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The Ultimate Nursing Care Plan Database

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Pathophysiology

Also known as acute kidney injury (AKI), is measured by the buildup of waste in your body and altered fluid levels because the kidneys are failing to do their job. The cause of the renal failure can also change the pathophysiology. There are three main causes: 1) decreased blood flow to the kidneys, 2) direct injury to the kidney/tissues, and 3) blockage of urine excretion. Inflammation to the kidneys or their structures (nephrons) can cause the kidneys to fail. Blockage of urine can cause a backup in the kidney, not allowing them to continue to filter out waste from the body or manage fluid levels.

Etiology

There are many causes of kidney failure. For example, low blood perfusion to the kidneys can cause acute kidney failure from causes such as an infection/antibiotic use, hypotension potentially from blood loss (hemorrhage) or fluid loss (vomiting/ diarrhea), or even other organ failure (heart attack, liver failure). Another reason for kidney failure could be direct damage to the structures of the kidney itself. The biggest offender of kidney damage is sepsis, but also anything that can cause inflammation in the vessels of the kidneys (Vasculitis) as well as the attempt to treat it with too many NSAIDs can cause direct damage to the kidneys. Lastly, if the urine cannot be excreted, this can cause kidney failure. Kidney stones, enlarged prostates and some cancers can present problems for the urinary tract’s ability to excrete urine.

 

Desired Outcome

Return normal functioning of the kidney’s, including the nephrons, blood vessels, urethra, and ureters. Have the kidney labs be within normal limits and hopefully not have the patient on dialysis.

Subjective and Objective Data

Subjective Data
  • Increased thirst
  • Dizziness
  • Flank pain
  • Hematuria
  • Oliguria
  • Recent antibiotic usage
  • Over usage of NSAIDs
  • Recent blood transfusion
  • Chest pain/pressure
  • Confusion
Objective Data
  • Hypertension
  • Orthostatic Hypotension
  • Atrial fibrillation
  • JVD
  • Pulmonary Edema/Rales
  • Edema

Nursing Interventions and Rationales

  1. Strict intake and output measurement
    • It is important if the kidney’s are not functioning to measure the patient’s I&Os. Notify the physician if there is a deficit greater than 5-10%.
  2. Medications to watch: Statins, NSAIDS, Aspirin
    • Be mindful of medications that can become toxic when the kidneys aren’t functioning at their prime.

      Try to limits these drugs, watch labs and antibiotic troughs. Look out for signs
  3. Statins NSAIDS Aspirin Acetaminophen Insulin Some antibiotics Herbal supplements
    • Be mindful of medications that can become toxic when the kidneys aren’t functioning at their prime.

      Try to limits these drugs, watch labs and antibiotic troughs. Look out for signs and symptoms of overdose.

      Here are the most common signs and symptoms of overdose. *note this is not a comprehensive list*

      Statins: muscle pain and weakness.

      NSAIDS: N/V, headache, dizziness and blurred vision.

      Aspirin: ringing in the ears (tinnitus), decreased hearing.

      Acetaminophen: N/V/D, irritability, convulsions, coma.

      Insulin: Hyperinsulinemia from the body building up resistance to insulin.

      Some antibiotics: Neuro symptoms like seizures, confusion, neuropathy.

      Herbal supplements: Various, depends on the herbal supplement.
  4. Monitor lung sounds and edema
    • You want to make sure fluid balance is carefully monitored. A backup in the lungs would cause crackles and a back up systemically would cause pitting edema in the legs.
  5. Diuretic administration: Furosemide (Lasix) Bumetanide (Bumex) Spironolactone (Aldactone)
    • This is very important… diuretics are going to make the patient PEE… lots and lots of PEE. Do not under any circumstances administer a diuretic without a bathroom plan. And a word to the wise, have a backup plan. Meaning if you have a walkie talkie patient with functioning arms and a strong call light finger, I still would set up a bedside commode just.in.case. I walk them to the bathroom or assist them in any way needed, but it is possible that they do not know how urgent their situation is and I can clean up pee, but you can’t clean up that patients dignity.

      Diuretics work on different parts of the nephrons. The goal of diuretics is to help the kidneys rid the body of salt (notice I didn’t say sodium (Na+)?) and fluids. It is important to note for every Na+ molecule there is a compound of one water (H20) that follows it. Psssst: potassium is a salt...

      There are three kinds of diuretics: Loop, Thiazide, and potassium sparing.

      Loop: works on the loop of henle and excretes Na+, K+, and Ca-. (Yikes! Watch your patient’s electrolytes!)

      Thiazide: Works on the distal convoluted tubule and blocks the Na+/Cl- symporter (which reabsorbs...you guessed it Na+ and Cl-). This symporter is responsible for about 5% of Na+ reabsorption. So monitor your patient’s sodium and chloride. Oh, and your K+...Why? Because K+, Cl- and Na+ have direct relationships!

      Potassium-Sparing: Works on the Na+/K+ pumps in the collecting ducts of the kidney by blocking the effects of aldosterone at that site. Aldosterone has the collecting ducts reabsorbing Na+ and thus water, and for ever Na+ absorbed, one molecule of K+ is excreted. So this diuretic does the opposite of that, saves a K+ and excretes a Na+ and H20.

      Most commonly used diuretics in acute kidney failure:
      -Furosemide: Loop
      -Bumetanide: Loop
      -Spironolactone: Potassium-Sparing
  6. Monitor Potassium Potassium (K+) Normal range: 3.5 - 5.0 mEq/L
    • As Furosemide is the front line and best treatment for kidney failure, nurses must be careful to watch the patient’s potassium levels (Remember: Furosemide is potassium wasting).

      Potassium (K+): is the most abundant intracellular cation and plays a vital role in the transmission of electrical impulses in cardiac and skeletal muscle. It plays a role in acid base equilibrium. In states of acidosis hydrogen with enter the cell as this happens it will force potassium out of the cell, a 0.1 decrease in pH will cause a 0.5 increase in K+
  7. Diet changes and control Fluid restriction Salt restriction
    • Educating the patient on decreased sodium intake as well as strict fluid intake is vital when in any sort of kidney failure.

      However, if patient is on a potassium wasting diuretic, educate about potassium (bananas, sweet potatoes, etc.)
  8. Monitor Kidney Labs Blood Urea Nitrogen (BUN) Normal Range: 7-20 mg/dL Creatinine (Cr) Normal Range: 0.7-1.4 mg/dL
    • This measures how well treatment is working, you want the labs to be moving back to normal limits.

      Blood Urea Nitrogen (BUN): measures the amount of urea in the blood. When protein is broken down ammonia is formed. Ammonia is converted to urea in the liver and is eventually excreted in the kidneys.

      Creatinine (Cr): is a byproduct of creatine metabolism, and it is excreted by the kidneys. Creatinine is created in proportion to muscle mass and usually stays stable.

Pathophysiology

A decrease in red blood cells (RBC) or hemoglobin (HGB). The body uses the RBCs to transport Oxygen via HGB (HGB binds oxygen to the RBC). The oxygen is then bussed around the body and dropped off to the cells for the cell to perform cellular respiration creating ATP AKA energy. With oxygen (aerobic cellular respiration) the cells produce their ATP and have a byproduct of CO2, which we breath out. Without oxygen (anaerobic respiration) the cells use fatty chains to get their energy which has the byproduct of ketones (super acidic). Having the body be in a state of low oxygenation (hypoxia) creates an unbalanced pH which then denatures proteins making cells not be able to read their code/instructions because the code (DNA/RNA) is made out of proteins… While being anemic for short term is easier for the body to bounce back, long term anemic or rapid severe anemia is a bicycle kick to the body… AKA no good. It is important to note that you need BOTH RBCs and HGB for a working system of oxygenation.

Etiology

There are many causes of anemia, the most life threatening is massive hemorrhage, but other causes such as lack of iron, severe burns, cancers, bone marrow disorders like multiple myeloma or leukemia can be just as detrimental.

