Med Surg FINAL REVIEW

LAB values WBC → 5000-10,000

Glucose → 70-110 RBC → 4.7-6.1 (M); 4.2-5.4 (F)
K → 3.5-5.0 Hgb → 14-18 (M); 12-16 (F)
Na → 135-145 Hct → 42-52 (M); 37-47 (F)
Ca → 9.0 -10.5 Platelets → 150k-400k
Mg → 1.3-2.1 PT → 11-12.5
Albumin → 3.5-5.0 aPTT → 30-40
BUN → 10-20 INR -> 0.9-1.2
Creatinine → <1.3 (anything over is a bad kidney)
pH → 7.38 Write any other lab values yall think of
GFR → 60
ICP
Gout is at the end btw

1
Respiratory

2
Chest Tube Care of Patient
What is it? To re inflate the lung, as well as drain fluid / air 1. Occlusive dsg and Petroleum gauze
What conditions need use of chest tube? Pneumothorax or a hemothorax that 2. Connected to low suction
need to move the fluid or air that is disrupting normal lung function; inserted 3. Subcutaneous emphysema ( crackling sensation)
into pleural space in most pt’s w/ penetrating wounds of the chest to achieve 4. Sterile technique
rapid & continuing expansion of the lungs 5. Encourage cough, deep breathing, incentive spirometer
6. Monitor amt/color of drainage (is it clear or blood?)
Problems with Ventilator and Solutions 7. Keep Drainage system below chest and make sure Connections tight/taped
- low pressure alarm → usually due to a leak in the circuit 8. “Milk” tube clots
- could be a disconnected tube → connect a bag quickly 9. Resp. assessment
- Attempt to find the problem and if problem CANNOT be fixed bag pt 10. No kinks in tubing
and call your respiratory therapist
- high pressure alarm → caused by a kink in the tubing
- A blockage in the circuit (water condensation)
- Pt is biting on the tube
- Mucus plug →attempt to fix the problem OR bag the pt and call RT

Ventilator Nursing Management

1. Assist-control ventilation (AC)OR (CMV) → Most often used; volume and rate a. Monitor and evaluate response to ventilator
are preset b. Assess VS, breath sounds → Q30 minutes at first
2. Synchronized intermittent mandatory ventilation (SIMV) → Allows c. Monitor pulse oximetry, ABG values
spontaneous respirations (pt can gradually resume breathing work) d. Prevent Infection/pneumonia
3. Bi-level positive airway pressure (BiPAP) → delivers positive pressure air on e. Assess ETT Q2H → Whenever pt is moved, Note secretions: type, color,
inhalation and exhalation amount, Note skin: color, tenderness, skin irritation
4. Continuous positive airway pressure (CPAP) → delivers positive pressure air f. Meet communication needs of client
on exhalation for spontaneous breathing; Allows alveoli to stay open/prevents g. Manage the ventilator system safely
collapse h. Perform and document ventilator checks according to the institution
5. Positive end-expiratory pressure (PEEP) i. Check the amount of fluid in humidification bottle
- Increases pressure at expiratory phase Increases gas exchange; Prevents j. Check temperature level
atelectasis k. Remove any excessive secretions in tubing
- Disadvantage: prolonged use with increased FiO2 = O2 toxicity l. Maintain sterility
m. All alarms must be functional at all times 3
n. High & Low Pressure
TB Manifestations
What is it? An infectious disease that is cause by the mycobacterium tuberculosis - Symptoms 2-3 weeks post infection, Dry cough –secretions
that can affect the lung, brain, kidney, bone; CDC 2 billion /world TB - Fatigue, Anorexia, wt. Loss. Low grade fever , night sweats, Flu symptoms
At Risk - Crackles, SOB late symptom, Hemoptysis
- HIV, Minorities, Homeless, IV drug abuse, Underserved, Foreign born Diagnostics
How is it spread? Spread via Airborne talking, coughing, breathing, sneezing 1. Tuberculin skin test (TST)
Patho → Lodge in bronchioles causing inflammation 3. Mantoux Test
Complications → Lung scarring and It can affect other organs 4. Purified Protein Derivative (PPD) → Implanted intradermal forearm; Results 48-72
Classification hrs by inspection/palpation
Primary TB - have organism no disease (when bacteria inhaled) **Induration + TB exposure** → induration of >10 mm diameter (+) exposure
Latent TB - Positive skin test / infected with Mycobacterium Tuberculosis / no active 5. CHEST XRAY (not only chext x ray) (Upper lobe infiltrates
TB / not infectious / no symptoms 6. Sputum specimens → 3 specimens / 3 days early morning
- Can develop at any time 7. Sputum culture and smear for Acid Fast Bacillus (AFB) which takes 8 weeks for
- Has TB bacteria that are alive, but inactive results so Start treatment if suspected
Active TB - individual infectious (+) chest x ray, (+) Sputum Patient is in airborne isolation, negative airflow room, negative pressure, N95
a. ISOLATE PT IF SUSPECTED UNTIL RULED OUT

Treatment Nursing management

ACTIVE TB / DRUG Therapy Health promotion
1. Initial Phase → 2 months / 8 weeks Isoniazid (INH) QD, Rifampin QD - Screening programs for high risk , Treat latent TB, Report to public health dept.
Pyrazinamide QD and Ethambutol QD - If positive TST → need chest x ray & sputum for active TB
2. Continuous Phase → Isoniazid (INH) & Rifampin QD X 18 wks Education
Latent TB - Cover mouth / nose, HAND WASHING, Wear mask if out of room, Minimize
Isoniazid QD X 9 months → Prevention of active TB visitors, Screen close contacts
Decrease risk factors → Like drug/ETOH abuse, smoking, HIV, malnutrition
Adverse Effects of Meds Care After
- Infectious 2 weeks after treatment starts - Negative sputum culture is needed before pt noninfectious; pt should sleep alone and
Strict adherence or else there could be a relapse avoid public settings/travel
- SE → avoid ETOH/hepatotoxicity/hepatitis - Adherence to drug therapy
- Rifampin SE → orange color sputum, tears, and urine - Adequate tx → negative cultures, full course of meds, clinical & x ray improvement
- Smoking cessation
- Teach symptoms of relapse if not compliant with meds 4
COPD Complications of COPD
What is it? A progressive disease affecting your lungs and the ability to breathe; 1. Cor Pulmonale → body is trying to compensate and this leads to RSHF →
the airway becomes thick, inflamed along with increased mucus and damage to more blood is now being back up causing edema
the alveoli 2. Pulmonary Hypertension
Risk Factors
3. SOB, Crackles or decreased LS,
1. Cigarette smoking
2. Second hand smoke 4. Use of accessory & intercostal muscles,
3. Occupational chemicals and air pollution 5. Rt sided HF → body tries to increase amount of blood going to the lungs and it
4. Infection causes the RS to overwork and it can lead to failure
5. Genetics - Antitrypsin deficiency - distended neck veins → blood gets stuck in the vena cava and it can back
6. Aging up to the neck veins
7. Asthma - Edema→ excessive fluid retention
- Wt gain → fluid retention leads to wt gain

Stabilize COPD Treatment

1. Keep up to date on immunizations → Flu Vaccine and Pneumonia Vaccine - Bronchodilators
2. Smoking cessation - Diuretics,
3. Bronchodilators PRN
- O2 low flow b/c too much oxygen will reduce the pts drive to breath
4. Albuterol, combivent
5. Spiriva

5
Shock

6
Anaphylactic Shock
What is it? A severe allergic reaction. Massive vasodilation: the third spacing of fluids
due to the massive vasodilation and increased capillary permeability.
There are three defining characteristics:
1. Acute onset of symptoms
2. Presence of 2 or more symptoms that includes respiratory compromise, reduced BP,
GI distress, and skin/mucosal irritation
3. Cardiovascular compromise from minutes to hours after exposure to the antigen
What Causes Anaphylactic Shock?
An allergic reaction to: Foods (especially peanuts), meds, or Insect stings & bites
Nursing Management of Anaphylactic Shock
- assess all patients for allergies or previous reactions to antigens and communicate
patients allergies to other
- find out how much the patient knows about their previous reactions and what they
did to help solve these reactions and what the patient will do to prevent further
exposure to antigen
- advise patient to wear allergy bracelet/identification
- observe for allergic reaction when giving new meds
- if patient says they’re allergic to a med, be aware of risks involved in new meds you
may give
- identify patients at risk to dye like substances that contain iodine
- know s/s of anaphylaxis and give family edu on anaphylaxis
- administer epi IM
S/S of Anaphylactic Shock ( present from 2-30 min of exposure to the antigen)
- lightheadedness, anxious, confused
- swelling lips, tongue, pruritus, erythema, generalized flushing
- chest pain and feeling of impending doom
- dyspnea (laryngeal edema), bronchospasm
- cardiac arrhythmias and hypotension (due to the vasodilation of the vessels)
Medical Management of Anaphylactic Shock
- remove the causative antigen
- EPINEPHRINE: IM: GIVEN TO VASOCONSTRICT
- DIPHENHYDRAMINE (Benadryl): IV; REVERSES THE EFFECTS OF
HISTAMINE AND REDUCE CAPILLARY PERMEABILITY
- ALBUTEROL: NEBULIZER TO REVERSE BRONCHOSPASM
- CPR for cardiac/respiratory arrest, endotracheal intubation to establish airway
- IV lines inserted to provide access for administering fluids and meds
Obstructive Shock → physical Obstruction of blood
Can cause → decreased CO & increased afterload
Manifestations → resp distress, tachycardia, hypotension, chest pain, tachypnea
Causes
- Cardiac tamponade, tension pneumothorax
- Pulmonary embolism
Stages of Shock (CPI) (if one stage is not corrected it will move on to the next)
1. Compensatory → increased HR, increased RR, skin cool clammy,
2. Progressive stage → decreased BP, increased HR, weak pulse, cool clammy,
hypothermia/hyperthermia
3. Irreversible stage → LOW BP, LOW CO, bradycardia, hypoxemia, pupils
dilated, hypothermic, RECOVERY IS UNLIKELY AT THIS STAGE → organ
failure one by one
7
Septic Shock
What is it? It is the most common type of distributive shock. It is caused by a
widespread blood-borne infection that overwhelms the body or sepsis; The
mortality rate is 28-50%; Do a quick assessment if you suspect shock
What Causes Septic Shock?
HAI’s that originate in the bloodstream (bacteremia), lungs (pneumonia), and
urinary tract (urosepsis). Other infection include intra-abdominal infections and
wound infections and Urinary catheter
INCREASED RISK OF
- increased use of invasive procedures
- indwelling medical devices
- Aging population due to the aging immune system
- patients who are undergoing surgical or invasive procedures
- malnutrition patients
- immunosuppressive patients
Diagnostics of Septic Shock
- positive blood cultures
- WBC high or low, High glucose levels, Low sodium, low platelets b/c of clots
- High lactate levels (normal is 0.5-1.0 mmol/L)
- High Specific gravity (dependent on the kidney function)
Medical Management of Septic Shock
- Correction of Underlying Causes → remove urinary catheter; collect specimens
of blood, sputum, urine, wound drainage, and tips of catheters
- Fluid Replacement Therapy
- Pharmacologic Therapy → unknown infection will be treated with
broad-spectrum antibodies until culture report is received
- nutritional therapy → give aggressive supplementation within 24-48 hrs
Pathophysiology Of Septic Shock
Gram-negative bacteria traditionally were the most common but now there is an
increased incidence of gram positive bacterial infections, viral infections, and fungal
infections. Microorganisms invade the tissues, and causes the SYSTEMIC
INFLAMMATORY RESPONSE SYNDROME which is basically increased capillary
permeability and vasodilation which decreases tissue perfusion. Because of SIRS, it
activates the coagulation system which forms clots whether or not bleeding is present
which results in microvascular occlusions and an inappropriate consumption of
clotting factors.
3 EFFECTS
1. Vasodilation
2. Maldistribution of blood flow
3. Myocardial depression
Septic Shock Manifestations → ULTIMATELY LEADS TO MOD AND DEATH
- hypotensive, tachycardia, tachypnea
- hyperthermia and fever with warm flushed skins and bounding pulses
- UO decreases
- altered mental status such as confusion or agitation
- lactate level is increased due to the maldistribution of blood
- WBC count is elevated
- Respiratory alkalosis (because of hyperventilating) then resp acidosis (because
of the increased levels of CO2 and increase in PH)
- As sepsis progresses the skin becomes cool, pale and mottled.
Nursing management
- careful hand hygiene for invasive procedures; monitor IV lines, infection control;
8
identify pts at risk for sepsis
Cancer

