingers toes. Janeway lesions not tender. Heart murmur, enlargement, failure. Hemiparesis or change in LOC. PE. Splenic Embolization pain in LUQ radiates to left shoulder. Rigid Abdomen. Blood cultures + for causative organsism. Elevated WBC and ESR. Anemia. IV antibiot for 4-6 weeks--penicillin, amphotericin B. Arthralgia. Amox before dental work, childbirth.
  • AAA 1 ½ times the stretch. 6:1 risk w/ first degree relative. Check yearly. Silent but may have prominent pulse in the abdomen when supine. Dx usually made when looking for something else. Rupture is Coming if---low back pain, abdominal pain, flank pain. Ruptured--intense low back pain. Lower abd pain, collapse, shock, mottling of lower extremities, decreased Hgb. Sx= resection of aneurysm. Low mortality stats if repaired before rupture, 5%. 50-80% mortality stat if repaired after rupture. Pre Op--compare peripheral pulses. Skin for color and temp, Mark pulses. During Sx- emboli risks from clamped aorta. Risks= MI, CHF, CVA, Kidney damage. Post Op= OUTPUT measured hourly. Assess for bleeding b/c heparin used during Sx. Check for Distal Arterial Perfusion= check for color pain level, motion sensation, temp. Check for distal arterial occlusion==darkened patches in soles/toes of feet. S/s of hemorrhage…drop in CV pressure. Drop in arterial pressure. Decreased urine output. Assess for spinal cord ischemia--assess motor and sensory function. Assess for pain from long incision. Assess for ischemic colitis--bloody diarrhea before bowel function is expected to return--normal return is 4-5 days post op. Assess mobility--OOB 1-2 days post op. discharge plan in 5-7 days. Lifting only to 5lbs. No driving. Showers ok. Assess family members after age 50.
  • Hepatitis--pt hospitalized for dehydration or a prolonged PT. Rest, hydration. NO ETOH. Low fat high CHO diet. Corticosteroids. Need Vitamins B--liver can not absorb. K--for coags--C for healing. Education---Gamma globulin indirect contact for Hep A. Hep A vaccine for travelers. Hep B vaccine for health care workers, newborns, and adolescents. Prevention for Hep C. No vaccine for E.
  • Cirrhosis--Early signs=vague, flu like. General weakness. Fatigue. Anorexia. Indigestion. Consitpation/diarrhea. Late signs= Jaundice, dry skin, pruitus. Edema. Ascites. Anemia. Bleeding. Infections (lost Kupfer cells). Menstrual irregular. Impotence. Gynecomastia. Renal failure. Dark amber urine. Clay colored stools.
    The Fs of distention= fluid, flatulence, fat, feces, fibroid tumors.
  • Rupture of Esophageal varicies. Med emergency. IV fluids, lytes, volume expanders. Sengstaken-Blakemore tube to stop the hemorrhage. Meds= Vasopressin.--constricts the arterial bed. Somatistatin--decreases bleeding w/out vasocontriction. Propranolol--beta blocker to decrease portal pressure.
  • Increased intracranial pressure--Bp up. Pulse down. Resps down.= cushings triad.
  • Shock--BP down. Pulse up. Resps up.
  • Tx for Hyperkalemia in ARF--Insulin +glucose IV. Sodium bicarb. Calcium gluconate IV. Dialysis. Kayexalate.
  • Diet for ARF= decrease protein. Increase calories. Low K+ and low phosphorus (bananas, citrus, coffee). Low Na+. Increase iron.
  • Colon Cancer locations of lesions= R. sided lesions--dull abd pain. Black tarry stools. L. sided lesions---bright red blood in the stool. Rectal lesions--tenesmus. Rectal pain. Constipation/diarrhea. Bloody stool.
  • Hyperflexion of the neck--chin to chest
  • Hyperextension of the neck--think falling down stairs chin first. Head back

Sunday, December 17, 2006

Some more review for final

Lung Cancer
Late clinical manifestations
= non specific= weight loss, anorexia, fatigue, n/v/ and hoarseness. Persistent pneumonitis. Hoarseness. Hemoptysis. Unilateral paralysis of the diaphragm. Dysphagia. Palpable lymph nodes in the neck. Medistinal involment will show cardiac signs and symptoms. Clinically silent, and the symptoms appear late. Persistent productive cough. Chest pain, dyspnea, wheezing. Unexplained fever.
CT scan is the single most effective non invasive technique for diagnosis.
Squamous cell
Large cell undifferentiated.
Oat cell.