 

Some of the types of anemia:

  • Iron Deficiency Anemia: Usually caused by hemorrhage or lack of Iron (or lack of ability to absorb iron). Treated with iron supplements/diet changes and blood transfusions.
  • Vitamin Deficient Anemia: Due to Folic Acid (vitamin B12) deficiency or lack of ability to absorb B12. Treated with B12 supplements and diet changes.
  • Aplastic Anemia: The bone marrow is not producing enough RBCs. Treated with blood transfusions and also bone marrow biopsies to diagnose specific issue with the bone marrow.
  • Hemolytic Anemia: Due to RBCs being destroyed. What is causing the lysing of the RBCs can be from a range of problems including infection, autoimmune disorders, etc. Treatment is dependant on the cause. If due to infection, treatment is antibiotics, if autoimmune treatment may be medications that suppress the autoimmune system. Cardiac and vascular specialists should be consulted for this condition in case it is due to a mechanical factor like the heart valves.
  • Sickle Cell Anemia: This is a genetic disorder where the blood cells become sickle shaped, causing clots, hemolysis, and poor perfusion. Treatment is focused on pain control, fluid resuscitation and sometimes blood transfusions.

Desired Outcome

Stopping the cause of the anemia and returning the blood counts (RBC/HGB) back to normal limits.

Subjective and Objective Data

Subjective Data
  • Fatigue/weakness
  • Dizziness
  • Lightheadedness
  • Shortness of Breath (SOB)
Objective Data
  • Bleeding/Hemorrhaging
  • (internal and external)
  • ***consider stroke like symptoms, patient may be have a hemorrhagic stroke!***
  • Pale skin
  • Shortness of Breath (SOB)
  • Potential ECG changes
  • Hypotension (from blood loss)
  • Tachycardia (from hypotension/blood loss)
  • Syncope (also from hypotension/blood loss)
  • Low lab values: HGB/RBC.

Nursing Interventions and Rationales

  1. Assess for bleeding/Hemorrhage and stop source if found. GI bleed: Give pantoprazole (Protonix), potential surgical intervention to stop the bleeding. External hemorrhage: Don’t forget about menstruation for females, soaking more than 1 pad in an hour is very concerning for too much blood loss! Internal hemorrhage: outside of the GI tract but inside the skin.
    • GI bleeding: This entails my least favorite thing to do, and the nurse doesn’t even do it, but the nurse usually needs to be present because it invades the patient’s self respect and dignity. Therefor you get to be in the patient’s visual field while they are being pillaged in their back end.

      The provider will place a gloved finger into the rectum and needs to have feces on it when it comes out. The feces is placed on a hemoccult card where a developing solution is married with the stool giving the provider insight of whether or not there is blood in the stool. If the card turns blue it is positive for blood.

      As a nurse you will ask the patient if they have black/tarry stools (upper GI bleed) or bright red blood (lower GI bleed) in their stools.

      Give pantoprazole (Protonix), a proton pump inhibitor (PPI) that decreases the amount of acid in the GI lining. This reduces the ulceration which could be (and most likely is) causing the GI bleed.

      External hemorrhage: Found by examining the patient’s full body (front and back). Apply pressure to any hemorrhage. Replace lost volume if hemoglobin is below 8 (this number is different per hospital, per doctor and per situation, but 8 is a general number that you don’t want people’s hemoglobin to be below).

      Internal hemorrhage: Can be from a laceration to the liver or the spleen. Assess for abdominal pain and swelling.

      Don’t forget about hemorrhaging in the brain- look for signs and symptoms of stroke.
  2. HGB Normal Value: Male: 13.5 - 16.5 g/dL | Female: 12.0 - 15.0 g/dL RBC Normal Value: Male: 4.5 - 5.5 x106/cells/mm3 Female: 4.0 - 4.9 x106/cells/mm3 Folic Acid (B-12) Normal Value: 2 - 20 ng/mL Ferritin Normal Value: 20-300 ng/mL Iron Normal Value: 50-175 ug/dL
    • There are many blood lab values a nurse can monitor while treating a patient with anemia. Here are the most important.

      HGB: Hemoglobin (Hbg), an iron containing compound, is the main protein in Red Blood Cells (RBCs). It enables oxygen and carbon dioxide (CO2) to bind to RBCs for transport throughout the body.

      This is the most commonly looked at lab value to assess need for a blood transfusion. Every institution, Doctor, and person is different but as a general rule, a hemoglobin below 8 requires a blood transfusion.

      RBCs: Red Blood Cells (RBCs) contain hemoglobin which is responsible for oxygen transport throughout the body. RBCs are primarily produced in the bone marrow, they have a life span of 120 days and are destroyed in the spleen and liver. RBC production is regulated by erythropoietin (EPO) which is produced and released from the kidneys.

      Folic Acid (B12): Folic acid is an essential water soluble B vitamin. It is stored in the liver and is an important part of Red Blood Cell (RBC) and White Blood Cell (WBC) function, DNA replication, and cell division.

      Ferritin: Ferritin is a protein that stores iron. It is formed in the liver spleen and bone marrow. Ferritin in the blood is usually proportional to stored ferritin. Ferritin is a more sensitive and specific test for identifying iron-deficiency anemia, however, it is usually measured in conjunction with total iron binding capacity and iron.

      Iron: Iron (Fe) is an element that is an important component of hemoglobin in red blood cells. Hemoglobin transports oxygen from the lungs to all the cells of the body. Most of the iron in the body is located in hemoglobin, but some iron is located in myoglobin as well as some iron is stored in the liver, bone marrow, and spleen. The storage form of iron is ferritin. Iron is transported in the blood by a protein called transferrin.
  3. Blood product administration: Packed Red Blood Cells (PRBC) Fresh Frozen Plasma (FFP)- one unit for every 4 units of PRBC
    • If the source of the anemia is blood loss, you want to stop the source if possible and replace the blood. If you are unable to stop the source and the patient losses greater than 40% of their blood, give a massive blood transfusion rapidly.
  4. Cardiac Monitoring: 12-lead ECG 5-lead monitoring
    • Decreased blood volume is problematic for the heart, so make sure the heart is still kicking it the proper way (normal sinus rhythm) or as proper as it can. Monitor for any changes in ECG, tell the patient to inform you of any new symptoms like chest pain or shortness of breath.

      Anemic patients are more likely to experience ST depression, QT prolongation, T wave depression, and R wave difference.
  5. Fall Precautions
    • High risk of syncope, especially if the patient is hemorrhaging. Keep the patient lying flat or in trendelenburg position if hypotensive.
  6. Oxygenation monitoring/Administration
    • The purpose of your RBCs binding hemoglobin and oxygen is to deliver oxygen to your cells so they can perform aerobic respiration, giving you the energy to perform ADLs.

      If you limit the number of RBCs or HGB, you limit the O2 in your blood.

      Check for oxygen saturation, monitor it, and if it falls below 94% give 2L NC to start with, increase as needed. Oh and call your Respiratory Therapist because they are your best friends and need to monitor the patient too. Friends don’t let friends drive drunk monitor oxygenation alone.
  7. Iron or B12 Supplements/Diet changes
    • Educate the patient on foods that are high in iron (red meats, dark leafy vegetables, etc) or high in folic acid AKA B12 (rice, pasta, beans) and if the patient is unable to get enough through their diet, they may have to use supplements.

      Review the patient’s medication list.

      Iron supplements are likely to decrease absorption of Quinolone and Tetracycline Antibiotics as well as Levodopa, Levothyroxine, Methyldopa, CellCept, Penicillamine, and Bisphosphonates.

      Folic Acid supplements are likely to increase side effects of 5-Fluorouracil and Capecitabine. It might also decrease the efficacy of Fosphenytoin, Methotrexate, Phenobarbital, Phenytoin, Primidone, and Pyrimethamine.

Pathophysiology

Bronchoconstriction and increased mucus production decreases the ability to bring air into the alveoli, decreasing the amount of oxygenation red blood cells are able to exchange. This can also lead to increased amounts of carbon dioxide (CO2) retention due to lack of ability to exhale the CO2.

Etiology

Swelling and mucus aggregated from an irritant or “trigger” cause difficulty in breathing, wheezing lung sounds and hypoxia. Triggers include dust, pollen, smoke, infection, etc. Asthma can also be genetic, environmental, triggered by exercise or from allergies.

 

Desired Outcome

Decreased work of breathing and proper oxygenation to tissues.

Subjective and Objective Data

Subjective Data
  • “I can’t breath”
  • Chest Pressure
  • Chest Pain
  • Chest Tightness
  • Cough (both objective and subjective depending on if the cough is happening now or if they are reporting a cough)
Objective Data
  • Pursed lip breathing
  • Low pulse oximetry (< 90)
  • Blue lips/fingers
  • Tachypnea
  • Wheezing
  • Tripod position

Nursing Interventions and Rationales

  1. Check pulse oximetry Apply oxygen if O2 saturation is less than 90%, start at 2 liters nasal cannula (2L NC)
    • Get subjective data to determine if patient is receiving proper amounts of oxygen.