9
Radiation Surgery → can include removal of tumor and some tissue nearby to get rif o the
What is it? It be used alone, w/ chemotherapy/surgery & effects tissues within field tumor
Types of Radiation
1. External radiation (Teletherapy) → most common radiation; It uses high-dose Radiation can be used alone, w chemo, or surgry
radiation to destroy cancerous cells or shrink tumors.
- During an EBRT procedure, a machine directs external beams of radiation into
cancerous areas inside your body with extreme precision. This method helps
reduce damage to healthy tissues.
Care for Patients Undergoing Teletherapy
1. Do not remove markings during treatment time
2. Wash gently with water alone or mild soap; Rinse soap thoroughly
3. Pat skin dry rather than rubbing; Use clean towels
4. Avoid direct exposure of the skin to the sun; Avoid heat exposure
5. Wear soft, cotton, loose clothing; No belts near radiation site

2. Internal radiation (Brachytherapy) → insertion of radioactive material into Precautions with Brachytherapy (PTS ARE RADIOACTIVE)
tumor or near tumor so it involves minimal exposure to healthy tissue by 1. Private room with a private bath
implants of seeds, rods or wires 2. Place “caution radioactive material” sign on the door of pt’s room
- Used for prostate, breast, head and neck, cervical cancer and uterine cancer, lung 3. Wear dosimeter badge (will tell how much nurse has been exposed)
cancer, rectal cancer, eye cancer, bladder cancer and skin cancer 4. Visitor precautions → no more than 30 min per day; 6 feet away (LIKE
Nursing Care with Brachytherapy COVID)
- Temp implants – radioactive only when source is in place 5. Never touch the radiation source with bare hands
- Permanent implants – have short half life exposure is low 6. Save all linens, dressings in pt’s room until radiation is removed then dispose
of it
Adverse Effects of Chemotherapy & Radiation Therapy and Related Nursing Care 7. Wear special protective clothing
a. Systemic: Altered Taste Sensation 8. No pregnant staff should be assigned to pt
b. Hypogeusia – decreased taste 9. Radiation safety office checks pt and room for radiation levels daily, using a
c. Dysgeusia – unpleasant taste meter
d. Ageusia – without
e. Mucositis/stomatitis
10
f. Xerostomia
Cardiac

11
Angina → episodes of pain in the anterior chest that are caused by insufficient
coronary BF which results in decreased oxygen while there are increased
demands for oxygen. The demand for oxygen is due to physical activity/stress.
Pathophysiology of Angina → When there is an increase in demand for oxygen, the
flow for coronary arteries needs to be increased. When there is a block in the coronary
arteries the demand for oxygen cannot be met, causing pain.
What Causes Angina?
- physical exertion, stress/emotional stress, eating a heavy meal
- exposure to the cold, stimulants like cocaine and amphetamines
- CA can go into spasms, accumulation of plaque in the arteries & decrease in BF
Types Of Angina
1. Stable Angina:predictable pain that occurs on exertion;relieved by rest /NTG
2. Unstable Angina: happens at random times, is more severe, may not be
relieved by rest or NTG
Assessment & Diagnostic Findings
- PQRST- when did it start? What were you doing when it started? Did you take any
medication to help the pain? Did the pain subside? Can you rate it on a scale of 1-10?
Has the pain spread anywhere else?
- 12-lead ECG → may show changes indicative of ischemia (T-wave inversion,
ST-segment elevation, abnormal Q-wave)
- Lab test for cardiac biomarkers to rule out ACS such as myoglobin, troponin
- Stress Test: patient does something to exert stress on heart and the heart is monitored
on the ECG, echocardiogram
- EBCT (electronic beam)
- CAT Scan (expensive): it gauges the amount of plaque in the arteries
- Chest X-RAY: to see if heart is enlarged
Clinical Manifestations of Angina
- choking or heavy sensation of the chest & the feeling of impending doom
- may radiate from the sternum→ to the jaw→ to the shoulder→to the left upper arm
- heavy choking/strangling sensation- crushing chest pain
- the feeling of weakness or numbness in the arms, wrist, hand
- SOB, pallor, diaphoresis, lightheadedness, nausea, vomiting (REMEMBER
WE’RE HAVING LACK OF O2 SO IT WILL AFFECT BREATHING)
Nursing Interventions for Angina
- have patient stop all activities and have them sit or rest in bed
RATIONALE: to reduce O2 requirements of the ischemic myocardium
- ask if this angina is the same this patient typically experiences
RATIONALE: if it is not, it could be indicative of something worse
- Give NTG up to 3 doses if pain unchanged, you will monitor BP, HR, and ECG
- administer 2L of O2 through Nasal Cannula
*IF THESE DON’T WORK, PATIENT WILL be EVALUATED FOR ACUTE MI*
Pharmacologic Therapy
1. NTG- vasodilator: improve BF to heart muscle & relieve pain → decreases O2
demand & chest pain (check BP before giving, headache & dizziness is a SE)
2. Beta-Blockers- metoprolol- blocks the beta-adrenergic stimulation to the heart.
3. ACES/ ARB- lisinopril, losartan- will further vasodilate vessels & decrease the
workforce of the heart
4. Calcium Channel Blockers: amlodipine and diltiazem- decrease the conduction
resulting in slower HR & a decrease in strength of myocardial contraction
5. Antiplatelet & Anticoagulant Med:Aspirin, Plavix - prevents platelet aggregation &
subsequent thrombosis which impedes BF through the CA → keeps blood thin
6. O2 Administration: increase the amount of oxygen to increase O2 to myocardium
and decrease the pain 12
7. Lipid Lowering Drugs- Crestor, Lipitor
STEMI
What is it? The patient has ECG evidence of acute MI with characteristic
changes in two contiguous leads on a 12-lead ECG (ST- elevations). In this type of
MI, there is significant damage to the myocardium. *THIS IS AN EMERGENT
SITUATION*
TX: GET PT TO CATH LAB STAT & OPEN THE VESSEL IN 90 MIN FOR A
PCI; IF CATH LAB IS NOT NEAR OR TOO FAR AWAY, TREATMENT WILL
BE THROMBOLYTIC THERAPY WHICH WILL DISSOLVE THE CLOTS
Manifestations
- chest pain, SOB, not relieved by rest, sudden onset of pain, heaviness and
tightness in chest
- note what the pt was doing when it started; were they digging a ditch or were
they relaxing on the recliner?
ECG → know diff rhythms and what interventions to do (no strips on exam)
Sinus Bradycardia → give atropine (increase HR); pacemaker if not corrected
Sinus Tachycardia → treat the cause
SVT → non-drug tx 1st (valsalva maneuver/bear down); adenosine (consent, dr at
beside, crash cart available, pt is on EKG); electrocardioversion (baby shock)
*CARDIOVERSION IS NOT DEFIBRILATION*
A-fib/A-flutter → anticoagulants, beta-blockers, cardioversion digoxin
V-Tach → PULSE (give amiodarone and then cardioversion) NO PULSE (start CPR
stat until defibrillation, than give epi and follow cardiac arrest protocol)
V-Fib → immediate defib (if not available give CPR), epi, ACLS protocol
Asystole → start CPR stat, call code, grab crash cart; get IV access; deliever advanced
cardiac life support drugs (epi); vasopressin) squeeze blood to heart)
*NO PULSE IN ASYSTOLE = NO SHOCK WITH DEFIB; UNTIL CPR IS DONE
& A SMALL PULSE, THAT IS WHEN YOU WILL DEFIB THE HEART
PCI→ TO OPEN THAT OCCLUDED CA & PROMOTE REPERFUSION TO
THE AREA WITHIN 90 MIN
- THROMBOLYTICS: RETAVASE, ACTIVASE, TNKase (TPA)- initiated
when primary PCI is not available/ transport time to the PCI-capable
hospital is too long; given within 30 min/IV (dissolve thrombus in the CA
→ increase BF & infarction is minimized)
*if a patient has active bleeding, history of stroke, bleeding disorder, recent
surgery or trauma, uncontrolled hypertension or pregnant, WE WILL NOT DO
THIS THERAPY UNDER NO CIRCUMSTANCE*
Pacemaker
What are they used for? → they are used to pace the heart when the normal
conduction pathway is damaged through the use of pads.
*if client has pacemaker, you will see the pacemaker spikes on the ECG*
- usually used with coronary bypass patients just in case
- clients who have sinus bradycardia at the bedside till they can get a
permanent one
How Does It Work?
- if the HR falls below the rate it’s set at, it will beat the heart for the
patient
13
Surgery
1. Cardiac Catheterization → thread catheter through femoral artery to the
coronary arteries and put dye to see if there are any occlusions
PROBLEMS: → Death, Acute MI, dysrhythmias (usual), stroke (check neuro status
prior), Bleeding, Hematoma, vascular injury, pulmonary edema, air/clot embolism
- contrast induced nephrotoxicity: make sure kidneys are functioning by
checking the BUN (10-20mg/DL) and Creatinine Levels (0.6-1.2 mg/DL)
→ if they are high they are not functioning
- allergic reactions/ anaphylaxis- if they’re allergic premedicate with
antihistamines
PREOP FOR CARDIAC CATH
- NPO 6 hours, neuro baseline
- Consent and clip/prep femoral or radial area
- neuro baseline, allergies, renal status
POST-OP FOR CARDIAC CATH
- lay flat (femoral) - check distal pulses every hour, cap refill, temperature
- check neuro status, check site for bleeding or hematoma
- check for retroperitoneal hematoma with CT or ultrasound→ can go
undetected→ s/s is hypotension and flank pain
- anticoagulants after surgery to prevent clots
PCI → IF 70% + OCCLUDED- put a catheter through the coronary artery and
thread it. The balloon blows up to open up the clot & the stent is left in place to
have the BF run through. With these stents, they have chemotherapy medications
that will avoid the platelets from occluding that area )Drug Eluting stents)
-we give Aspirin and plavix post procedure to thin out the blood
*IF THERE IS A 3 VESSEL DISEASE/ LEFT MAIN→ SURGERY CABG
WILL BE PERFORMED AND IT WILL BYPASS THE CA IF ALL THREE
ARE OCCLUDED*
CABG → (coronary artery bypass graft) a surgical procedure in which a blood
vessel is grafted to an occluded CA so that the blood can flow BEYOND the
occlusion
Bypass surgery → ST elevation MI → 3 or more vessels occluded → rather than
put in stents then they do a bypass graft (use mammary artery to bypass where
the obstruction is)
What Are the Indications of a CABG?
1. Alleviation of angina that can’t be controlled with medication or PCI
2. Treatment for left main coronary artery or three-vessel disease
3. Not a candidate for PCI (blockages are long or difficult to access)
4. Failed PCI with ongoing chest pain 14
5. CA have to be at least 70% occlusion/at least a 50% occlusion in left main CA
Diabetes