2 functions of the pancreas= endocrine--insulin and glucagon production and exocrine--digestive. Secretes 500-1000cc digestive juices/day.
Pancreatic Enzymes= Amylase breaks down starches. Chymotripinsinogent, elastase, trypsinogen break down proteins. Lipase, phospolipase A & B break down fats.
Pancreatitis is acute or chronic inflammation of the pancreas. Auto digestion (it is eating itself). The enzymes are activated BEFORE being secreted into the pancreatic duct. The cause may be----
Gall bladder disease 80%
ETOH abuse
Cysts, tumors, viral infection, trauma, surgery, mumps, steroids, thiazide, diuretics, oral contraceptives.
extreme abdominal pain umbilical pain that radiates to the back. Abd distention and decreased bowel sounds. N/v. chronic steatorrhea. Low grade fever. Tachycardia. Dyspnea. Hypotension, restless confused.
Sign of hemorrhage
Cullen’s sign= bluish color around the umbilicus.
Turners sign= bluish color on the flank.
Lab Tests
Just remember that everything is going to be up EXCEPT the serum calcium.
What is up
***Amylase is going to be up
WBC--tissue damage inflamation
SGOT, SGPT, LDH--tissue destruction
Alkaline Phospatase
Down is the Ca+….hypocalcemia leads to Tetany so watch for signs.
Reduce the anxiety. Anxiety stimulates the vagus nerve which will increase the secretions.
IV therapy w/ I&O and daily weights.
Anticholinergics--reduction of enzymes. Decrease spasms of Oddi.
Calcium gluconate IV
Histamine blockers
NGT--removes gastrin
Mouth Care
Blood glucose
Diet is progressed from NPO to low fat bland diet high in CHO after inflammation is over.
NO Coffee. NO ETOH
Avoid heavy spicy meals.
Give pancreatic enzymes with meals.

The start of Final Review.

  • Tricuspid Atresia
    This is a failure of the tricuspid valve development. There is no communication between the RA and the RV. There is no opening where the tricuspid should be. The blood is going to flow…into the Vena Cava then through an ASD or PDA to the left side of the heart. Then goes through a VSD to the RV to the lungs. You will see cyanosis. Palliative Sx is the same for TETs. Corrective Sx= Convert the RA into an outlet for the pulmonary artery called Fontan procedure. Survival stats= 80-90% w/ complications.
  • Tetralogy of Fallot TOF. Remember the aorta is riding the septum. Cyanotic.
    4 defects=
    Ventricular Septal Defect. Pulmonic Stenosis. Overriding aorta. Right ventricular hypertrophy.

Unoxygenated blood enters the aorta.
The shunting in TOF varies.
Right to Left shunt….unoxygenated blood enters the aorta when the pulmonary vascular resistance is higher than the vascular resistance.
Left to right shunt….if systemic resistance is higher than the pulmonary vascular resistance.
S/S= Blue, cyanotic, squatting, clubbing, syncope.
Blue Spells, hyper cyanotic spells, TET spells. The O2 needs are not med by the blood supply usually during crying, feeding or defecation. The cause is an infundibular spasm which decreases the pulm blood flow and increases R to L shunt. The risks from these spells are brain damage, death, neuro complications, polycythemia and increased blood viscosity which increases the risk for CVA. To treat these spells the infant is placed in the knee chest position. Stay calm. 100% O2 via mask. Morphine SQ or IV to reduce the spasm. IV fluids and expanders to decrease the viscosity. More morphine.
Sx= Palliative= Blalock Taussig shunt. But not preferred treatment.
Complete repair= First year of life. Closes the VSD…resection of the infundibular stenosis with pericardial patch to enlarge the right ventricular outflow tract. This is open heart and post op complications include dysrhythmia and CHF. Survival stats are at 95%.