      This is both a comfort measure as well as physiologically helpful. In other words, it can’t hurt the patient (at higher amounts and flows it could hurt the patient!). Eliminate hypoxia, move up by 1L if not improving after re-checking every few minutes, call respiratory therapy if they require more than 6L NC.
  2. Educate about triggers/make sure the patient's room does not have any triggers
    • Dust is near impossible to completely get rid of, however, other triggers like pollen (no flowers), animal dander (no visiting puppies), etc. can be eliminated.

      Make sure the patient knows about their asthma triggers and help them problem solve how to eliminate the trigger from their life.
  3. Auscultate lung sounds
    • If wheezy they may need a breathing treatment
      If you hear crackles they may have pneumonia and potentially could use suctioning.
  4. Positioning patient in an upright position
    • Opens lung bases and airway
  5. Have the patient perform a peak flow meter
    • Peak flow meters tell us how much air that patient can exhale. The smaller the number the less amount of air they are moving.
  6. Breathing treatments and medication therapy
    • Beta-Agonists: Such as albuterol work as bronchodilators

      Anticholinergics: Such as Ipratropium work to relax bronchospasms

      Corticosteroids: Such as Fluticasone work as an anti-inflammatory
  7. If the patient is a child or the patient has been working very hard to breath for a long period of time and is getting worse, be prepared with an airway cart. And for the love of the airway, have your respiratory therapist aware of the patient
    • Safety! Plus you do not want to wait until the impending airway closure happens to try to secure their airway. Sometimes the patient will be sedated and intubated to try to correct any respiratory acidosis or alkalosis.

Pathophysiology

An electrical activity disturbance in the heart that causes an irregular and often rapid heartbeat. The atria quiver sending confusing electrical signals to the ventricles, leaving them unsure of when to contract thus beating irregularly. During atrial fibrillation, the heart is a less effective pump because of the quivering as well as not emptying completely. This causes the blood to pool and a clot can form. The clot can venture out of the heart into the lungs (PE), brain (stroke) or extremities (DVT).

Etiology

The specific cause of atrial fibrillation is unknown but there are risk factors that put someone at higher risk of developing afib. Risk factors such as smoking, hypertension, and obesity as well as conditions such as diabetes or heart disease increase the likelihood that a patient may get atrial fibrillation. Post surgical interventions present a major risk for atrial fibrillation as well. Approximately 30%-40% of cardiac surgery patients develop atrial fibrillation.

Desired Outcome

Decreasing risks of clot formation, a heart rate within normal limits and rhythm control. The ultimate outcome is converting back to normal sinus rhythm, however, many people live with atrial fibrillation, especially if rhythm control doesn’t work or isn’t necessary.

Subjective and Objective Data

Subjective Data
  • Heart Palpitations
  • Feeling like the heart is beating out of the chest
  • Feeling a fluttering sensation in the chest
  • Nausea
  • Lightheadedness
  • Weakness
  • ***Patient may not have any symptoms at all***
Objective Data
  • Irregular heartbeat
  • Tachycardia

Nursing Interventions and Rationales

  1. Obtain a 12 lead ECG
    • Used to diagnose atrial fibrillation

      The waves are more chaotic and random

      The beat is irregular

      You can see the atria quivering between the QRS (ventricles pumping)

      No discernible P waves The ventricular rate is often 110-160 bpm and the QRS complexes is usually less than 120 ms.
  2. Potential rhythm control: Electrocardioversion, Ablation, Pacemaker
    • -Electrocardioversion: AKA cardioversion, is used to “reset” the heart’s electricity.

      The patient will be shocked on the outside of the chest wall. This treatment is used for patients who have infrequent episodes of atrial fibrillation because if the patient has it frequently, they have a high probability of the afib returning after being cardioverted.

      ***If there is a blood clot in the atria, cardioverting may send the clot out of the heart to the brain, lungs, or extremities. The chance of a blood clot increases the longer the patient is in afib, consider anticoagulation prior to cardioversion***

      Ablation: used for patient’s that have not been able to control their afib for a long time with medications or cardioversion. A catheter is inserted into the patient’s heart and destroys cardiac muscle cells so they scar, causing the electrical activity to stop in those cells, thus eliminating the passing of chaotic electrical activity.

      Pacemaker: This is placed under the skin and is a device that sends electrical signals to the heart to help it beat with the right rhythm and pace.
  3. Heart rate control: Beta Blockers: -Propranolol -Metoprolol -Atenolol Calcium Channel Blockers: -Diltiazem -Verapamil Cardiac Glycosides: -Digoxin
    • A heart can only sustain rapid beating for so long before it tires out. Using beta blockers, calcium channel blockers and cardiac glycosides will help control the rate of the heart beat.

      Beta Blockers: They block beta 1 receptors from being stimulated. Stimulation of Beta 1 causes positive inotropic (force of contraction) and chronotropic (pace of heart beat) effects. If you block beta 1 you will have decreased force of contraction and decreased heart rate.

      Calcium Channel Blockers: They block calcium channels… Duh. When calcium enters the cell in causes the cell to contract, thus when the channels are blocked, it decreases the production of electrical activity innately decreasing the heart rate.

      Cardiac Glycosides: This medication stimulates the Vagus nerve, which when stimulated slows the heart rate down. The vagus nerve is a CNS nerve that also works with the PNS- specifically the autonomic parasympathetic system… AKA rest and digest… So if this is stimulated your body will rest/slow down, thus decreased heart rate.


      It also blocks the Na+/K+ channel in cardiac myocytes. When this channel is open, K+ moves into the cell and Na+ moves out of the cell, called repolarization and is the relaxation part of a heart beat. When it is blocked it causes increased contractility of the heart. If your heart is beating stronger it will inherently slow down.
  4. Anticoagulant Therapy: Coumadin Aspirin Lovenox Plavix Eliquis
    • Thinning the blood helps to disintegrate and break up the clot as well as increasing flow of blood. There are many options for blood thinners each with their own pro’s and con’s. The most common are listed to the left.
  5. Fall education
    • Being on a blood thinner, the patient needs to be informed of their risk of bleeding out especially if they fall and hit their head.

      Make sure to go over environmental hazards such as good lighting and eliminating throw rugs.

      If a patient does fall and hit their head they need to go to the ER immediately, even if they are not experiencing any adverse effects.
  6. Stroke education Use the FAST Mnemonic: F: Facial drooping A: Arm weakness S: Slurred speech T: Time to call 911
    • The risk of a blood clot forming and moving to the brain is fairly high. It is important to teach the patient and their family members the signs and symptoms of stroke.

      Teach the patient that if they feel confused or feel weakness on one side to call for help.
  7. Cardiac enzyme monitoring: Troponin I Creatine Kinase MB
    • Initial measurement of the cardiac enzymes is important because it helps with any trending information, the sooner you get this information the better. Also getting trending results over specific periods of time is helpful.

      Troponin I: Is an enzyme that helps the interaction of myosin and actin in the cardiac muscle. When necrosis of the myocyte happens, the contents of the cell eventually will be released into the bloodstream.

      Troponin can become elevated 2-4 hours after in ischemic cardiac event and can stay elevated for up to 14 days.

      Creatine Kinase MB: This enzyme is found in the cardiac muscle cells and catalyses the conversion of ATP into ADP giving your cells energy to contract. When the cardiac muscle cells are damaged the enzyme is eventually released into the bloodstream.

      CKMB levels should be checked at admission, and then every 8 hours afterwards.

Pathophysiology

Blood clots formed from any source, lodging in the patient leg or arm, impeding blood flow. This backup of blood pools in the extremity causing swelling, redness, warmth and pain.

Etiology

Narrowing or occlusion of the vessels in an extremity. If caused by plaque (cholesterol and other substances) this could be from poor diet, lack of exercise, or genetics. However, blood stasis can cause aggregation of platelets and other blood products forming a clot that travels to the extremity (or heart, lungs or brain!). The most common cause of blood pooling (stasis) is Atrial Fibrillation (AFib). Other major causes are prolonged sitting, pregnancy, smoking, and birth control.