15
Hypoglycemia → too much insulin < 70mg/dl DKA → occurs when Serum glucose > 250mg/dl
Hypoglycemic unawareness : no symptoms, unaware of hypoglycemia until critical; Ketosis, Acidosis, dehydration and usually occurs with Type 1 DM
Low blood glucose Causes:
At risk: frequent episodes, older, on beta blockers - Deficient Insulin, inadequate Insulin dose
S/S - Illness, infection
- Cold / clammy skin; ncreased heart rate - Under diagnosed Type 1 DM
- Headache; Nervousness / dizziness - Poor management, neglect
- Unsteady gait/ slurred speech Clinical Manifestations
- Hunger - Dehydration (glucose make you urinate alot), Poor skin turgor; Tachycardia,
- Changes in vision; Sz, coma low B/P
**COLD AND CLAMMY YOU NEED SOME CANDY** - Lethargy, weakness
CAUSES - Abdominal pain N, V
- Too little food or Too much insulin
-Ketones in the urine
- Meds at wrong times
- Increased exercise/Loss of wt - Kussmaul breathing ( rapid deep, then labored)Acetone on breath fruity odor
- Use of beta blockers Laboratory Finding
- ETOH without food - Glucose > 250mg/dl
- Ph < 7.30
- Serum bicarb < 16meq/L; Moderate to large ketones in urine

Rule Of 15 DKA / CARE

IF BG < 70 mg/dl - Fluid and electrolyte replacement
- 15 grams fast acting carbohydrate 4-6 oz fruit juice, soda, gels, tablets avoid - IV access 0.45% /0.9% N/S
fats ice cream whole milk
- D5W may be used to prevent hypoglycemia
- Recheck BG 15 mins
- BS < 70 repeat and recheck in 15 mins - Potassium level before insulin given
- Contact MD if no response after 3 Xs - IV REGULAR Insulin 0.1U/kg/hr by infusion
Acute Setting Treatment :
- IV D 50%
- Glucagon 1 mg IM or SQ 16
- Glucose gel
Endocrine

17
Goiter → It is an enlargement of the thyroid gland with benign tumors. It can Thyroidectomy → removal of thyroid gland; manipulation of the gland can
cause overproduction or underproduction of the thyroid hormone which can cause them to have a thyroid storm
result in hyperthyroidism or hypothyroidism. 1. Surgery Thyroidectomy: client will need to go on thyroid hormones for life
What Causes Goiter? (Hormone replacement of synthroid when we have a complete thyroidectomy)
1) Iodine intake is deficient (iodized salt, broccoli, cabbage, kale, peanuts) 2. Subtotal Thyroidectomy: client will have partial thyroid gland removed
2) Autoimmune where there is TSH, T4, and thyroid antibodies Thyroidectomy Complications
Treatment of Goiter 1. Hypothyroidism: replace the hormones → ALWAYS want to have a trach at the
1) Surgery to remove goiter bedside and O2 just in case of this and the RR is depressed
2) Thyroid hormone to prevent further enlargement 2. Hypoparathyroidism: when they take the thyroid out they also take out these glands
(Tingling toes and fingers)
DON'T PALPATE B/C IT CAN INC SECRETIONS OF HORMONES AND LEAD 3. Watch out for signs of hemorrhage, infection
TO PROBLEMS 4. Damage to the laryngeal nerve causing vocal paralysis
5. LOOK FOR ANY SIGNS OF SPASTIC AIRWAY OBSTRUCTION
6. Lab work, Fluids, and Electrolytes

18
Cushings → is the excessive levels of corticosteroids due to chronic exposure
S/S of Cushing's Syndrome *primary a result of oversecretion of glucocorticoids
and androgens although mineralocorticoid may be be affected as well*
- Growth, MSK changes, Moon face; oilness of the skin and acne
- Obesity → Fatty buffalo hump in the neck, Heavy trunk, Relatively thin
extremities
- Thin fragile skin that is easily traumatized (do not use adhesives because we
will rip the skin and it can lead to formation of a peptic ulcer
- Bruises and striae, Slow healing of minor cuts, bruises
- Weakness , Osteoporosis, Kyphosis and backache
- Diabetes can develop → increase amount of glucose in the system if not
controlled can lead to Diabetes (they have a high glucocorticoid level which
produces glucoses)
SYMPTOMS GO AWAY AFTER RECEIVING TREATMENT
Treatment → depend on the cause and the severity of the symptoms
1. If it is caused by tumors from the pituitary rather than the tumors of the adrenal
cortex, treatment is directed at the pituitary gland it can be treated with surgery or
with radiation
- Adrenalectomy for adrenal tumors; Laparoscopic/open (it is open when malignant)
1. Post-Op → Symptoms of adrenal insufficiency may begin to appear 12-48
hours after surgery because of the reduction of high levels of circulating
adrenal hormones; Temp replacement therapy with hydrocortisone
- Insulin therapy → Blood glucose monitoring before and after surgery
- Drug Therapy to decrease the production of corticosteroids (Nizoral, Cytadren, &
Lysodren)
- Gradually (taper) discontinuing prednisone so they don’t go into addisonian crisis →
IV Solu Cortef → gives the necessary corticosteroids.
What Causes Cushing Syndrome?
1. Use of corticosteroid medications such as Prednisone
2. Excessive glucocorticoid production secondary to hyperplasia of the adrenal cortex
3. Tumor of the pituitary gland that produces ACTH and stimulates the adrenal cortex
to increase its hormone secretion despite production of adequate amounts
Diagnostic Findings of Cushing Syndrome
a) High Cortisol Serum Levels
b) Abnormal ACTH level levels
c) CT or MRI to rule out any tumors
Monitoring and Managing Potential Complications
Addisonian Crisis → High risk pt who is treated by withdrawal of corticosteroids, by
adrenalectomy, or removal of a pituitary tumor
Nursing Interventions for Cushing Syndrome
Maintaining Adequate Cardiac Function → Monitor for HTN & hypokalemia
Decreasing Risk of Injury → Establish protective environment to prevent falls
fractures and other injuries to bones and soft tissues; Foods high in protein,
Decreasing Risk of Infection → pt should avoid unnecessarily exposure to infection
Promoting Skin Integrity → avoid traumatizing pts fragile skin; no adhesive tape
Improving Body Image → Wt gain & edema modify w/ a low-carb, low-sodium, &
high-protein diet
Improving Coping → Patient and family education
Patient Education
- Inform that meds should not be stopped abruptly b/c it can cause a rebound effect
- compliance with medications
- Educate patients on wearing a medical alert bracelet 19
- Close monitoring of the adrenal function returning to normal
GI

20
PUD → Can affect the esophagus, stomach, or duodenum; it is a hollowed-out Manifestations
area that forms in the mucosa of the stomach 1. Gastric → High epigastric pain, Burning after meal & eating may increase pain,
Causes Pain on palpation of epigastric region
- H. Pylori (most common), Stress & Family hx , Smoking , Diet, Coffee, alcohol 2. Duodenal (D → decrease pain with food) (WORSENS AT NIGHT B/C IT TAKES
- NSAIDs → destroys the prostaglandins which will neutralize the acid when you TIME TO DIGEST)
have to much and destroys the protective gastric mucosa ) - Low epigastric pain below xiphoid process, Pain occurs 2 to 3 hours after meal,
Types Back pain, Bloating, N, V, Full feeling; relief w/ Antacids, H2 blockers, & eating food
1. Gastric Ulcers ( Less common and Occur in women over 50) Diagnostics Studies
2. Duodenal Ulcers (80% of ulcers and most commonly caused by H. Pylori) 1. Endoscopy to visualize stomach/duodenum
Conservative Therapy 2. Biopsy (to determine H. Pylori presence)
- Rest the GI tract, Drugs/No NSAID use, Smoking cessation/alcohol cessation 3. Barium Contrast is done to view obstruction (drink white chalky fluid and
- Modify diet and Stress management take x-ray)
Health Promotion 4. Gastrin level test to see how much acid they are producing
- Take NSAID’s with food to reduce irritation; Take meds as prescribed CBC (to determine extent of blood loss), liver enzymes, amylase, check stool (for
- Lifestyle changes(stress, smoking cessation, diet); Early detection, Teach S/S of occult blood)
PUD, Prevent reoccurence