  • CHF in children.
    The heart is not meeting the demand of the body. Seen a lot when there is increased blood flow to the lungs or problems w/ the left side of the heart .
    The subtle signs= poor feeding, irritable, tired when feeding and lethargy.
    2 things happen
    I. Impaired myocardial function
    …Seeing tachycardia, weak pulses, decreased BP and a gallop rhytm. Fatigue restless, anorexia, pale cool mottled extremites. Diaphoresisi. Cardiomegaly. Decreased urinary output.
    II. Systemic Venous congestions…seeing weight gain. Hepatomegaly. Peripheral edema, per orbital edema. Ascites. Neck vein distention. Rales, resp distress…retractions, nasal flaring.
    Therapeutic Management Goals
  • Improve cardiac function by increasing the contractility and decreasing the after load. Decrease the preload…remove accumulated fluid and sodium retention.
  • Decrease the cardiac demands…control the work of the pt.prevent cold stress. Treat infections. Semi fowlers position. Sedation. Rest.
  • Decrease O2 consumption to improve tissue oxygenation.
    Digitalis is a Cardiac glycoside--improves contractility. Increases the force of contraction--positive inotropic. Decreases the heart rate--negative chronotropic. Slows the conduction of impulses through the AV node--negative dromotropic. Enhances duresis indirectly by increases renal perfusion…..
    Concerning Digoxin and Pediatrics.
    The dose is calculated in micrograms. 1000ug=1 mg. The digitalizing dose is given to bring the serum dig into a therapeutic range. The maintenance dose is 1/8 of the digitalizing dose.
    The therapeutic range is from 0.8-2ug/L
    Check the apical pulse for one full min is a must. For infants hold the med for pulse below 90-110 bpm. For older children do not give if apical is less than 70 bpm.
    Signs of Dig Toxicity
    = bradycardia. Anorexia. Nausea. Vomit often unrelated to feedings. No interest in eating. Decreased oral intake.
    Other meds and treatments.
    ACE inhibitors Vasotec and Capoten to reduce the after load on the heart which makes it easier to pump.
    For severe CHF other inotropic meds given IV in the ICU = dopamine, dobutamine, Amrinone to improve contractility.
    Diuretics= to remove fluid and sodium…but CAUTION a fall in the serum K+ can potentiate the effects of digoxin and there is then an inceased risk of toxicity.