Desired Outcome

Stabilization of the blood clot or disintegration of the blood clot as well as prophylaxis treatment for future blood clots.

Subjective and Objective Data

Subjective Data
  • Painful extremity
  • Numbness and tingling on affected extremity
  • Potential subjective data to be concerned about and monitor for: (this is if the clot moves)!
  • Pulmonary Embolism (PE): Difficulty in Breathing (DIB)/Shortness of Breath (SOB), Chest Pain (CP)
  • Myocardial Infarction (MI): Chest Pain (CP)
  • Stroke: facial asymmetry, confusion, one sided deficit,  
Objective Data
  • Warm, red, firm and swollen leg
  • Decreased peripheral pulse on affected extremity

Nursing Interventions and Rationales

  1. Assess a full neuro exam, assess breathing-Pulse oximetry, difficulty in breathing, chest pain, obtain an EKG.
    • Assess and monitor for potential complications d/t the blood clot moving into another area such as the lungs (PE), heart (MI), or brain (CVA).
  2. Heparin- initial therapy to break up clot. Transition into a SubQ or oral anticoagulant to prevent future clots.
    • This is an anticoagulant that breaks up blood clots (as well as prevents them).

      Monitor aPTT or Anti-Xa Q6H to adjust and maintain therapeutic levels.

      Bolus: 80 units/kg

      Initial dose: 18 units/kg/hr
      -Adjust according to your organization's nomogram (Q6H- based on results of aPPT or Anti-Xa)
  3. Enoxaparin (Lovenox)/Warfarin (Coumadin)
    • Both SubQ and oral anticoagulant therapy use as prophylaxis (prevention) therapy.

      Patient will need to have frequent blood draws to monitor their INR. Therapeutic range is between 2 and 3.

      Enoxaparin: 1-1.5 mg/kg

      Warfarin: initial dose is 2-4 mg, and typically can range up to 10 mg.
  4. Educate about avoiding vitamin K (both supplements as well as food)
    • Vitamin K works to help increase clotting, this is opposite of what we are trying to do for this patient, unless of course they are bleeding out, in which case the treatment may be vitamin K with Fresh Frozen Plasma (FFP)
  5. Continuous monitoring: 3 or 5 lead cardiac monitoring pulse oximetry monitoring
    • This monitors for changes in the heart and allows for quick intervention if the clot moves and is stuck in the heart.

      This monitors for changes in oxygenation if the clot moves to the lungs.
  6. Bleeding/fall precautions because of anticoagulant therapy
    • This isn’t just for in the hospital, it is also for when the patient goes home. The patient is at major risk for bleeding out, thus educating about s/sx of internal bleeding as well as educating about fall precautions is vital.

      GI bleeding: Dark, tarry stool (Upper GI bleed) OR bright red bloody stools (lower GI bleed)

      Epistaxis: Nosebleeds are obvious, however, inform the patient that if they bleed through nasal packing for longer than 15 minutes they should go to the ER. Also they they feel dizzy, faint, or are losing color in their face they should go to the ER.

      Cuts that don’t stop bleeding: if the cut has had pressure applied for longer than 15 minutes and the gauze is being soaked through the patient should go to the ER.

      Brain bleed: Have patients and the people who are around them look for S/Sx such as confusion, facial droop, one-sided weakness.

Pathophysiology

Cardiac muscle tissue death from lack of blood flow. The blood carries oxygen and nutrients to the cells. When this is decreased, cells die also called necrosis. Cardiac muscle cells dying is problematic as they do not regenerate (although there is some debate of this topic: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3042154/ )

Etiology

Narrowing or occlusion of the cardiac vessels that perfuse the heart. The plaque that causes this could be from poor diet, lack of exercise, or genetics. It can also be from a deep vein thrombosis (DVT) that has broken free (embolus) and landed in the heart.

Desired Outcome

Re-perfusion to cardiac muscle and return of cardiac muscle functionality, or as much as possible.

Subjective and Objective Data

Subjective Data
  • Chest Pain
  • Chest Pressure/Squeezing
  • PQRST pain assessment
  • P- provoke, precipitate, palliate
  • Q- quality
  • R- radiate
  • S- severity, symptoms
  • T- time
  • Patient may report a feeling of impending doom
Objective Data
  • ST elevation on the ECG- Called an STEMI
  • Decreased oxygenation
  • Signs of left ventricular failure such as crackles in the lungs or S3 heart sound
  • Tachycardia (Bradycardia can be seen if patient is having an inferior MI)

Nursing Interventions and Rationales

  1. MONA: Morphine Oxygen Nitroglycerin Aspirin (ASA)
    • Initial treatment for acute coronary syndrome.

      Morphine: given if aspirin and nitroglycerine do not relieve chest pain. Initial dose is 2-4 mg IV.

      Oxygen: helps for you to remember to check oxygenation for chest pain- if under 94% or if patient is short of breath give 2L NC initially. Evidence based research has left the use of oxygenation and its helpfulness in these situations inconclusive. Oxygen can cause vasoconstriction thus worsening the situation and decreasing blood flow. Administer oxygen when clinically relevant.

      Nitroglycerin: This is the initial medication given, along with aspirin. This medication dilates the blood vessels to help allow any blood flow that might be impeded. Give 0.4 mg sublingual tab, wait 5 minutes, if the chest pain is not relieved administer another dose. This can happen 3 times total. Monitor a patient’s blood pressure, hold for a systolic BP of less than 90 mmHg.

      Aspirin: given to thin the blood. A total of 4 baby aspirin (81 mg each) can be given for a total of 324 mg.
  2. 12 lead ECG If inferior wall MI- do a right sided 12 lead ECG.
    • Assess a 12 lead ECG immediately on anyone complaining of chest pain to determine if an ST elevated MI is occurring. If it is-Take the patient to the cath lab STAT! If the ECG is a normal sinus or otherwise non-concerning rhythm, place them on a 3 or 5 lead cardiac monitor for frequent re-assessing.

      Right sided 12 lead ECG shows the right side of the heart to assess for right ventricular ischemia.
  3. 3 or 5 Lead monitoring
    • No matter the outcome of the 12 lead ECG, placing a patient on a form of cardiac monitoring is key. You are worried about a worsening condition such as cardiac arrest.
  4. Cardiac Catheterization with Percutaneous Coronary Intervention (PCI)
    • A patient who has an ST elevated MI (STEMI) will be rushed to the cath lab so they can locate the clot and place a stent to regain blood flow to the heart.

      A patient may also go to the cath lab without having a STEMI, and they may still find a clot. Most NON-STEMI’s are treated without catheterization.
  5. BP Monitoring The measurement is determined by the doctor, who is determining this based on evidence based research married with patient factors. It can be measured by the systolic BP or the Mean Arterial Pressure (MAP). This can also be monitored by an arterial line.
    • This is important because the higher the blood pressure, the more pressure is on a clot. It isn’t out of the question for someone to have more than one clot, and increased pressure could break free a clot lodge itself somewhere else either in the heart, lungs, brain, or extremity.
  6. Heparin
    • This is an anticoagulant that breaks up blood clots (as well as prevents them).

      Monitor aPTT or Anti-Xa Q6H to adjust and maintain therapeutic levels.

      For STEMI
      Bolus: 60 units/kg (max 4,000 units)
      Continuous infusion: 12 units/kg/hr
      -Adjust according to your organization's nomogram (Q6H- based on results of aPPT or Anti-Xa)

      For N-STEMI
      Bolus: 60-70 units/kg (max 5,000 units)
      Continuous Infusion: 12-15 units/kg/hr
      -Adjust according to your organization's nomogram (Q6H- based on results of aPPT or Anti-Xa)
  7. Monitor Cardiac Enzymes: Troponin I Creatine Kinase-MB (CKMB)
    • The values of these enzymes are based on your institutional laboratory technique. If they are elevated it indicates that the cardiac muscle is stressed out or injured.

      Troponin I is an enzyme that helps the interaction of myosin and actin in the cardiac muscle. When necrosis of the myocyte happens, the contents of the cell eventually will be released into the bloodstream.

      Troponin can become elevated 2-4 hours after in ischemic cardiac event and can stay elevated for up to 14 days.

      Creatine Kinase MB: This enzyme is found in the cardiac muscle cells and catalyses the conversion of ATP into ADP giving your cells energy to contract. When the cardiac muscle cells are damaged the enzyme is eventually released into the bloodstream.