Complications Drug Therapy

1. Hemorrhage → most common from duodenal & caused by an ulcer through a major
blood vessel ( Hematemesis & Melena; black tarry stool)
2. Perforation → high mortality rate **SURGICAL EMERGENCY**
- A deep whole in the stomach, Distention, rigid/firm abd, NO BOWEL SOUNDS;
Pt will have sudden upper abd pain to back
- Perforation can lead to bacterial peritonitis → sepsis → shock → death
3. Pyloric Obstruction → manifested by vomiting, edema and causes gastric dilation
- Relief obtained by belching/vomiting
-s/s Abd bloating and distention, N&V projectile, Constipation, dehydration, swelling
in stomach and upper abdomen
1. PPIs; drug of choice (it decreases bone density it can contribute spinal
fractures (prilosec, prevacid, aciphex, protonix, nexium)
2. H2-receptor antagonists → block histamine stimulate gastric secretion (can be
used for indigestion and heartburn) (Zantac, pepcid, axid)
3. Antacids → buffer gastric acid and prevent the formation of pepsin
4. Sucralfate → forms a protective layer in the intestine, esophagus, and stomach
5. Misoprostol → synthetic prostaglandin that protects the gastric mucosa from
agents that cause ulcers (NSAIDS/ASA)
(if h pylori is the cause → 2 antibiotics and a PPI for 7-14 days to prevent 21
ulcers/heal ulcerations/prevent recurrence)
PUD CONT
Nutrition Therapy is directed toward neutralizing acid and reducing hypermotility
1. A bland, non irritating diet is recommended during the acute symptomatic phase
2. Avoid bedtime snacks, hot spicy foods
3. Avoid alcohol, carbonated drinks, caffeine, tobacco
Acute Care PUD
- NPO to rest da tummy; an NG tube may be placed to relieve acids & give IV fluids
- Gastric pH testing, blood, bile → NORM pH is 1.5-3.5
- CBC; V/Ss, orthostatic BP (this can be a sign of bleeding/a shift in fluids)
- Rest and Pain meds (remember the goal is to relieve pain)
PUD Surgery
1. Partial gastrectomy → removal of half of stomach (causes the food to dump
straight out because we have removed half of the stomach)
2. Vagotomy → severing the vagus nerve to decrease gastric acid secretion
3. Pyloroplasty → surgery to widen the opening in the lower part of the stomach so
that contents can empty into the duodenum
Post-OP care
1. NPO/NG tube to decompress and rest tummy
(Aspirate NG tube for color, amount, odor and Irrigate to keep patent)
2. Check BSs and do abd assessment (pain, distention), V/Ss and I&Os
3. Pain meds, IV fluids and give fluids PO when tolerated
4. Splint the area, teaching deep breathing and coughing;
5. Check drainage for blood, odor, or infection
6. Pt may develop anemia (loss of intrinsic factor will cause malabsorption of vit b12)
Hemorrhage care
- Presence of blood in NG tube drainage (KEEP TUBE PATENT; if blood is present
in tube clots will form; irrigate!!)
Perforation
Manifestations → Sudden upper abd pain, Rigid abd, rebound tenderness, Increased
HR, RR, weak pulse , Absent bowel sounds
- NPO/NG tube feedings (always not drainage from NG tube and I&O
- Tx → Pain meds, antibiotics, surgery (emergency!!)
Obstruction
- NG tube → to decompress stomach
- IV fluids (check electrolyte levels)
Post-OP complications
1. Dumping syndrome → may occur as a result of any surgical procedure that
involves the removal of a significant portion of the stomach or resection of pylorus
- Manifestations → weakness, palpitations, dizzy, diaphoresis, abd cramping, loud
BSs and urge to defecate Lasts less than 1 hr
(Hypoglycemia (pancreas will release insulin in response to excess carbs)
THINGS THAT ARE A NO GO → No fluids with meals & No high carbs
2. Postprandial hypoglycemia → secondary hypoglycemia occurs w/ symptoms
approximately 2 hours after meals
- S/S → sweating, weakness, mental confusion, palpitations, tachycardia, and anxiety
3. Bile reflux gastritis → occurs following pyloroplasty because of the manipulation
of the pylorus (the pylorus prevents reflux of duodenal contents back into stomach)
- Epigastric pain after meals (vomiting DOES NOT provide relief) 22
Gastric Obstruction → Intestinal obstruction exists when blockage prevents the
normal flow of intestinal contents through the intestinal tract
Types of obstruction
1. Mechanical/physical obstruction → can be extrinsic lesions from outside intestines
or intrinsic lesions within intestines that can obstruct flow
- Hernias → A strangulated hernia is EMERGENT
- Adhesions
2. Nonmechanical → paralytic ileus → this is caused by abd surgery and handling of
the intestines (sometimes the nerve endings can be damaged and cause a decrease in
peristalsis causing obstruction)
Manifestations
1. Initial symptoms is pain that colicky; Constipation, no flatulence, dehydration
2. Abd pain, N, distention/firm/tenderness, abd rigidity, FEVER
3. Vomiting may turn malodorous with fecal smell (vomiting also causes
hypovolemia and loss of electrolytes → dehydration)
Treatment
1. Surgery is depending on the cause of obstruction
- Bowel resection (take a piece of intestines out)
- Colostomy → surgically creates an opening into the colon that diverts fecal
drainage into the abdomen via a stoma(could be temp/permanent)
Nursing care
1. Monitor fluid/electrolytes and monitor I&O
2. Monitor for shock or sepsis
3. Record vomitus (color, amount, fecal odor)

Peritonitis → “Hot belly” it is the inflammation of the lining of the abd cavity Management
Manifestations - Antibiotics (broad spectrum)
- Tachycardia, hypertension, dehydration, pain, decreased BSs, Fever - NGT to decompress tummy
- Rebound tenderness, Board-like abdomen, Abd pain, distention, & rigidity , N, - IV fluids to replace fluid and electrolyte
V - Pain meds and antimetics
- Movement aggravates pain - Surgery → to find out cause and clean abd
**peritonitis can lead to sepsis → shock → death and it can also lead to ARDS** Nursing management
Risk factors - Monitor pain level
- Abd surgery; Ectopic pregnancy; perforation caused by trauma, ulcer, appendix - Monitor I&O’s, electrolyte status
rupture, diverticulum) - Keep pt NPO/NGT (If NGT is in record amount of drainage and color)
Diagnostics - Monitor for signs of shock (hypotension)
1. CBC, WBC (increased) - Abd assessments 23
2. Abd X-ray/ CT scan
Renal

24
UTI → Caused by pathogenic microorganisms that move up the urinary tract Cystitis (lower UTI) → Lower UTI involves the bladder and urethra and it refers
from the external urethra to the bladder and so on; it can involve the upper or to inflammation of the bladder
lower urinary tract depending on patient - Usually does not have systemic manifestations, but when a fever, flank pain,
- Most common in women (we know why) and chills are present it indicates that there may be an infection
- 90% are caused by E.Coli, trauma, and irritation S/S
- Catheter related infections (#1 HAI) - Increased urinary frequency
Urethritis → refers to inflammation of the urethra - urgency
Risk factors include - dysuria,
- supra pubic pain,
- HAI’s (most commonly catheter acquired infections)
- WBC’s in urine,
- Obstruction and calculi (because urine is stasis it can cause infection) - cloudy/foul smelling urine
- DM → spilling out a lot of glucose can cause an infection b/c bac loves sugaaaa - hematuria
- Alkalotic urine (should be acidic remember 4-8, ideally 6) - fatigue
- Gender (female), age
- Sexual acitivty → introduction of bacteria into urinary tract
- Poor hygiene (wash yourself)