    Cancer of the Larynx
    At risk= smoking and ETOH. Pollution. Nutritional deficiency. Family predisposition. Vocal straining.
    Early signs= hoarseness. lump in neck, pain in throat when drinking hot fluids or juice.
    Late Signs= Dysphagia, Dyspnea, Foul breath. Chronic cough. Hemoptysis. Sore throat or sores in throat.
    Signs of Metastasis= Enlarged cervical lymph nodes. Weight loss. General debility. Otalgia.
    Most are squamous cell.
    Laryngectomy 3
    Partial--½ or more of the larynx removed. High cure rate stats. It is a vertical midline incision. Trached first few days. VOICE HOARSE. No dysphagia.
    Supraglottic--removes hyoid bone. Epiglottis and false cords. It is radical neck dissection. Tracheotomy. NG tube for 2 weeks. Voice is preserved. Post op dysphagia because some muscles removed.
    Total--removes hyoid bone. Epiglottis, cricoid cartilage and 2-3 rings of the trachea. Permanent tracheal stoma. NO VOICE. It is radical neck dissection.
    Complications= resp distress. Hemorrhage. Infection.
    Post op--be alert for serious complication of rupture of carotid artery. If it happens apply direct pressure. Call for help. And provide emotional support until it can be ligated.
  • Spinal Cord injuries
    4 types of injury. Hyperflexion&Hyperextension (think car wreck). Axial Loading (think fall from ladder). Excessive Rotation.
    Complete (total cord transection) or Incomplete (partial cord transection).
    Injuries affect motor & sensory fx at and below the level of the injury.
    Spinal shock= areflexia (loss of reflex fx). Decrease in BP & bradycardia. Below the injury paralysis and no sensation and no diaphoresis. Check for distended bladder. Lasts days or months.
    Paraplegia= paralysis of lower body. Injury level in the thoracic spine or lower.
    Tetraplegia= Quad= injury in the cervical spine=arms, legs, trunk and pelvic paralysis.
    Maintain patent airway. Cervical injury edema.
    High does Corticosteroids within 8 hours.
    Mannitol to decrease edema around the spinal cord
    Baclofen=muslce relaxer to reduce plasticity
    Dextran= prevents BP from dropping and improves the capillary blood flow.
    Traction= tongs such as the Gardner Wells or Crutchfield. Halo.
    Weights hang free.
    Do not remove.
    Clean tongs with betadine
    Assess for infection.
    Surgical immobilization….via anterior/posterior decompression and fusion w/ bone grafts. Decompression w/ laminectomy will remove bony fragments that cause compression…remove the foreign body causing compression. Fusion-anterior/posterior using Harrington rods.
    SOMI=sterno occipital mandibular immobilizer
    CTLSO= cervical thoracic lumbar sacral orthotic.
    Complications may include= DVT. Orthostatic hypotension. Autonomic Dysreflexia.
    Nursing Interventions
  • Promote Adequate Breathing and airway clearance--I am not going into this as we should know this by now! But I will say that if suctioning is needed--be careful because this can stimulate the vagus nerve which can lead to bradycardia and cardiac arrest.
  • Improving mobility--maitain proper body alignment at all times. Feet are prone to foot drop. Use splints removing and reapplied q 2 hours. Trochanter rolls to prevent external rotation of the hip. If the pt is not on a rotating bed do not turn unless the spine is stable and the MD must order. PROM to avoid contractures.
  • Promote adaptation to sensory and perceptual alterations.
  • Maintain skin integrity--Prevent pressure ulcers. They can happen very quickly.
  • Maintain Urinary Elimination--intermittent cath. Teach family. Neurgenic bladder. Prevent UTI--increase fluid, high acid fluids, no ETOH, avoid alkaline fluids.
  • Improve Bowel function--paralytic ileus from Neutrogena paralysis of the bowel. NG tube to relieve distention and prevent aspiration. Bowel activity usually returns in a week. After BS are heard pt given high calorie, high protein, high fiber diet.
    Remember Again that the Emergency Autonomic Dysreflexia
    1. Immediately the head of bed up and BP q 5 min,
    2. Rapid Assess to find the cause and alleviate
    3.Urinary Cath but never drain more than 700cc--can lead to Hypovolemic shock.
    4. Check for fecal mass. Topical anesthetic for 10-15 min…then remove.
    5. Check skin for pressure
    6. Remove all stimulus.
    7. Report to MD immediately if BP does not drop.
    Meds for Autonomic Dysreflexia.
    Arfonad IV / Apresoline IV--ganglionic blocker to lower BP fast. relaxes arteriolar smooth muscle.
    Low spinal anesthetic at L4 in nothing works.
  • Burns- Some nursing Care. NG tube to decompress. Foley Cath for I&O--HOURLY! Putting a lot of fluids in so we need to see what is coming out. Urine glucose levels. Pain relief. Continuous assessment of extremity pulses and ventilation. Emotional support. Check for GI bleed--stool for OB, coffee ground emesis.
    Nursing care for pt w/ grafts
    Occlusive dressing. Check for infection and foul smell. If the graft is dislodged cover w/ sterile saline dressing. Keep the pressure off and elevate. The donor site is more painful than the burn site!
    Pain is severe and may need PCA pump w. morphine.
    For Rehab… the pt set realistic goals and include the pt in decision making…give them some control.
    S/S of smoke inhalation damage from burns
    Focus on signs of resp and cardiac involvement. Burned nasal hair. Cyanotic lips. Hard time talking, facial burns, Dyspnea, Tachypnea, Cough, Stridor, Hoarseness, Sooty sputum. Rales, Wheezes, Rhonchi.