      CKMB levels should be checked at admission, and then every 8 hours afterwards.

Pathophysiology

Even after bone are done growing after childhood, bones are constantly being broken down and replaced. Bone truly is living tissue. Osteoporosis occurs when the production of new bone isn’t keeping up with what’s being broken down. There is primary and secondary osteoporosis. Primary osteoporosis is from the normal age-related bone loss, while secondary osteoporosis is due to some other disease process.

Etiology

During younger years, bone is regenerated faster than old is broken down. Therefore, the overall bone mass will increase. Typically, bone mass peaks in the early 20’s.  As individuals age they continue to break down bone, but the rate in which they produce new bone can’t keep up.  If the patient had a high amount of bone mass when they peaked in their 20’s, they have more stored up, therefore the likelihood of developing osteoporosis with aging decreases.

There’s quite a bit that can put someone at a higher risk for developing osteoporosis. See the table below for a comprehensive list.

Desired Outcome

Address any underlying causes and prevent fractures

Subjective and Objective Data

Subjective Data
  • Pain
Objective Data
  • Fractures
  • Stooped posture
  • **The challenge with osteoporosis is that there typically is no sign of it until a fracture occurs, and a subsequent bone density test is performed

Nursing Interventions and Rationales

  1. Prevent injury (initiate fall precautions)
    • Injury can be catastrophic for patients with osteoporosis, as a fall could much more easily cause major fractures
  2. Control pain
    • Patients with fractures typically experience pain; pain control is essential to participating in rebab
  3. Consult physical and occupational therapy as appropriate
    • Establishing rehab needs and plan for nursing to assist with implementation; also safely evaluates their max functional level
  4. Assist with ROM activities
    • Patients may require assistance to ensure appropriate movement occurs to prevent atrophy from immobility
  5. Try to avoid using restraints if possible
    • A patient is much more likely to cause a fracture from restraints if they have osteoporosis and confusion. It is especially important to avoid restraints in these patients.
  6. Assist with repositioning every 2 hours if needed
    • Repositioning skin breakdown; assist patient with this if they are unable to do so themselves
  7. Promote appropriate bowel habits
    • Decreased mobility, pain, medications, and so forth all contribute to constipation. Being proactive rather than reactive will safe the patient discomfort, additional pain, and increase compliance with treatment regimen.
  8. Promote nutrition
    • Prevents skin breakdown, promotes healing. Increasing calcium intake and supplementation as appropriate
  9. Support fracture stabilization
    • Whether cast or splint, ensure it is on appropriately and evaluate for skin irritation and breakdown. Assess for appropriate circulation.
  10. Monitor for fat embolism
    • Fat embolism is a complication from a fracture (respiratory insufficiency, rash

Pathophysiology

Pneumonia is essentially when fluid or pus gets trapped in the alveoli of the lungs (pictured below) and impaired gas exchange results. This can impact one or both lungs.

 

Below are the important differentiations of pneumonia (these definitions, except the first one, are from Cleveland Clinic). Establishing the kind of pneumonia is essential, in that the treatment course can differ.

 

    • Community-acquired pneumonia (CAP): pneumonia acquired out in the community, not in a healthcare facility (source)
    • Hospital-acquired pneumonia (HAP): pneumonia diagnosed 48 hours or more after hospital admission
    • Health-care acquired pneumonia (HCAP): pneumonia that presents within 90 days of a hospitalization, nursing-home or long-term care facility stay, or received chemo, wound

 

  • Ventilator-associated pneumonia (VAP):  pneumonia acquired 48 hours or more after endotracheal mechanical ventilation

 

 

The first picture below is normal, unobstructed gas exchange.  If you look to the second picture, you see the alveoli have an accumulation of fluid in them, which impairs the gas exchange that should occur to provide appropriate oxygenation into circulation. What results is coughing (many times producing phlegm), fever, chills, chest pain or pain when coughing, or cold/flu like symptoms. Inflammation can also occur.  Antibiotics are administered, and the choice of which is dependent upon the offending pathogen, any other medical conditions going on with the patient, and if there are any antibiotic resistances present . Oral antibiotics are given typically for community-acquired pneumonia, however if the patient is hospitalized, they will most likely receive IV antibiotics. Steroids are typically administered to address inflammation.

 

Etiology

Pneumonia can be caused by a virus, bacteria, fungus, or from inhaling something (a chemical, inhalant, or aspirating on food or fluid). This can be of particular risk to those with a weakened immune system or unable to keep your own airway clear (for example, unable to cough or maintain consciousness due to neurological or other injury).

Desired Outcome

Resolve the infection, optimize gas exchange, minimize impact from impaired gas exchange.

 

Subjective and Objective Data

Subjective Data
  • Chills
  • Pain
  • Shortness of breath
  • Increased work of breathing
  • Nausea
Objective Data
  • Cough
  • Phlegm
  • Elevated temperature
  • Low temperature (not as common)
  • Vomiting
  • Loose stool
  • Mental status changes
  • Increased or decreased RR

Nursing Interventions and Rationales

  1. Obtain appropriate labs (antibiotic troughs, sputum cultures, ABGs, etc.)
    • Gives us a baseline; identifies pathogens, and enables us to evaluate if interventions are effective
  2. Complete a full respiratory assessment to detect changes or further decompensation as early as possible, and notify MD as indicated
    • Enables quicker interventions and may change them (for example, wheezing noted on auscultation would potentially indicate steroids and a breathing treatment, while crackles could require suctioning, repositioning, and potential fluid restriction)
  3. Promote normothermia (warm patient if hypothermic, cool patient and administer antipyretics if hyperthermic)
    • Normothermia optimizes oxygen consumption
  4. Cluster care
    • Activity intolerance is common because of decreased gas exchange; cluster your care to conserve your patient’s energy for essential tasks like ambulation, coughing and deep breathing, and eating
  5. Promote airway clearance
    • We want to encourage coughing to remove phlegm; do not suppress cough unless clinically indicated. If patient is able to clear their own airway, continue to encourage this. If not, suction frequently and consider an advanced airway to ensure a patent airway, which ultimately maximizes gas exchange. Getting phlegm out is important.
  6. Optimize fluid balance
    • Patients with pneumonia may not be consuming adequate oral intake due to fatigue or not feeling well, but hydration is essential to healing. Patients may need IV fluids if PO intake is inadequate.
  7. Assess and treat pain
    • If patients are not coughing because of pain, it will only allow fluid to continue to build. Treat pain appropriately and encourage them to cough to clear phlegm.
  8. Encouraging coughing and deep breathing
    • Coughing and deep breathing encourages expectoration, which enables better gas exchange
  9. Promote nutrition
    • Patients with pneumonia typically tire easily and have poor appetites, but need appropriate nutrition and hydration to heal
  10. Administer supplemental oxygen as appropriate
    • Due to the impaired gas exchange, oxygen doesn’t make it into circulation as easily. Providing additional oxygen supports this as much as possible. Use caution in patients with underlying lung conditions.
  11. Ensure patent airway
    • If a patient has unmanageable secretions or is unable to maintain consciousness and keep their airway clear, they must be supported (positioning, advanced airway, etc) to ensure adequate oxygen delivery
  12. Promote rest
    • Energy conservation is essential; patients should focus on breathing, providing self care, coughing/deep breathing, and ambulation. Patients cannot adequately participate in these important activities if they are not maximizing their time to rest. Appropriate sleep promotes healing.
  13. Administer antibiotics in a timely fashion, draw troughs appropriately
    • Patients may be on antibiotics, therefore it’s essential to ensure they are administered at the appropriate time and not delayed, as this will impair their efficacy. Also, trough levels will most likely to be ordered to assess if the patient is getting too much, too little, or just enough of the antibiotic. The timing of these labs related to administration times are essential for accuracy.
  14. Prevent further infection
    • Patients may have invasive lines like a internal urinary catheter, central venous catheter, endotracheal tube, and so forth. It is essential to care for these devices properly to prevent further infection.
  15. Educate patient and loved ones on the importance of energy conservation, effective airway clearance, nutrition, as well as coughing and deep breathing
    • Patients must be aware of how these aspect of recovery are pertinent so they will be more likely to participate and remain compliant.

Pathophysiology

Essentially, at its most basic level, respiratory failure is inadequate gas exchange. Not enough oxygen is being exchanged in your lungs, and therefore it’s not getting into circulation.  