Diagnostics Treatment (PTS MUST BE COMPLIANT AND TAKE FULL COURSE OF

- Hx & Phx (previous UTI? Symptoms?)
- Urine dipstick → tells us if there’s any WBC, proteins, RBC, glucose, ketones, pH
- Urinalysis → remember helps determine WBC and bacteria presence
- Urine culture → helps us know what exactly is growing so we can treat it
- CT and renal ultrasound→ if there is an obstruction is used view if there is a
mass/calculi
Interventions
- TAKE FULL COURSE OF ANTIBIOTICS
- Prevent unnecessary catheterizations or promote early removal of catheter
- Cranberry juice might help (research is still being done)
- EDUCATE PT OF THE S/S OF UTI AND TO NOTIFY HCP → DUFF → dysuria,
urgency, fever, frequency
MEDS
1. Bacinfection → give antibacterial agent that will eradicate bacteria
- Bactrim, Septra, Ampicillin, amoxicillin, cephalosporin, Cipro, levaquin
- Macrodantin (tell pt there urine will be orange)
2. Fungal infection → give Diflucan
3. Analgesic → give pyridium which is used for dysuria (anesthetizes bladder if
there is a lot of pain), but let pt know that it may turn urine and mucus
membrane orange
GOAL of Tx is Relief of UTI symptoms, Prevention of upper UTI, and
Prevention of recurrence of UTI
25
UTI CONT
Pyelonephritis (upper UTI) → Inflammation of kidneys, renal cortex, renal
pelvis and ureters; typical UTI S/S are present → fever, chills and flank pain
S/S → Typical UTI symptoms and because infection is traveling
- Nausea, vomiting, CVA tenderness, pyuria (pus in urine)
Causes
- Could begin with infection of the lower urinary tract
- Bacteria → E.coli, Proteus, Klebsiella
- Vesicoureteral reflux (urine backflows from bladder into ureters and into
kidney)
- Obstruction (causes stasis of urine; the perfect medium for bacteria to grow)
- Frequent catheterizations (remember #1 HAI)
- Pregnancy (because the uterus presses on the bladder it makes it harder to let
out all the urine therefore some stays in and can obstruct the pathway of urine)
Treatment
1. Mild symptoms
- Give antibiotics for 14-21 days → pt must be compliant
- Adequate fluid intake (HYDRATION IS KEY)
- NSAIDS/antipyretic (for pain control if needed and for fever control)
- Antiemetics can be given for nausea
- Receive a follow up culture to make sure that once the pt is done with
antibiotics that nothing is growing
a. Severe symptoms
i. HOSPITALIZATION (usually pregnancy and elderly will be
hospitalized)
ii. IV antibiotics/fluids
Diagnostics
- Hx and Phx; ask about any recent UTI’S
- Urinalysis (CBC will have an increase in WBC)
- Urine culture → helps identify bacteria so we can treat it before it gets worse (i.e.
septic shock)
- Blood culture (to know if bacteria entered into blood stream)
- CT and renal ultrasound to rule out abscess, mass, stones, and any scar tissue
Nursing interventions
- Early tx of cystitis (lower UTI; remember bacteria will travel up so destroy it)
- Continue meds as prescribed BE COMPLIANT!!!
- Fluid intake 8oz of water a day and Rest
- Have the pt understand the rationale for the tx (if they understand they are more
likely to be compliant and you can explain the worst case scenario)
1. Explain that if the bacteria travels up to the kidneys, it can enter into the
blood and cause septic shock and can lead to death
Chronic pyelonephritis → Occurs when acute pyelonephritis are recurrent; the
kidneys are small, atrophied and loss function from scarring
- CAN PROGRESS TO END STAGE KIDNEY FAILURE (because of the
progressive loss of nephrons due to chronic inflammation and scarring)
- Diagnosis by renal biopsy and imaging
Health promotion for UTI’s
1. Use ASEPTIC TECHNIQUE for all procedures and HAND WASHING
2. Avoid incontinent episodes (don’t let urine sit there)
3. Emphasize taking full course of antibiotics even if there are no symptoms
4. Explain to call HCP if lower tract symptoms persist beyond treatment or if sudden
flank pain/fever appear REPORT STAT
26
5. Instruct on follow-up care (aka repeating culture PRN to make sure bacteria is no
longer there)
Glomerulonephritis → It is inflammation and damage to the filtering part of the Diagnostics
kidney (glomerulus) → 3RD LEADING CAUSE OF ESRD - Hx and Phx (any previous/recent strep infection?)
- Can be acute (sudden symptoms, temporary and reversible) or chronic - Renal biopsy to confirm
(progresses slowly and can lead to irreversible renal failure) - Proteinuria/ Urinalysis
Most common type → Acute Poststreptococcal Glomerulonephritis → it is an - HIGH BUN and creatinine → indicate the kidney is not filtering properly
infection caused by the streptococcal bacteria, occurs after a strep infection
S/S Prevention
- Generalized edema because kidneys aren’t filtering out fluid which also causes - TREAT sore throat/skin lesions early
HTN - We want to prevent it because it can lead to ESKD
- hematuria, rust colored urine, proteinuria (remember that's not normal), wt
gain, We see pts with a lot of edema because they cannot filter out anything; which is
- Abdominal or flank pain why we restrict a lot of electrolytes and protein because our kidneys are not
- decreased GFR (there is decreased blood going to kidney therefore a decreased working
GFR therefore decreased urine output) → EDEMA

Treatment
1. Treat the symptoms and Rest
2. Restrict sodium, protein, potassium (because kidneys are not filtering
out/removing it, i.e K is not being excreted)
3. Restrict fluids (because the glomeruli are inflamed they aren't working well so
fluids can leak from the blood vessels into surrounding tissues) with this you want
strict I&O and daily wt
4. Drug therapy
- Diuretics to remove the excess fluids
- Antihypertensives
- Antibiotics (penicillin for strep infections)
27
Chronic Kidney Disease → progressive, irreversible loss of kidney function;
characterized by a GFR of <60/mi for 3 months and presence of kidney damage
Causes:
1. DM 50%; HTN 25%
With DM → you are constantly urinating a lot → takes a toll on the kidney over time
HTN → constant pressure entering the kidney can damage

GFR Rates Treatment

Stage 1 → GFR <90 (kidney damage with norm or increased GFR) High K? → give insulin/IV glucose/Kayexalate (MAKE SURE THEY HAVE
Stage 2 → GFR 60-89 ( kidney damage with mild decreased GFR) BS’s)
Stage 3 → GFR 30-59 ( moderate decreased GFR)
Stage 4 → GFR 15-29 (severe decreased GFR) preparing for dialysis/kidney Dialysis
transplant 1. Peritoneal dialysis (PD) → done at home 4x a day for 30 min or left on
Stage 5 → GFR <15 (kidney failure) renal replacement therapy is initiated overnight and can be transportable → allows for more independence (P →
portable)
2. Hemodialysis (HD) → 3-4 hours 3 days a week to a dialyzer center (H →
Hospital)

Kidney transplant → best option; however there is a long wait list; this will
eliminate the need for dialysis
- However rejection may occur and pts must take very good care of new
organ 28
Hematology

29
Anemia → is characterized by low RBCs, ,Hemoglobin and Hematocrit Manifestations
LABS 1. Mild anemia
a. HGB → Palpitations, SOB, fatigue → increase in HR to get more blood flowing
b. HCT 2. Moderate anemia
c. RBC → Cardiac symptoms → decrease in Hct, Hgb, and RBC can cause pain because heart
Causes won't get O2
1. Decreased RBC production caused by 3. Severe anemia
- Deficient nutrients → Multibody systems → no system will be getting enough O2 and blood
- Decreased erythropoietin → produced by kidneys if O2 levels are low → Pallor, weakness, fatigue jaundice (destruction of RBC), increased hr, chest pain,
- Decreased iron HF, cardimegaly (enlarged heart b/c its overworked), edema
2. Blood loss caused by GI bleed or trauma
3. Increased RBC destruction caused by
- Sickle cell anemia
- Medications
- Incompatible blood → complication of blood transfusion

Nursing Intervention Types of Anemia

1. CORRECT THE CAUSE 1. Iron-defiency anemia
- Blood transfusion 2. Thalassemia
- Drug therapy 3. Megoblastic anemia
- Vitamins and Diet 4. Aplastic anemia
- O2 level 5. Hemolytic anemia
2. Balance physical activity, exercise, and rest Maintain adequate nutrition 6. Sickle cell disease
3.Maintain adequate perfusion 7.
4.Patient education to promote compliance with medications and nutrition
5.Monitor VS and pulse oximetry; provide supplemental oxygen as needed
6. Monitor for potential complications

30
Iron-deficiency anemia → (common in young, poor diet, pregnant women)
Causes → blood loss, malabsorption, GI bleed Collaborative Care
S/S 1. Diet Teaching (liver, beans, leafy green veggies, vitamin C enhances iron
→ Pallor, glossitis (sore tongue), cheilitis (inflamed lips), brittle spoon shaped nails, absorption)
headache 2. Supplemental iron → Iron therapy for 2 to 3 months after Hgb levels return
Diagnostics a to norm
- CBC H/H RBCs Iron Vit B12 Folate 3. INCLUDE PT IN TX PLAN and emphasize compliance
- Stool for occult blood
- EDG/colonoscopy
- Bone marrow biopsy
Treatment
1. Drug therapy → PO Iron (before meals, use straw and dilute) → will cause
constipation, diarrhea, dark stools (Iron IV, IM Z track (can stain skin)
2. Treat cause
3. Nutrition
4. PRBC’s may need to be transfused

Thalassemia → genetic to middle eastern Megaloblastic anemia

What is it? A group of hereditary anemias that is characterized by a decrease in RBC What is it? Majority result from deficiency in Cobalamin (vitamin B12) & Folic acid
production Folic acid → water soluble found in green leafy veggies, organ meats, yeast & fruits
S/S - Absorbed from the gut and a common cause is ALCOHOLISM → alcohol
→ Growth both mental and physical is slowed (shown by the age of 2), enlarged liver, increased folic acid requirements, but at the same time their diet lacks the vitamin
spleen, heart, pale, anemic Cobalamin (Vit B12) Deficiency → caused by pernicious anemia which is caused by
Management → blood transfusions (PRBC’s) an absence of intrinsic factor and with no IF there is no B12 absorption and RBC
production is diminished (IF is a protein produced by gastric parietal cells)
- This dietary deficiency is extremely rare and seen only in strict vegetarians
Causes of B12 deficiency → GI surgery, Chronic disease of GI tract, Chronic
alcoholics, Long term use of H2-histamine receptor blockers and PPIs, Strict
vegetarians (no B12 is being absorbed from diet)
S/S → GI → sore tongue, anorexia, N, V, abd pain, pallor, fatigue, wt loss
Neuromuscular → weakness, paresthesia feet & hands, muscle weakness
Management B12 supplements PO ( poor dietary intake) OR B12 supplements 31
IM →if there is no intrinsic factor because ti will not be absorbed orally
Aplastic anemia (RARE) Hemolytic anemia
What is it? A decrease in all blood cells because of damage to the bone marrow stem What is it? Destruction or hemolysis of RBCs at a rate that exceeds production
cells (RBC, WBC, platelets) Causes → by problems intrinsic or extrinsic to the RBCs
S/S → caused by suppression of any or all bone marrow elements - Intrinsic forms are usually hereditary & result from defects in RBCs
- Fatigue, dyspnea, petechiae (decreased platelets = easily bruised/bleeding - Extrinsic forms → Physical destruction, infectious agents, toxins
under skin), neutropenia (decreased WBC = no immune system) S/S → general manifestations of anemia
Diagnostics → specific manifestations → jaundice(b/c of RBC destruction and release of
- Low Hgb, WBC, and platelets bilirubin) and enlargement of spleen and liver
- Prolonged bleeding time (b/c of low platelets) Maintenance → focus on renal function because filtration of RBC can damage tubules
- Bone marrow aspiration and cause renal failure
Collaborative care
- Identify causative agents and remove them if possible (genetic?radiation?,
chemical?)
- Prevent complications from infection