Monday, December 11, 2006


The relationship is between duration + temp.
Superficial Partial Thickness Burn= First degree burn=Epidermis and maybe some dermis. soothed by cooling. reddened, blanches with pressure. no scar. peeling. recovery in 1 week. ie: sun burn, or low intensity flash.
Deep Partial Thickness=Second Degree burn=epidermis and upper dermis, portion of deeper dermis. Pain! Blistered, mottled red base, weeping surface, edema. Infection may convert this to full thickness. ie: scalds, flash flame.
Full-Thickness= Third Degree burn= epidermis, all of dermis and some SQ and may involve muscle or bone. Symptoms= NO PAIN! shock, hematuria. Wound may look dry, pale white, leathery or charred. Fat may be exposed. Edema. Need grafting.
Rescuer should stay safe.
Airway-C-spine immobilization.
Breathing- 100% O2
Neuro-may be very alert w/ deficits later. So gather information now.
Deal with the wounds last.
Then find out how they were burned and Med history
MED History includes
P=past illness
L=last meal
E=events that preceded injury
Stop the burning process= flush chemical burns, remove contacts, cool water to stop the burning.
Airway management= humidified O2 @100%. Smoke inhalation is the leading cause of death in burn pt. The hemoglobin loves CO better than O2. it creates carboxyhemoglobin which competes with the O2.
Next to the respiratory system fluid and lytes are next in line.
The body is going to try and conserve fluids and can lead to kidney failure. A decreased BP+decreased cardiac output leads to shock.
LR is infused via a large bore IV.
Most common formula is the Parkland/Baxter formula=4ml pf LR x body weight in kg x % of BSA burned= the fluid replacement. 1/2 of that is given the first 8 hours. Then 1/4 for the next 8 hours. And then again 1/4 of that for the next 8 hours. Of course this depends also on the clinical picture. Assess--heart rate, BP, urine output HOURLY.
This is what is happening during the emergent phase... concerning fluids
General dehydration as plasma leaks through the damaged capillaries. Blood volume is reduced secondary to plasma loss, decrease in BP, and decreased cardiac output. Decreased urinary output secondary to fluid loss, decreased renal blood flow, Na+ and water retention. To much K+ because of massive cellular trauma releases K+ into the extracellular fluid. Na+ deficit because it is trapped in edema fluid and because of the K+ shift. Metabolic Acidosis because of a loss of bicarbonate ions that goes with sodium loss. Hemoconcentration-elevated hematocrit because liquid blood component is lost into the extracellular space.

Monday, December 04, 2006


Neuro Disorders
Myasthenia Gravis
The problem is with neurotransmission, a defect in acetylcholine receptors sites. Fatigue of the voluntary muscles. Dry eye corneal abrasion. Eyes droop. Fatigue of the resp muscles and limb muscles. The pt eventually choke on food because of difficulty swallowing. The tensilon test= pt given short acting anti-cholinesterase (tensilon or edrophonium chloride) this enhances neurotransmission and improves symptoms, this is short term. Atropine is given to reduce the side effects of the tensilon which is bradycardia, sweating, and cramping. If the pt has a positive test, the pt may be ordered drug therapy with anticholinesterase meds. Mestinon, Prostigmin. MUST be given on time. Side effects=abd pain, diarrhea, increased Oropharyngeal secretions. Other treatments=Corticosteroids given. Cytotoxic meds may be given, such as Imuran and cytoxan…why they work is still unknown. IVIG. Plasmapheresis. No cure. Surgical Tx= thymectomy results in clinical improvement. Produces antigen specific immunosuppression. It takes a year to start working because of the life span of the circulating T cells.
Myasthenic CRISIS
Severe generalized weakness and respiratory failure. After stress such as infection, high temp, surgery. Need Ventilatory support. ADLs, chest PT, suctioning.
Cholinergic CRISIS
From overmedicating with Anticholinergics. Can mimic the s/s of myasthenic crisis. It is differentiated by the tensilon test…ie…the pt in myasthenic crisis will improve after the tensilon. Stop all anticholinesterase med! Atropine sulfate to reduce increased, excessive secretions.
Nsg Care= teaching….use of meds on time and to keep a diary. .s/s of crisis. How to save energy, space activity, organize the house.…how to avoid aspiration soft food, neck slightly flexed
…eye care.
Parkinsons disease
Reduced amount of dopamine. Signs and symptoms= rigid, resting tremor, bradykinesia, a loss of postural reflexes. Bradyphrenia. Memory problems. Drooling dysphagia, speech problems, constipation, urinary frequency. Treatment= Eldepryl--protects the neurons and reduces the need for Levodopa till later. Levodopa--provides the missing dopamine. Amantadine--Anticholinergics that is given to reduce the symptoms and increases the release of dopamine from the storage sites. Sometimes pt need a drug holiday to find other drugs that may work when the current treatment not working.
Nsg care= routine for personal care. Safety. AROM, PROM, rigid facial expressions may hide true feelings. Thicken liquids. Eat sitting up…..
Multiple Sclerosis.
Demyelinating disease…nerve fibers of brain and spinal cord. Lesions throughout the white matter…some in the grey matter. There is an inflammatory response that attacks the myelin. Could be an autoimmune problem with a viral trigger…unknown. Exacerbations and remissions. MRI will demonstrate white matter lesions. New drug therapy= Avinex--interferon beta-1a--weekly IM
Betaseron--interferon beta 1b recombinant every other day SQ. Major side effect = suicidal tendency, depression. Older drug therapy= Corticosteroids. Cytoxan may produce temporary remission. Signs and symptoms= blurry vision, double vision, dysphagia, facial weakness, numbness, pain, paralysis, abnormal gait, tremor, vertigo, incontinence, short term memory loss, trouble finding words. Other meds to reduce the symptoms.
Nsg Care= self care balance. Urinary retention--straight cath or texas. Bowel routine. Skin integrity.