There are three main types:

  • Type I is low levels of oxygen in the blood (hypoxia) – also called hypoxemic respiratory failure
  • Type II is hypoxia with high levels of carbon dioxide (hypercapnia)  – also called hypercapnic respiratory failure
    • High levels of carbon dioxide result when your lungs can get rid of it (breathe out) and it begins to build up
  • Type III is also called perioperative respiratory failure is basically when patients get atelectasis after general anesthesia or shock
    • Type III is a subset of Type I

Your body desperately needs oxygenated blood to function. Therefore, if you’re not getting good gas exchange in the lungs and oxygenating your blood, your organs will suffer.

Etiology

Many situations and/or conditions can result in respiratory failure.  Trauma, medication (oversedation, for example), various disease processes (COPD, asthma, PE, pneumonia), damage to the actual lungs/surrounding tissue/spinal cord or nerves supporting the lungs/brain, and inhalation injuries are the major ones.

Desired Outcome

Restore oxygen levels of blood as appropriate and remove excess carbon dioxide

Subjective and Objective Data

Subjective Data
  • Feeling SOB
  • Respiratory distress
  • Confusion
  • Lethargy
Objective Data
  • Hypoxia
  • Hypercapnia
  • Blue skin, lips, nail beds, etc.
  • Arrhythmias
  • Increased RR
  • Decreased RR
  • Increased breathing workload
  • Low Sp02
  • Decreasing level of consciousness

Nursing Interventions and Rationales

  1. Maintain patent airway
    • Some patients with trauma or neurological injury may require frequent suctioning and/or oropharyngeal airway/nasopharyngeal airway/intubation to ensure adequate oxygen delivery
  2. Obtain and evaluate labs (ABG)
    • This will reveal the level of decompensation as well as if interventions are effective
  3. Complete a full respiratory assessment to detect changes or further decompensation as early as possible, and notify MD as indicated
    • Enables quicker interventions and may change them (for example, wheezing noted on auscultation would potentially indicate steroids and a breathing treatment, while crackles could require suctioning, repositioning, and potential fluid restriction)
  4. Provide supplemental oxygen as appropriate
    • Supplemental oxygen will ideally increase their oxygen levels. (Use caution with COPD patients, as they cannot breathe out the CO2 adequately, so over-oxygenation is a concern, and they also may have a lower baseline SpO2 level)
  5. Ensure patient is in optimal position to decrease work of breathing
    • Sitting up in bed to enable appropriate lung expansion allows for adequate inspiration and expiration, which facilitates better gas exchange (if clinically appropriate to be sitting up)
  6. Prepare for rapid sequence intubation, if necessary
    • Helpful to be prepared, as this can progress quickly. Know where the necessary meds and equipment are and how to get ahold of assistive personnel.
  7. Remove any negative/distracting stimuli: turn the TV off, encourage family members to be calm
    • When patients are anxious or cannot focus it can increase their work of breathing and exacerbate the issue. Promote a calming environment so all the patient has to worry about is breathing.
  8. Prevent ventilator acquired pneumonia (VAP) if patient is intubated
    • If the patient becomes intubated, prevent this major further complication
  9. Provide oral care
    • If a patient is intubated or receiving oxygen via nasal cannula/face mask or tent, or other method of delivery, oral care is essential to protect mucous membrane and prevent infection
  10. Cluster care
    • Decreases oxygen demands if patient’s rest can be maximized
  11. Promote appropriate nutrition
    • Malnourishment is common with chronic lung disease, and appropriate nutrition provides the patient support for healing
  12. Assist to treat underlying cause. If the patient has pneumonia, administering antibiotics is essential to healing, if the patient has a PE, administer appropriate blood thinners, if the patient has asthma, you’re auscultating lungs sounds before and after to evaluate effectiveness.
    • The underlying cause must be treated and routinely reevaluated for the patient to progress.
  13. Monitor for conditions that can increase the oxygen demands (fever, anemia)
    • Frequently other things are going on, so make sure you’re being diligent in addressing them to give the patient the best opportunity to maximize their gas exchange (treat the fever, administer blood products, etc.)
  14. Prevent aspiration pneumonia in patients who cannot maintain their own airway
    • Hypoxia can cause lethargy and a decreasing LOC; should they aspirate on their own secretions this will put them at a significantly increased risk for aspiration pneumonia, which would further impair gas exchange and respiratory failure
  15. Manage secretions
    • Tough to allow appropriate gas exchange in a patient if they cannot handle their own secretions and are using effort to cough/clear their airway, or if it is getting down into their trachea.
  16. Assess ability to swallow safely post-intubation
    • Vocal cords may be irritated and have edema if a patient has been intubated and if give oral intake too quickly too early, patients can easily aspirate. Many facilities require patients to wait 12-24 hrs post intubation to resume regular oral intake as well as a swallow evaluation.

Pathophysiology

Essentially, skeletal muscle is destroyed (for various reasons) and their intracellular contents (in particular myoglobin) leak into the bloodstream. The kidneys can’t handle this large amount of myoglobin and it can damage them, and in some cases (roughly 30-40% of patients with this develop acute renal failure) can cause kidney failure.

Etiology

Quite a few things can cause this. One that has been discussed more frequently recently is due to the increase in people engaging in high-intensity workouts (like CrossFit). This causes intense muscle breakdown, which can result in this condition. Trauma can also be a cause, as well as conditions of genetic origin, seizures, metabolic issues, temp-regulating issues, and many medications.  A few medications that can cause this to occur include statins, diuretics, aspirin overdose (salicylate toxicity), recreational drugs like cocaine and amphetamines, and narcotics.

Subjective and Objective Data

Subjective Data
  • Muscle pain*
  • Generalized weakness*
  • Nausea
  • Tender muscles
Objective Data
  • Dark urine*
  • Vomiting
  • Fever
  • Edema
  • Skin changes (may even look like necrosis)
  • Tense muscles

Nursing Interventions and Rationales

  1. Ensure fluid resuscitation
    • “Expansion of extracellular volume is the cornerstone of treatment and must be initiated as soon as possible.” (Source)
  2. Record I&O
    • The amount of urine output, or lack thereof, may dictate various treatment regimens. Patients may need dialysis if oliguria is present.
  3. Insert Foley and prevent infection
    • Enables nurse to closely and accurately monitor urine output, foley is a source of infection and must be cared for diligently
  4. Monitor labs
    • Labs can and will dictate treatment regimens, especially because symptoms can vary widely. CK, serum and urine pH, bicarb, and electrolytes to name a few
  5. Correct electrolytes per orders
    • Electrolyte imbalances are common (K, Ca, P are of particular importance)
  6. Monitor for compartment syndrome
    • If significant muscle injury occurred, compartment syndrome is a risk. Muscle injury is typical due to decreased perfusion.
  7. Discharge education r/t diet, activity level/prevention
    • Diet changes can prevent this in the future when there is a metabolic cause, patients who are active athletes need to ensure they are hydrated appropriately and use caution with intense exercise, and note if they’re experiencing heat stroke. If a medication was noted to cause this, it and alternatives should be evaluated with the prescriber. Prevention is key!

Pathophysiology

The exact patho of RA is not fully understood, although there is thought to be a genetic component leading to more susceptible individuals. Essentially, something triggers the immune response (that something could be an infection, trauma, or something of that nature) and this leads to synovial hypertrophy (synovial lining of the joint) and chronic inflammation of the joint(s).

Basically, this inflammation becomes uncontrolled and leads to the destruction of bone, cartilage, and even tendons, ligaments, and blood vessels.

Chronic inflammation and degenerative changes are the hallmark aspects of RA.

Etiology

Like the pathophysiology, the etiology is unknown. However there are some factors that seem to contribute to its occurrence. These factors include genetics, various infections, sex hormones, as well as immunological factors.

Desired Outcome

There is no cure for RA, therefore the goal is to manage symptoms and slow the disease progression. NSAIDs, steroids and DMARD’s are used, physical and occupational therapy are key, and in severe cases surgery and joint replacement may be necessary. Some alternative therapies like fish oil, tai chi, and various plant oils have demonstrated improvement in RA symptoms.