Sickle cell disease SCD CRISIS → make sure pt is getting adequate fluid intake
What is it? A genetic disorder that is diagnosed at birth that causes an abnormal form Causes
of Hgb in RBCs to form; this crescent shape & sticky abn RBC can clump together - infection, stress, surgery, blood loss, dehydration, or w/o cause BUT IS
clothing the flow of blood causing ischemia VERY PAINFUL
- Can cause damage to lungs (PE), kidney, brain (strokes), retina (blindness), Management
and bones - Prevention complications
Manifestations - Give PT o2, IV fluids, resp assessments,
- Anemic, pallor, PAIN (high pain levels in both U&L extremities), fever, - DVT prevention (TED stockings, elevate, ambulation, increase fluid intake,
swelling, HTN, N, V meds like heparin)
Complications - Pain relief, treat infection
- Infection is the major cause of death because it weakens the immune system - AVOID CRISIS → know what causes a crisis and how to avoid it)
Pneumonia (most common infection)
- Fever, chest pain, cough, dyspnea
- MI, HF
- Kidney failure, stroke, bone disease (osteoporosis) 32
SCD CRISIS → make sure pt is getting adequate fluid intake
Immune System

33
HIV Asymptomatic infection
What is it? A chronic disease that affects 1 million in US; it is a retrovirus that causes - HIV infection to aids is 10 years; in this state person can spread the disease
immunosuppression; THERE IS NO VACCINE Symptomatic infection
Transmission of HIV - More active stage; S/S include night sweats, fatigue; CD4 count declines
a. Contact with infected blood, semen, vaginal secretions, breast milk, blood products - Thrush, Shingles, Vaginal candida. Oral/genital herpes
b. Pregnancy/delivery - Kaposi sarcoma, Oral hairy leukoplakia
c. Unprotected sex - Swollen lymph nodes, Mouth ulcers, Fevers, Sore throat, Fatigue
d. IV drug HIV Care
Manifestations (WHERE PT ARE MOST INFECTIOUS) a. Monitor HIV progression
- Fever, Swollen glands, Sore throat, HA, Flu like symptoms b. Initiate ART
- Malaise, Nausea c. Prevent opportunistic disease; detect and treat infections
- Muscle/joint pain diarrhea, Rash d. Manage symptoms
Diagnostics e. Prevent complications from treatment
a. Blood, saliva f. Prevent HIV transmissions
b. CD4 count → marker for immune function normal range is 800-1200 GOAL is to decrease viral load and to stop progression to AIDS as well as
i. As CD4 count decreases, viral load will increase transmission of HIV

Treatment Drug therapy Main Goals

antiretroviral therapy: → goal suppress HIV replication ART does not cure HIV. a. Decrease viral load
- Reduce HIV-associated morbidity and prolong duration and quality of life b. Maintain/increase CD4+ counts.
- Restore and preserve immunologic function c. Prevent HIV-related symptoms and opportunistic diseases.
- Maximally and durably suppress plasma HIV viral load d. Delay disease progression w/ Drug Therapy
- Prevent HIV transmission and for individuals with HIV Extra info
PrEP → Pre-exposure prophylaxis is when people at very high risk for HIV take HIV - When to Evaluate CD4 T Cell Count → Every 3-6 months to determine when to
medicines daily to lower their chances of getting infected. initiate ART and assess immune response to ART
- Daily PrEP reduces the risk of getting HIV from sex by more than 90%. Risk
of getting HIV via sex is lowered if PrEP is used with prevention methods Most common infections is pneumocystis pneumonia (without prevention 80%
Antiretroviral Agents will develop PCP)
- Nucleoside Reverse Transcriptase Inhibitors (NRTIs) - Fever, chills, SOB, productive cough)
- Non-nucleoside Reverse Transcriptase Inhibitors (NNRTIs) - Treat w/ bactrim
- Protease Inhibitors, Fusion (Entry) Inhibitors, Integrase Inhibitors, CCR5
Antagonist 34
Gout → a type of arthritis due to the accumulation of uric acid in the blood that
crystalize to form in the joints causing inflammation to the joint and the tissue around
it

Occurs when there is an increase in uric acid production OR it is not being excreted
properly

Causes
1. High intake of purine rich foods
2. High intake of alcohol
3. Meds → aspirin, cyclosporine, diuretics,
4. Dehydration
5. Overweight
6. Physical stress

Why does it happen?

→ uric acid is the product of purine breakdown

s/s
1. Severe pain
2. Swelling
3. Warm at site of inflammation
4. Joint damage and bone deformity

Drug therapy
1. NSAIDS
2. Corticosteroids

35
Neuro

36
CVA → cerebrovascular accident Manifestations
- Both types of CVA result in death of brain cells; 7 million people over age of 20 - Right CVA → stroke occurs on RS body weakness occurs on the LS
have had a stroke; it is the 5th cause of death - Left CVA → stroke occurs on LS body weakness occurs on the RS
Face drooping Arm weakness Speech difficulty Time to call
- Sudden severe headaches, numbness/weakness face, arms,&legs, trouble seeing
Risk factors
- Mobility → sudden dizziness, balance loss, unable to walk; motor deficits
a. Modifiable RF
- Resp, Speech, gag, Hyporeflexia, hyperreflexia
- HTN, Cardiac disease, Diabetes , Hyperlipidemia, a-fib, TIA
- Affect → Can not control emotions
- Cigarette smoking, alcohol consumption and illicit drug use
- Intellectual→ Impaired memory/judgment (sudden confusion,trouble speaking)
- Lifestyle factors: obesity, lack of physical activity, and poor diet, Migraine
- Aphasia → inability to understand or express speech
b. Non-modifiable RF → Age, Gender, Race and ethnicity, Family history of stroke
- Receptive aphasia → loss of comprehension
Diagnostics
- Expressive aphasia → inability to produce language
- Rapid head CT/MRI → we want to determine type of CVA interventions are made
- Global aphasia → total inability to communicate
NIH Stroke Scale → 11 questions that are done quickly
- Dysphasia → impaired ability to communicate
0 → no stroke symptoms 1-4 → minor stroke 5-15 → moderate stroke
- Dysarthria → problem with muscle control of speech slurred, slow
16-20 → moderate to severe stroke 21-42 → severe stroke
speech
- Elimination → Constipation and incontinence

Transient Ischemic Attack (TIA) → Occurs when blood flow to the brain is Nursing management CVA
temporarily blocked by either a clot, narrow blood vessel, or restricted blood Assessment
flow from the carotid arteries could cause this **WARNING SIGN TO A CVA* - Respiratory → assess resp function, position, oral care; eval for aspiration pneumon.
unlike a stroke it alleviates after a couple hours - Neuro → assess neuro status/LOC/Pupil response/strength of extremities/V/S & ICP
S/S (Symptoms depend on area of brain affected) - Cardiovascular → Monitor cardiac rhythm, I&O & fluids, Heart& lung sounds,BP
a. Loss of vision (temporary) - Family hx/medical hx, surg hx, History of risk factors , Onset of symptoms, meds
b. Transient hemiparesis Acute Care CVA
c. Numbness, loss of sensation Musculoskeletal → Prevent joint contractures/muscle atrophy; ROM / positioning /
d. Inability to speak foot board; Prevent skin breakdown; Turn & position / good hygiene / nutrition
GI → constipation (Fluids / fiber / stool softener)
Urinary → incontinence / bladder training 37
Nutrition: with first 24 hrs g tube / ppn / swallow study / ot
Types of Stroke Ischemic Stroke
1. Hemorrhage Stroke What is it? Clots that stop blood supply to an area of the brain
2. Ischemic Stroke Types of Ischemic Stroke
1. Thrombotic Stroke → (MOST COMMON) formation of blood clot
Hemorrhagic Stroke
(thrombus) blocks flow of blood in brain
What is it? Blood leaks into the brain tissue via ruptured blood vessel (aneurysm)
- The vessel becomes narrow, than occluded and than infarction occurs
aka an intracerebral hemorrhage; prognosis is poor and most death within 48 hrs
RISKS → Older adults, DM, high cholesterol, HTN
Cause → HTN common cause
2. Embolic Stroke → fatty plaque or blood clot (embolism) breaks away and
S/S → Sudden symptoms
flows to brain where it blocks an artery (most originate from the heart via
- Headache, N,V, Decreased LOC, HTN, Weakness 1 side face, arm, leg,
afiv or MI)
Hemiparesis, fixed dilated pupils, Resp distress, Posturing, Coma
S/S → Headache and Neurologic deficits (can be temporary)
Types of Hemorrhage Stroke
Treatment → Treat cause of stroke
- Subarachnoid hemorrhage → Intracranial bleed into CFS that is caused by a
Acute Care Ischemic Stroke
ruptured cerebral aneurysm due to trauma and is known as the silent killer
a. Time of onset of symptoms → tells us how much time we have
Acute Care of Hemorrhagic Stroke
b. A, B, C → O2/ETT/vent
- Manage HTN less than 160 sys
c. Neuro assessment
- Sz prophylaxis
d. Stroke center → if hospital does not have a proper team, pt will be
- Evacuation of hematoma surgically → Clip or coil aneurysms
transferred)
e. CALL CODE STROKE → if suspected stroke, pt will be evaluated
f. Therapy ischemic stroke
- TPA → breaks down clots given IV bolus within 3-4 ½ hours of onset of
symptoms
- Monitor V/S and BP and Monitor neuro status
- Give heparin after TPA to prevent further clots
- Stent placement in blocked artery
**before starting intervention you need to rule out hemorrhagic CVA DO NOT GIVE
TPA IF PT IS ACTIVELY BLEEDING**
38
Seizures → Electrical disturbances in the nerve cells in one section of the brain,
these cells emit abnormal, recurring, uncontrolled electrical discharges
Causes (treat the cause)
- Many causes and it could Unknown cause
- Metabolic causes: Acidosis or Electrolyte imbalance, low GL
- Hypoxia, ETOH, barbiturate withdrawal, Dehydration or water intoxication
- Extracranial disorders: Lupus, DM, Sepsis, Kidney disease, Seizures
3 major classes of seizures
1. Generalized onset 2. Focal onset 3. Unknown onset
Seizure Triggers “STOP SEIZURE”
Stress; Trauma; Overexertion; Period, pregnancy; Sleep loss; Electrolyte&metabolic;
Illness; visualiZation disturbances; Undermedicated; Recreational drugs; ETOH
Health promotion → May need to wear helmet; maintain a proper diet, Rest, Exercise,
Avoid ETOH, loss of sleep, handle stress
Types of Seizures
1. Atonic Sz → Tonic episode or loss of muscle tone, Lasts about 15 sec, Stays
conscious (Risk for head injury / fall)
2. Generalized onset nonmotor SZ
3. Absence SZ → Staring spell and Last 10 sec; it can go unnoticed
4. Atypical absence SZ → Staring with eye blinking and lip movements
5. Focal onset seizures
6. Awareness SZ → Involve 1 hemisphere of brain, No Loc, strange feeling, déjà vu
7. Unawareness → May have loc; dreamlike state
- Motor→ Atonic – loss of muscle tone; Tonic/ clonic; Lip smacking
- Non motor → Strange feeling
8. Status epilepticus → Seizure lasting more than 10 mins
- Emergency; Stop SZ activity; can result in Permanent brain damage,
resp distress, arrhythmias
4 phases
1. Prodromal phase → Sensation that precedes seizure by hrs or days
2. Aural phase → Sensation that is the same with each seizure and part of the
seizure
3. Ictal phase →Duration of seizure
4. Postictal phase → Recovery period
Manifestations
a. Generalized onset SZ → Involve whole brain and impaired awareness
b. Tonic-Clonic SZ → Tonic phase – stiffening/Clonic phase – jerking movements
- Cyanosis, tongue biting, incontinence; Post ictal sleepy, sore, no memory of SZ
Diagnostics
1. Health history and Description of SZ
2. EEG (electroencephalogram)
4. CBC (chemistries, liver and kidney function, CT, MRI)
Tx/Drug Goal → Prevent Sz w/ minimal Side effects however, there is no cure
1. Tonic-clonic SZ: → Dilantin, Tegretol, phenobarbital
2. Non motor SZ: →Klonopin
3. Status Epilepticus: → Ativan, valium
Side effects: → Diplopia, drowsiness, ataxia, mental slowness
**PT NEEDS TO ADHERE TO MEDS **
1. Surgery → Resection of focal area
2. Vagal nerve stimulation → Increase blood flow to area of brain
3. Ketogenic diet → High fat, low carb; produce ketones in brain to replace glucose
Nursing Management
1. Teach risk of sz; record sz details: length of sz, loc, type of sz, vs, postictal period
2. Medication teaching side effects, monitor drug levels; teach caregivers
3. Assess airway, position on side; Give IV / po medications; Suction equipment, 39
ambu bag, o2, remove harmful objects, pad side rails; get V/S postilitical
Meningitis → bacterial or viral infection causing inflammation of the meninges Multiple sclerosis → disorder of the CNS/autoimmune; inflammation of the
;tissue around brain and spinal cord brain and spinal cord causing tissue and nerve damage; it is a
- population at risk → college dorm students/institutionalized pts chronic/progressive degenerative disorder with a gradual onset
Cause: → Unknown, infection, genetic, smoking, stress, fatigue, pregnancy, poor
Nursing interventions state of health
- antibiotics after cultures obtained → ampicillian, penicillin, vanco, ceftin Manifestations
- vaccinations → flu/pneumonia/meningococcal vaccine - Blurred double vision,blindness in one eye; dipplopia; weakness, trouble with
- health promotion coordination/balance, numbness, tingling, abd pain, speech problems, dysphagia,
- acute care → V/S, neuro assessment, pain relief, minimize stimuli, Diagnostics
- Hx and Phx, MRI, testing spinal Fluid
Diagnostics Treatment (NO CURE, tx symptoms on case by case basis and TREAT EARLY)
- blood C/S; CT scan; MRI; - DRUGS → IMMUNOMODULATOR (modify activity of immune
- Hx and Phx; neuro assessment system and decrease inflammation)
- Corticosteroids
STIFF NECK → nuchal rigidity - Physical, speech therapy, exerce
- Muscle relaxants for tremors → valium