Wednesday, November 29, 2006

NCLEX practice question ICP

A nurse is caring for a pt with Increased intracranial pressure. What trend in the following vital signs would indicate the ICP is rising?
1. Increasing temp, increasing pulse, increasing respirations, decreasing blood pressure.
2.Increasing temp, decreasing pulse, decreasing resps, increasing bp
3.decreasing temp, decreasing pulse, increasing resps, decreasing bp
4.decreasing temp, increasing pulse, decreasing resps, increasing bp

ICP positioning

What is the proper way to position the pt to reduce the ICP?
To promote the venous drainage…head neutral..cervical collar, keep the head of the bed up.
Compression of the jugular vein increases the ICP so…avoid rotation and flexion.
Avoid hip flexion to avoid…intrabdominal pressure which raises the intrathoracic pressure which increases the ICP.
Use turning sheets and pt should exhale when turning..
Colace and NO enemas
Space the care…ICP should not rise above 25mmHg and should return to baseline in 5 min.
NO isometric muscle contractions because this will raise the systemic BP and again therefore raise the ICP


Head injury
Closed or open
Grade I= Mild. Not admitted. Short loss of consciousness.
Grade II= loss of consciousness. Lethargy, confusion, hemi paresis, admitted and require surgery.
Grade III= unable to follow even simple commands. Serious damage. Dilated pupils. Without rapid attention may die.
Concussion.--mechanical force and release enzymes. Contusion--brain bruise. Blunt object like a baseball bat. Hematoma.
Epidural or extradural Hematoma=
arterial blood between the dura and the skull. Pt loss of consciousness and regains it. Vomit. hemi paresis. Pupil changes. all leading to rapid worsening. The Tx is to remove the Hematoma by craniotomy.
Subdural Hematoma.= venous bleeding below the dura. ICP.
Complications of head injury= cerebral edema, DI, SIADH, Stress ulcer from use of steroids. Epilepsy. Meningitis. Hyper/hypothermia.
Mannitol and steroids. Antibiotics.

Craniotomy--supratentorial or infratentorial.
Burr holes--used to remove clots.
Nutrition following head injury
May need TPN…stress and steroids increase catabolism.
Airway. LOC. Pupils. Movement. Sensation. Hand grasps. ICP. Resp changes. VS. headache. Glasgow coma scale.
POST OP Craniotomy care
Resp. Deep breath q 2. NO COUGHING! Neuro checks. Suction. Strict I&O. Seizure precaution. CSF leaks. S&S of meningitis.
Supratentorial--head of bed up 30 degrees. On back or unoperative side.
Infratentorial--FLAT on either side.
Assess for bleeding. GI bleeds, assess for emotional response or knowledge deficit.
Brain death--irreversible loss of brain function. EEG will confirm no activity. Cerebral blood flow studies. MD will determine.
Remember Diabetes Insipidus…caused by a decrease in ADH---increased urine output…anticipate to give VASOPRESSINS….give fluids and lytes.
SIADH--restrict fluids….caused by increase ADH. Volume overload and a decreased urine output.

Tuesday, November 28, 2006

Causes of ICP

Causes of ICP
. Abnormal amount of fluid accumulates in the ventricles of the brain.
Blockage--the CSF can not get to the subarachnoid space. Causes: malformations, neoplasms, infections, trauma.
Obstruction in the subarachnoid cistern at the base of the brain or in the space.
No blockage! Fluid paths are open….but not absorbed.
Early signs= increased head circumference. Bulging fontanels. Cranial sutures separated. Signs of ICP.
Late signs= Cracked pot head….;}….which is of course Macewen’s sign! Setting sun sign, arched back (opisthtonus) frontal bossing.
Treatment= correction of cause of obstruction. Ventricular shunting.
VP= ventriculoperitoneal= method of choice.
Older versions= ventriculpleural, ventriculoatrial.
Problems= infection…tubing issues, replacements
Position on unoperated side to prevent the pressure on shunt valve. Keep flat….prevent rapid reduction of fluid….to fast the cerebral cortex can pull away from the dura and produce a subdural Hematoma.
Gradually raise the head of bed as ordered.
Shunt obstruction will need to return to OR.
Infection---IV and Intraventricular antibiotics.