Subjective and Objective Data

Subjective Data
  • Fatigue
  • Joint stiffness
Objective Data
  • Warm joints
  • Swelling
  • Deformity
  • Rheumatoid nodules
  • Various deformities
  • Weight loss
  • Periarticular osteoporosis
  • Decreased ROM

Nursing Interventions and Rationales

  1. Manage both chronic and acute pain: use pillow supports and even specialty mattresses, administer PRN and scheduled meds
    • RA is painful and you must have a plan to address the chronic level that accompanies RA as well as the breakthrough and acute pain
  2. Promote self care
    • It may become difficult for patients to care for themselves, especially if they begin to have deformities of their hands
  3. Cluster care, promote rest
    • RA patients experience fatigue frequently
  4. Promote positive self-image
    • Patients experience joint deformities, which can produce a negative body image.

Pathophysiology

Seizures are a very complex neurological issue. Here is the definition from Medscape of a seizure: “a seizure results when a sudden imbalance occurs between the excitatory and inhibitory forces within the network of cortical neurons in favor of a sudden-onset net excitation” (source).  Basically, abnormal electrical discharges are occurring in the brain.  There are different kinds of seizures (epileptic, focal-onset, general-onset).

Etiology

The exact cause of a seizure can be extremely difficult to pinpoint. John Hopkins Epilepsy Center divides seizures into two categories: provoked and unprovoked.  

The etiology of provoked seizures can include: trauma, drugs or alcohol, tumors, medications, drug withdrawal, progressive brain disease, and more.

The etiology of unprovoked (or “natural”) seizures can include: fever, infection, metabolic issues, genetics, Alzheimer’s disease, and more. (Source link listed below)

Desired Outcome

Stop any current seizure activity as soon as possible, minimize damage, and prevent it from occurring in the future.

Subjective and Objective Data

Subjective Data
  • Loss of awareness
  • Confusion
  • A postictal state (drowsiness, nausea, vomiting, headache)
Objective Data
  • Rhythmic twitching
  • Loss of consciousness
  • Staring off
  • Repetitive behavior (lip smacking)

Nursing Interventions and Rationales

  1. Ensure safety and initiate seizure precautions for patients at-risk for seizures. This includes having suction set up and working, having an ambu-bag in the room, padding side rails, not restrain them or putting anything in their mouth if a seizure occurs, having all side rails up, and so forth.
    • Seizures frequently happen without warning, therefore we must ensure safety in case it occurs. Once one begins, it’s too late to try to implement the safety precautions
  2. Maintain airway
    • During a seizure, the patient may not be able to maintain their own airway, or they may not be able to handle their oral secretions and aspirate (this is why it is essential to have suction set up)
  3. Assess, monitor and document seizure activity
    • It is essential to know the precipitating factors, what actually happened during the seizure (rhythmic twitching and specific location) and the specific timing (30 seconds vs. 2 minutes vs. 6 minutes) - you must be as specific as possible to enable the medical team to make appropriate clinical decisions
  4. Administer antiepileptics (PRN and scheduled) medications per orders
    • Many patients with seizures, or who are at-risk will have schedule antiepileptic medications. They must receive these promptly, as ordered. Also be aware of your PRN antiepileptics and when to administer them (typically for seizures lasting longer than 2 minutes)
  5. Reevaluate any medications that may lower the seizure threshold (some antibiotics, antidepressants, narcotics, and many more may do this)
    • We want to do all we can to prevent seizures from occurring, therefore the healthcare team must evaluate meds that may increase the seizure risk and closely look at them to decide if the benefit is worth the risk, or if an alternative is available that does not lower the seizure threshold
  6. Educate patient and family on hospital procedures, and when to notify staff
    • Some patients with a history of seizures can tell when one is coming on, which is helpful to communicate to the nurse. Also, it’s helpful to let them know what you as the nurse will do when/if a seizure occurs so that they are prepared mentally and emotionally, as it can be somewhat scary for families to witness and patients to experience.
  7. Provide emotional support
    • Seizures are serious and upsetting to witness. The more empathy and support you can provide patients and loved ones, the better.

Pathophysiology

Sepsis is essentially an overactive/uncontrolled immune response to an infection. The immune system kicks into overdrive, for whatever reason, and cannot be calmed down. It’s like someone turned the dial all the way up on the immune system and ripped the dial off the dashboard. As the healthcare team, we are trying to turn the immune response down as best we can… but it is VERY challenging. This is a very complex issue which affects many body systems, with an overall mortality rate anywhere from 27-36% (and higher in patients in intensive care settings). The challenge is that it can present with very subtle symptoms and progress quickly. Time is of the essence in sepsis recognition and treatment.

Etiology

Essentially, the cause of sepsis is the original infection. Examples include pneumonia, urinary tract infection, infection in the bloodstream (bacteremia), etc. It doesn’t have to be a bacterial infection, it can be a virus or a fungus as well.

Desired Outcome

Lessening the immune response, prevention cellular death, resolution of infection, minimizing damage from cellular oxygen deprivation and lactic acid build up, maximizing cardiac output and resolution of the condition.

Subjective and Objective Data

Subjective Data
  • Pain
  • Difficulty breathing
Objective Data
  • Elevated temp (over 101 F)
  • Low temp (below 96.8 F)
  • HR over 90
  • RR over 20
  • Respiratory distress
  • Decreasing urinary output
  • Hypotension
  • Decreasing platelet count
  • Edema
  • Hyperglycemia (no hx diabetes)
  • Altered LOC
  • Mental status changes
  • Increase in WBC, bands
  • Low SVO2
  • High lactic acid
  • Increasing creatinine

Nursing Interventions and Rationales

  1. Prompt lab draws
    • Labs in sepsis diagnosis and treatment are very time sensitive. It is imperative the nurse is drawing labs promptly, as this evaluates the effectiveness of treatment and determines next steps.
  2. Appropriate administration of IV antibiotics
    • Baseline blood cultures must be drawn prior to the initiation of antibiotics to ensure the appropriate pathogen is identified. Drawing the labs, then starting antibiotics as ordered is the nurse’s responsibility.
  3. Optimize fluid-volume status
    • Patients suffering from sepsis usually require massive fluid resuscitation.
  4. Assess, monitor, and optimize cardiac output
    • Cardiac output is typically compromised in sepsis. The nurse must communicate with the MD about this and how to treat it, as some may need more fluid, or vasopressors, or both. Non-invasive cardiac output monitoring (NICOM) or central venous pressure monitoring (CVP) are options.
  5. Assess, monitor, and support oxygen status
    • Septic patients may need significant respiratory support, depending on severity. Oxygen delivery and utilization is severely impaired, therefore the nurse must assess frequently (ABG’s, SpO2) and work with medical team on interventions
  6. Prevent infection
    • This patient already has a heightened inflammatory response, we don’t want to make it worse with another pathogen. Asepsis is KEY with all patient care but in particular the septic patient. Frequently septic patients will require a central venous catheter and foley catheter. These are invasive lines that can easily get infected but are necessary when a patient is that ill.
  7. Assess, monitor, and manage body temp
    • Their body temp may be high or low, and we want to warm them if they’re too cold (increase room temp, warming blankets) or cool them if their fever is too high (antipyretic, cooling blanket, decrease room temp). Many septic patients with fluctuating body temps may have continuous temperature monitoring (via foley, rectal tube, or endotracheal tube)
  8. Communicate with and educate patient and loved one
    • Sepsis is serious and scary. It is essential to educate the patient and their support system at every step of the way so they are able to let you know if they feel/act differently, if things change, and also to prevent them from unnecessarily worrying or interfering with very needed interventions.

Pathophysiology

A stroke is essentially a neurological deficit caused by decreased blood flow to a portion of the brain. They will be classified as either hemorrhagic or ischemic. An ischemic stroke is the result of an obstruction of blood flow within a blood vessel. A hemorrhagic stroke is when a weaken blood vessel ruptures and blood spills into the brain where it shouldn’t be. Both of these can cause edema and cellular death. Lack of blood flow for greater than 10 minutes can cause irreversible damage.

Etiology

Various things can cause an ischemic stroke, which comprises approximately 85% of all strokes. Some of those who are at highest risk are those on anticoagulation therapy. People are on anticoagulants therapy for various reasons (mechanical heart valves, atrial fibrillation, etc.) and if they become sub therapeutic and therefore their blood is too thick, a clot can easily form and end up in the brain, causing an ischemic stroke. Diabetes is also one of the major risk factors, in addition to atherosclerosis, hypertension, cardiac dysrhythmias, obesity, substances abuse, and oral contraceptives. Hemorrhagic strokes (the remaining 15% of strokes) can be caused by an aneurysm rupture (which are very difficult to predict… frequently noted increased incidence in smokers, drug abuse, and people with family history of a first-degree relative with one), high blood pressure, or the rupture of an arteriovenous malformation (which is genetic).