Parkinsons disease → chronic, progressive neurogenerative disorder that causes

bradykinesia (slow movements), tremors at rest, and gait changes

Manifestations
- Shuffling gait
- Mask like face
- Tremors at rest
- Unstable gait
- Akinesia → loss of ability to move the muscle voluntarily

40
ALS Myasthenia Gravis

41
Neuro-Head Trauma

42
Traumatic Brain Injuries (TBI) →Result of external force applied to head &
brain causing disruption of physiologic stability locally, and globally w/
elevations in ICP & potentially dramatic changes in blood flow within & to brain
(the skull does not expand; if ICP increases & there is an accumulation of fluid
in/around brain, there is no place for the brain to expand)
Pathophysiology of Traumatic Brain Injury
Brain suffers traumatic injury → Brain swells/bleedings cause an increase in
intracranial volume → skull does not allow room for expansion of contents so ICP
increases → Pressure on blood vessels within brain causes BF to brain to slow→
Cerebral hypoxia & ischemia occur → ICP continues to rise & may cause brain to
herniate → Cerebral blood flow ceases
Manifestations
-LOC, persistent/severe headache, N, V, inability to wake up from sleep, Sz
Nursing Implementation FOR ALL TBI
Health promotion
- Prevent car and motorcycle accidents
- Promote driver safety
- Wear safety helmets
- Use seat belts and child car seats
- Do not drive under the influence of drugs or alcohol; do not text and drive
- Home safety to prevent falls
Cushing Triads → three primary signs that often indicate an increase in ICP
- Increase in BP, decrease in pulse, and decrease in respirations
Types of head injuries
1. Diffuse axonal injury → Damage to axons (by either edema or disconnection)
resulting in decreased LOC, increased ICP, cerebral edema, decortication, decorations
**LIFE THREATENING*
2. Focal head injury→ Injury to local area in the brain
3. Lacerations. Of brain tissue from open or closed skull fracture
4. Contusions: bruising of brain tissue; damaged in a specific area b/c of severe
acceleration-deceleration force/blunt trauma; the impact of the brain against the skull
5.. Intracerebral bleed → Bleeding into the brain tissue, watch for sz size and location
of bleed aneurysms subarachnoid bleed
6.. Cranial nerve injuries
7. Hematomas→ Collections of blood in brain that may be epidural (above the dura),
subdural (below the dura), or intracerebral (within the brain)
a. Epidural → bleeding btw inside of skull & outer covering of brain
**NEURO EMERGENCY** could contain either venous/arterial blood
Manifestations → LOC, headache, N, V
Interprofessional care → Evacuate hematoma & Manage increased ICP
b. Subdural → a collection of blood outside of brain that could be acute,
subacute, or chronic
Acute manifestations → LOC, HA, pupil size and reaction, High ICP
Subacute manifestations (can occur up to 2 weeks post injury)
Chronic manifestations (can develop over weeks, months)
43
Concussion→ A temp loss of neurologic function with no apparent structural Primary Survey and Resuscitation Interventions order of approach to patient by:
damage to the brain (A)Cervical Spine/Airway (B)Breathing (C)Circulation (D)Disability (E) Exposure
Manifestations → Lethargy, headache **ALWAYS PLACE HARD COLLAR ON NECK; ESPECIALLY IF YOU DON’T
Interprofessional Care KNOW WHAT HAPPENED AND IF THERE IS A SPINAL INJURY → C Collar
- OBSERVE PT stays in place until it is ruled out (via CT/ X-Ray) that there is no spinal fracture
- Make sure to teach home care and pt teaching Airway Assessment
- Wake up pt to make sure that they are responsive - Assume cervical spine injury with any suspected head and neck injury.
- If patient has persistent V/N, severe headaches or any changes in LOC bring - Apply a cervical collar → this hard cervical collar will protect the neck from being
back to ER/SEEK MEDICAL ATTENTION manipulated &v Relieve airway obstruction
Post-Concussive Syndrome Breathing
→ Could happen weeks or months later depending on the injury - Admin O2 as needed; Monitor RR, rhythm and depth; Symmetry of breath sounds;
Monitor ABGs and O2 Saturation
Circulation

Skull Fractures and Lacerations→ A break in the continuity of skull caused by - assess circulatory status (pulse, BP, UO, LOC); check for and control hemorrhage;
forceful trauma shock
S/S of a Basal Fracture Disability
- Battle sign → an area of bruising/echomyosis - Do a priority assessment of the person’s neurological status including: LOC,
- Raccoon eyes Pupillary response, and Glasgow Coma Scale
- Rhinorrhea → thin, clear nasal discharge (CHECK NASAL & EAR DRAINAGE) Exposure
- Otorrhea → drainage of liquid from the ear - Prevent hypothermia; Keep person in a quiet and calm environment; Position person
Types of Skull Fracture with head midline and in cervical collar
Primary Injury → MVA/Falls/recreational; Blunt force trauma; Damage to any
component of brain (tissue, blood, CSF)
Secondary Injury → Occur several hrs/days after injury
- Hypoxia, Ischemia, Hypotension, Edema, Increased ICP
Nursing Management 44
- GCS, Neuro status , CSF Leak
HEAD INJURY CARE
Diagnostic Testing → NO lumbar puncture
a. Skull /Cervical neck radiographs; CT Scan / MRI → to rule out spinal cord
injury
b. Arterial blood gasses (to detect hypoxia & hypercapnia)
c. EEG; Cerebral angiography; Doppler and evoked potential studies
d. ICP and brain tissue oxygenation measurement (LICOX catheter)
Treatment
a. Maintain Airway and Maintain Spinal Cord Precautions
b. Continuous monitoring of neurological status
c. Prevent/treat Increased Intracranial Pressure
d. Maintain cerebral perfusion and implement Seizure Precautions
Surgical Management
a. ICP monitoring devices: Intraventricular catheter (IVC); Subarachnoid screw
or bolt; Epidural catheter; Subdural catheter (monitor pressures)
b. Craniotomy may be performed in extreme instances of elevated ICP.
Neuro Assessment
1. Skull for lacerations or soft tissue injury
2. Cleanse any lacerations and cover with dressing.
3. Do NOT remove any protruding objects from the skull.
4. Battle’s Sign (ecchymosis behind the ear)& Raccoon eyes (periorbital ecchymosis)
5. Check for CSF leaks from nose & ears (“halo effect,” positive for glucose)
6. Assess pupils (size, equal, reaction to light);Abn eye movements (nystagmus, doll)
7. Sensory/motor changes
Be aware and prevent bleeding
Decortication (IN) decerebration (OUT)
ICP Drug Therapy
a. Mannitol/furosemide → decrease ICP by diuresis and vasoconstriction
b. Glucocorticoids → decrease inflammation and ICP
c. Opioids → pts are sedated b/c any stimulation will increase ICP (naloxone)
d. Neuromuscular blockers; Antipyretics;Barbituratecoma/sedatives;
Antiepileptic
e. Hyperventilation → decrease cerebral blood flow and cerebral blood volume
f. IV 0.9% NaCl → hypertonic solution decreases ICP increase BP and CO
(pulling fluid out of brain) (NO D5W WILL INCREASE ICP DO NOT GIVE)
Treatment and Prevention of ICP and Maintain Perfusion
- Head Midline & Elevated 15-30 deg (keep ICP down); Decrease activities that
increase ICP (suction quickly, sneezing, coughing)
Manifestations
- headache, HTN, decreased LOC, vision problems, N/V, seizure precautions
Nursing Care
- Airway management, Neuro functioning, V/S and fluid & electrolytes, Nutrition
- Maintaining temp (FEVER CAN INCREASE ICP), Skin integrity (pt may not
mobile), Coping, Potential complications , NO NGTs, no sneezing→ can increase ICP
Acute care post head injury
- Neuro assess, Monitor icp readings, Lubricate eyes (loss of corneal reflex), Maintain
norm temp, Loose pad under nose, No sneezing, No NTG, Monitor SZ, Rehab
Nutrition
- Prevent protein calorie malnutrition, Monitor serum albumin levels
- Initiate feedings within 72 hrs of post-injury (SHOULD BE STARTED ASAP)
- Maintain normoglycemia, Assess gag reflex, Use of enteral tube feeding 45
Neuro-Spinal Trauma