Infection of the pia mater…arachnoid membrane…and CSF fills the subarachnoid space. Because of bacteria, virus, or fungal organism. The organisms can get there by…..nasal pharynx, lumbar puncture, penetrating wounds, fractures, spina bifida.
S & S
Neonate= hypothermia or fever….not eating, poor muscle tone.
Infants= fever, high pitch cry, headache, bulging fontanel.
Children/Adolescents= fever, photophobia, headache, nuchal rigid, +Kernigs, + Brudzinski’s signs.
All= Irritable, Seizures, vomiting.
***CSF examined***
Pressure is measured--the normal is 0-15mmHg. Increased ICP is greater than 15mmHg.
The CSF is sent to the lab…Grain Stain to identify the shape of the organism…Blood cell count--increased WBC…Glucose--decrease in glucose….Protein--increase in protein…within the hour…C and S will take longer….

Antibiotics AFTER sending CSF to the lab…penicillin, cephalosporins, vancomycin alone or with Rifampin. Dexamethasone given 15-20 min before the first dose and q 6 hours for next 4 days.
Isolation for first 24 hours of antibiotics
Control seizures, fever, strict I & O to avoid edema…..
Shhhh….no pillow! Seizure precautions, be careful with the neck…VS, neuro checks, LOC q 1-2 hours. NPO if decreased LOC.
If you are exposed the CDC recommends treatment with Rifampin.
Rifampin side effects: n/v/d…headache, dizzy orange urine, contact lenses will turn orange, Cannot be given to pregnant women. Or Tx w/ Cipro or rocephin.

ICP to start

  • ICP
    Skull volume= brain tissue + blood + CSF.
    There is a limited space inside the skull for expansion and an increase in any of the components will lead to a change in the volume of the other components.
    There will be an increased absorption of the CSF and a decreased cerebral blood volume.
    The ICP will rise leading to decreased cerebral perfusion which will lead to edema. Then the brain tissue will shift through openings in the rigid dura leading to herniation and death.
    Remember that an increased ICP leads to decreased cerebral blood flow…leading to ischemia and cell death.
    The systemic response---vasomotor centers are stimulated which increase the BP
    ***Slow bounding pulse and irregular respirations***
    How the body deals with cerebral edema…..
    The goal is to maintain blood flow and prevent tissue damage. 2 ways the body deals= Auto regulation of blood vessel diameter, and decreasing production of the CSF.
    Seen with pressure on the medulla from brain stem herniation.
  • Pathological Conditions that can cause ICP
    Head injury, CVA, brain tumor, intracranial Sx, meningitis, encephalitis, subarachnoid hemorrhage.
  • Early symptoms of ICP= a change in the LOC= slow speech, delayed responses, irritable, restless and increased effort of resps. Change in pupils, weakness on one side, headache that increases.
  • Late symptoms of ICP= Worsening LOC leading to coma. Sluggish pupil response, decreased HR, decreased RR. Bradycardia to tachycardia. BP and temp will rise. The pulse pressure widens, Cheyne stokes resps, PROJECTILE VOMITING, hemiplegia, decorticate or decerebrate posture, flaccid before death. Loss of brain stem function. Increased systolic pressure.
    LOC, pupil response, VS, motor activity
    VS=pulse decreases, resps decrease, BP increases, Temp increases.
    Diagnostics= CT scan, MRI, PET
    Goal is to relieve the ICP by decreasing edema, decrease volume of CSF, decrease cerebral blood volume while still maintaining adequate perfusion.
    Monitoring the ICP
    Intraventricular catheter= ventriculostomy.into lateral ventricle. Allows for drainage. Meds can be instilled. Risks are infection and ventricle collapse.
    Subarachnoid bolt=or screw…hollow device through the skull and dura mater into the cranial subarachnoid space. No ventricle puncture. Negative aspect = blockage leading to decreased accuracy of reading.
    Epidural/subdural catheter= non electrical basis. Low incidence of infection. Can not withdrawal CSF for analysis.
    ***Remember the ventricles are the storage tanks for CSF***
    To decrease the cerebral edema
    Mannitol=and osmotic diuretic to dehydrate the brain tissue. This works by drawing the water across intact membranes. Need strict I&O
    Corticosteroids--dexamethasone is given to reduce the edema
    Fluid restrictions--- to lead to dehydration and hem concentration which is again drawing fluid across the osmotic gradient which will decrease the edema.
    Maintain the cerebral perfusion
    Manipulate cardiac output to provide enough perfusion to the brain. Improve Cardiac output. This is done by fluid volume and inotropic agents= dobutamine hydrochloride. This is checked by monitoring the cerebral perfusion pressure and it should be maintained at 70mmHg or greater.
    Reduce the CSF and intracranial blood volume with drains…but be careful of over drainage can lead to collapse. Hyperventilation of patients is only used for patients that do not respond to the other therapies.
    Control the fever….shivering increases ICP…fever increases cerebral metabolism and edema.
    Reduce metabolic demands
    Barbiturates= Nembutal, pentothal, diprivan. When administering paralyzing agents…..require intubation, arterial pressure monitoring…ICP monitoring.
    ASSESSMENTS based on location in the brain
    ICP on the frontal lobes will lead to Cheyne stokes resps
    ICP in midbrain will lead to hyperventilation
    ICP in stem (pons, medulla) leads to irregular resps and apnea.
    Elevate the head of the bead 30-40 degrees as prescribed.
    Avoid Trendelenburg’s position
    Prevent flexion of neck and hips
    Monitor resp status and hypoxia
    Avoid morphine sulfate
    Maintain PaCO2 at 30-35mmHg. This will result in vasoconstriction of the cerebral blood flow vessels, decreased blood flow and a decreased ICP.
    Maintain body temp--anti pyretics ,
    Prevent shivering.
    Decrease environmental stimuli
    Monitor lyte and fluid balance
    Limit fluid intake 1200mL/day--decrease edema
    Avoid straining, coughing sneezing
    Avoid valsalva maneuver.
    Seizure precautions--pad rails, have O2 and suction.
  • Avoid straining, coughing sneezing
    Avoid valsalva maneuver.
    Seizure precautions--pad rails, have O2 and suction.