Desired Outcome

Restoring as much blood flow as possible as quickly as possible, and minimizing cellular death/damage is key. Clot-busting meds can be given to restore blood flow for ischemic strokes. Hemorrhagic strokes are managed by keeping the blood pressure controlled, controlling intracranial pressure, reversing any anticoagulants on board, and even very invasive procedures or surgery to relieve increased intracranial pressure. You want the patient to gain back as much function as possible. This is done slowly over time by the brain creating collateral circulation around the infarcted area. Physical, occupational, and speech therapy are essential aspects of stroke recovery. Some patients may make a complete recovery, while others may have profound deficits.

Subjective and Objective Data

Subjective Data
  • Numbness
  • Tingling
  • Decreased sensation
  • Difficulty swallowing
  • Headache
  • Pain
  • Nausea
  • Dizziness
Objective Data
  • Hemiparesis
  • Hemiplegia
  • Ataxia
  • Dysmetria
  • Facial droop
  • Paralysis
  • Aphasia
  • Dysphagia
  • Dysarthria
  • Vomiting
  • Increased secretions
  • Incontinence
  • LOC changes

Nursing Interventions and Rationales

  1. Use assistive ambulatory devices
    • Facilitates ambulation/transfers safely
  2. Frequent neurological assessments (per orders)
    • Alerts nurse to neurological changes as early as possible, enables them to notify MD and intervene when needed
  3. HOB at 30 degrees unless otherwise indicated
    • Increases venous return, decreases ICP
  4. Initiate DVT prophylaxis (mechanical and/or chemical)
    • Decreases risk for subsequent stroke, as patient most likely will not be as mobile as they are at baseline
  5. Ensure PT/OT/ST is ordered
    • Rehab is essential in stroke recovery; all must complete a baseline assessment and provide recommendations
  6. Fall prevention measures (non-skid socks, bed in lowest locked position, call bell within reach, and so forth)
    • Injury prevention; patient will most likely not be able to ambulate as they could prior to stroke and will require assistance
  7. Prevent contractions
    • Extremities that are now paralyzed are at risk for becoming contracted; ensure pillow supports are in place as well as rolled towels and adaptive devices
  8. Prevent aspiration: follow ST recommendations, keep HOB at 45 degrees during oral intake and keep patient upright after a meal, have suction available, assess lung sounds and body temp
    • Stroke patients frequently have impaired swallowing, and are at high risk for aspiration from their own oral secretions and oral intake.
  9. Cluster care; promote rest
    • Maximizes time with the patient so they can rest when care is not being provided
  10. Monitor vital signs appropriately; know BP limits
    • Closely monitoring BP is essential in managing ICP
  11. Prevent edema: elevate limbs, utilize compression stockings, promote ambulation, promote complete bladder emptying
    • Patients who are in bed more will have a harder time clearing fluid out, especially if they have any underlying heart condition causing a decreased cardiac output (like atrial fibrillation)
  12. Promote self-care
    • Patients will have a decreased ability to care for self due to new deficits; promote confidence and participation in caring for themselves as much as possible
  13. Promote cerebral tissue perfusion (interventions per orders, as this can differ depending on kind of stroke, location, and other factors)
    • This prevents additional neurological damage
  14. Facilitate safe swallowing: ensure bedside swallow screening completed and/or speech therapy assessment prior to oral intake
    • Frequently, brain injury results in an impaired ability to swallow safely. This is not always apparent as patients don’t always cough when aspirating and have silent aspiration.
  15. Promote adequate nutrition
    • Once a patient is cleared to eat, do what you can to encourage appropriate intake… as patients cannot heal if they don’t eat
  16. Initiate discharge planning
    • Stroke patients typically require multiple needs at discharge (follow up appts, rehab/therapy, and may need to go to long-term care or inpatient rehab, depending on the situation) begin getting your mind around their discharge needs at the beginning even if it’s not clear yet what their needs will be
  17. Prevent skin breakdown: turn q2hrs, ensure adequate protein intake, off-loading, pillow support, keep linen clean and dry
    • There are many reasons why a stroke patient will be at risk for skin breakdown… from an inability to feel or move extremities, incontinence, inability to communicate needs/pain/discomfort, decreased nutritional status.
  18. Facilitate communication; promote family coping and communication
    • Having a stroke is a major life event. Roles within families and support systems may change, especially if the patient played a caregiving role within their family structure

Pathophysiology

Syncope is essentially a loss of consciousness, which is typically caused by hypotension. The brain lacks adequate blood flow and a temporary loss of consciousness results.

Etiology

Syncope typically has a cardiac etiology, but can also be due to many other things (like a side effect from a med, neuro issue, psych issue, or lung problem). When a cardiac etiology is suspected, a cardiac workup is completed. This typically includes cardiac monitoring, labs, and routine vital signs (specifically blood pressure and heart rate).

Desired Outcome

No additional syncopal events, no injury, identification of cause and treatment to prevent further episodes

Subjective and Objective Data

Subjective Data
  • Nausea
  • Feeling cold, clammy, or warm
  • Tunnel vision
  • Blurred vision
Objective Data
  • Vomiting
  • Loss of consciousness
  • Arrhythmias
  • Hypotension
  • Pallor
  • Bradycardia
  • Confusion/disorientation

Nursing Interventions and Rationales

  1. Prevent injury (nonskid socks, doesn’t walk without assistance, bed in lowest locked position, necessary items within reach, call bell within reach, side rails up x3)
    • Sudden loss of consciousness puts patients at a higher risk for falls and injury, therefore it would be prudent to be with the patient when OOB
  2. Educate patient to change positions slowly
    • This enables the blood pressure to accommodate to position changes and hopefully prevent future episodes
  3. Reevaluate medications, review any that may cause syncope with MD
    • BP meds may need to be spaced out, or dosages may need to be adjusted; discuss
  4. Monitor for changes in level of consciousness.
    • Monitor appropriately and notify MD if needed, promote safety
  5. Promote adequate fluid intake
    • Prevents worsening hypotension

Pathophysiology

Infection within the genitourinary system, which then causes inflammation. The urinary tract is sterile above the urethra and pathogens gain entrance via the perineal area or the bloodstream.  When these pathogens enter this sterile environment, infection ensues.

One can acquire an infection in the bladder itself (cystitis), or the an infection in the urethra (urethritis), which is essential a urinary tract infection.

Etiology

Females are most prone to UTI’s due to their natural anatomy. Females have a shorter urethra and it has a close proximity to the anus (and therefore e. Coli, which is normally found in the GI tract). Males become more susceptible as they age due to urinary stasis. Urinary catheter use (particularly indwelling) significantly increase the risk for a UTI, sexual intercourse, certain birth control methods (spermicide, diaphragms), blockages in the urinary tract, abnormalities in the anatomy of the urinary tract, or a suppressed immune system can all increase the risk for a UTI.

Desired Outcome

Resolution of infection, restoration of normal bladder functioning

Subjective and Objective Data

Subjective Data
  • Painful urination
  • Burning
  • Lethargy, urinary urgency, pelvic pain, chills, back pain
Objective Data
  • Malodorous urine
  • Dark/cloudy/discolored urine
  • Sediment or pus in urine
  • Sediment in urine
  • Altered mental status
  • Positive urine culture
  • Increased WBC
  • Increased frequency
  • Fever
  • Discharge
  • Nausea and vomiting

Nursing Interventions and Rationales

  1. Assess pain, Assess urine color, clarity, odor Assess mental status Assess body temperature
    • Must obtain baseline assessment data
  2. Discontinue indwelling catheter if applicable
    • May be source of infection
  3. Draw appropriate labs (CBC, UA)
    • Identifies infection, follow ups can show if treatment is effective
  4. Encourage increased fluids (start IVF if necessary)
    • Increased urinary output helps flush out bacteria
  5. Promote routine voiding
    • Taking the patient to the bathroom on regular intervals will help facilitate emptying the bladder completely
  6. Educate on proper perineal cleansing techniques to decrease risk of infection
    • Improper wiping can cause infections
  7. Administer meds as ordered (antibiotics, antispasmodics, analgesics)
    • Decreases discomfort and kills bacteria causing infection