Monday, November 27, 2006

more review...acute renal failure

  • Acute renal review. Some…alot of work for kidneys.
    Think about the kidney…waste and water balance, acid base balance, controlling BP, controlling anemia.
  • 3 f(x)= glomerular filtration, reabsorption and secretion.
  • How does the kidney exrete nitrogenous waste ? Conserve electrolytes? and concentrate urine?
  • Standard renal f(x) test= the GFR. Creatinine clearance test done over 24 hours. Normal rate is 80-125ml/min.
  • Streptomycin--is nephrotoxic…be careful…
  • Hypotension, extreme bleeding associated with pre renal failure.
  • Oliguric phase--10-14 days….anticipate, urinary changes decreased output decreased GFR, cant concentrate urine. fluid volume excess, assess edema, neck vein distention, pulm. Edema, CHF, bounding pulse. Metabolic acidosis…see increased rr. Sodium balance…excreting to much Na+. Supposed to excrete K+ …but it is not. Anemia decreased platelets, RBC. Calcium deficit + Phosphate excess.
  • What to expect to do….treat Hypovolemia w/ albumin IV. (remember 3rd spacing?) Treat HTN with meds, Treat hyperkalemia…R insulin IV + glucose. To help K+ into cells. Sodium bicarbonate to Tx acidosis. Calcium gluconate IV. Dialysis, to get rid of K+ for arrhythmias. Kayexalate to get rid of K+ in through stool excretion. Restrict dietary K+. to 40mEq.
  • Diet
    Decrease the protein to 1gm/kg
    Increase the calories
    Decrease K+ and phosphorous (banana, citrus, coffee)
    Increase the Fe
  • Hemodiaylsis
    Access = AV shunt, fistula, graft.
    Nsg Care
    Assess for change in BP, disequilibrium reaction, alterations in clotting from heparin solution.
  • Transplant.
    Major concern=rejection. Rx given to immunosuppressive=Imuran, Prednisone, cyclosporin.
    Next concern is infection
    Assess for increased temp. pain. Tenderness over grafted area. Decreased output, edema, sudden weight gain. Assess for rise in serum creatinine and BUN values. in essence the s/s of ARF.