46
Spinal cord injury → Trauma or damage to the spinal cord that can cause temporary Nursing Implementation Health Promotion
or permanent dysfunction - Identify high-risk populations and provide teaching
- occur as a result of concussion, contusion, laceration or compression of - Support legislation to:
spinal cord - Prohibit texting while driving; Mandate use of seat belts in cars
Other Information: - Mandate helmets for motorcyclists/ bicyclists; Mandate child safety seats
- 17,000 SCI each year and 282,000 americans living with SCI - Promote programs for older adults to prevent accidental death and injury
- Males account for 80% of SCI; Average age is 42 - Recommend tougher penalties for impaired driving
- 30% rehospitalization rate **Caring for these patients a Major concern for critical care nurses and treatment is
Risk Factors needed to prevent partial injury from developing into more extensive, permanent
- Young age, Male, Alcohol and drug use damage**
**decreased life expectancy and increased mortality so WE WANT TO PREVENT!!* Causes
Types of Injuries: - Most are from direct trauma to the vertebral column, affecting the spinal cords
1. primary injury ability to send and receive messages to & from the brain
2. Secondary injury - Impairment w/ motor, sensory or autonomic functions occurs below level of injury.

Classification of Injury Complications of SCI

Mechanism of injury s/s Increased ICP → headache HTN, decreased LOC, vision problems, N/V;
- Flexion injury → forward dislocation that causes damage to spinal cord (causes seizure precautions
ruptured posterior ligaments) Treatment
- Hyperextension injury → 1. Mannitol, opioids
- Compression fracture → 2. Head midline; decrease activities that will increase ICP
- Flexion-rotation injury →
Level of injury
- Symptoms, degree of paralysis, extent of injury, and disability depends on the level of
cord that is injured
- Cervical (C1-T1) → Tetraplegia (arms are rarely completely paralyzed)
- Thoracic / Lumbar (T2-lumbar) → Paraplegia (full use of arms)
- Degree of injury 47
Effects of Spinal Injuries Brown-sequard Syndrome → a rare neurological condition characterized by a
Anterior Cord Syndrome → an incomplete cord syndrome that affects the anterior lesion in the spinal cord which results in weakness or paralysis (hemiparaplegia)
2/3 of SC resulting in motor paralysis below the level of the lesion; the loss of pain & on one side of the body and a loss of sensation (hemianesthesia) on the opposite
temp at & below level of lesion (MPT) side
**Since posterior columns are pared, position, light touch, and vibration input are There is more pain on the injured side while there is loss of pain and sensation on
preserved** (PVT) the opposite side
CAN CAUSE
Causes → ischemia within anterior spinal artery (ASA), which supplies blood to a. damage to the lateral half of the spinal cord by a lesion
anterior 2/3 of the SC b. loss of motor on the same side as the injury as well as vibration and
Treatment → in the initial phase of anterior cord injury is to treat the underlying proprioception (MVP)
cause. This may take the form of medications such as steroids and blood thinners, and c. preservation of pain on same side
some conditions causing spinal cord damage will need surgical treatment. d. loss of pain and sensory deficits on opposite side of injury
e. penetrating wound or tumors on same side

Cauda Equina Syndrome → a rare disorder that usually is a surgical emergency.

In patients with cauda equina syndrome, something compresses on the spinal nerve
roots. You may need fast treatment to prevent lasting damage leading to incontinence
and possibly permanent paralysis of the legs
Causes: a massive disc herniation in the lumbar spine (low back)
Symptoms Asymmetrical
- distal weakness and patchy sensation in lower extremities
- Flaccid paralysis of lower extremities
- Complete loss of sensation in saddle area
-Areflexic (flaccid) bladder and bowel
-Sciatica (lower extremity pain )
Treatment 48
- decompression by a lumbar laminectomy or steroids to reduce inflammation
Care Of SCI Nursing implementation
Diagnostic Studies - Cervical traction
a. CT Scan - Cervical collar
b. Cervical x rays (b/c it is hard to see C7 and T1) - Halo systems for cervical and thoracic injuries
c. MRI hypothermia/hyperthermia
d. Comprehensive neurological examination - SCI impairs ability of hypothalamus to regulate core temp
e. CT angiogram - Injuries above T6
Interprofessional Care - poikilothermia: the inability to regulate core body temperature
nonoperative stabilization→Stabilization of injured spinal segment & decompression - Monitor environmental temperature, as this can affect body temperature.
- Traction/realignment - a form of decompression therapy that relieves pressure on - Hypothermia may worsen bradycardia and hypotension.
spine (Eliminates damaging motion & prevent secondary damage)
a. Promotes early realignment of unstable fracture-dislocation Preparation for Getting Your Patient Out of Bed who Experiences Orthostatic
a. Closed reduction through craniocervical traction Hypotension
Surgical therapy → used following acute SCI to manage instability and depress SC - Gradually elevate the head of the bed; use wheelchair tilts; Tilt table
- reduces secondary injury and improves outcomes - apply thigh high anti embolic stockings
- Surgery within 24 hours of injury is recommended for central cord syndrome and - Electric powered wheelchair (joy stick/wheel controller)
adults with any SCI → Posterior approach; Anterior approach; Fixation and/or fusion

Nursing process Bowel Management and interventions

a. Respiratory a. Autonomous bowel
- Promotion of effective breathing & airway clearance - Habit training, Exercise, Increased fluids & high fiber to firm stool, Valsalva
- Monitor for resp failure, prevent and remove secretions; suction w/ caution;
maneuver, Manual digital removal
breathing exercises, assisted coughing; humidification and hydration
b. PE/DVT Prevention b. Reflex bowel
a. Improving mobility - Habit training, Exercise, Increase in fluids and high fiber, Suppository program,
b. Maintain proper body alignment; Turn if spine is stable & indicated by Digital stimulation
physician - Abdominal massage (right to left) and Stool softener
c. Monitor blood pressure with position changes Long term complications w/ SCI
d. ROM at least four times a day; Use neck brace/collar, as prescribed, when a. Respiratory
patient is mobilized
b. Pressure ulcers
e. Move gradually to erect position
c. Renal 49
c. Pain management d. Sepsis
Incomplete SCI
Central Cord Syndrome → Damage to central spinal cord, most commonly in the
cervical region that can cause motor weakness and altered sensation in upper
extremities (lower extremities are not usually affected)
Other Info → More common in older adults
Symptoms → Dysesthetic (burning pain in upper extremities)
Spinal Shock → Temporary reduction or loss of reflexes following a spinal cord
injury. It usually lasts for days or weeks after spinal cord injury and the average
duration is 4 to 12 weeks
- Can occurs shortly after injury and lasts days to weeks
- A sudden depression of reflex activity below the level of spinal injury
- muscular flaccidity, lack of sensation and reflexes (bladder/bowel)
- Paralytic ileus within first 2-3 days
- Maintain MAP > 85mm/Hg (Hypotension makes secondary injury to cord)
Most common cause MVA
Conus Medullaris Syndrome → Result from damage to conus medullaris (lowest
portion of spinal cord) that may cause motor function in legs to be preserved, weak, or
flaccid but it will cause a decrease in or loss of sensation in perianal area
Areflexic bladder and bowel → reduced reflex control of your anal sphincter. You
can't feel the need to have a bowel movement, and your rectum can't easily empty by
itself (Pain is uncommon)
Neurogenic Shock → Occurs in cervical or high thoracic (at or above T6) injury;
can last 1 to 3 weeks
Causes → the loss of function of the autonomic nervous system below level of
lesion
**S/S → Blood pressure, heart rate, and cardiac output decrease**
Other symptoms
a. Temperature dysregulation
b. Venous pooling occurs because of peripheral vasodilation
C. Paralyzed portions of the body do not perspire
50
Autonomic Dysreflexia **Acute Emergency; it can be life threatening!** Interprofessional Care (prehospital)
What is it? Occurs after spinal shock has resolved and may occur years after the injury a. Immediate goals
(specifically in SCI lesions above T6) this can cause the autonomic nervous system - Patent airway
AD can lead to - Adequate ventilation/breathing
- Stroke, seizures, or cardiac arrest - Adequate circulating blood volume
Symptoms - Prevent extension of spinal cord damage
a. severe pounding headache
b.Initial assessment and diagnostics
b. sudden increase in blood pressure
- Initial immobilization → Collar, Sandbag, Spinal board, Keep supine;
c. profuse diaphoresis, nausea
log-roll for transfers
d. nasal congestion
- Detailed neurological exam is performed; Assessment for other injuries
e. Bradycardia
Triggering stimuli - Lateral cervical spine x-rays & CT required initially
- distended bladder (most common cause); distention or contraction of visceral organs - MRI done if ligamentous or cord injury suspected; EKG monitoring
(e.g., constipation); stimulation of the skin

Nursing interventions
- Place patient in place patient in seated position to lower BP
- Rapid assessment to identify and eliminate cause
- Empty the bladder using a urinary catheter or irrigate or change indwelling
catheter
- Examine rectum for fecal mass
- Examine skin
- Examine for any other stimulus
- Administer ganglionic blocking agent such as hydralazine hydrochloride
(Apresoline) IV
- Label chart or medical record that patient is at risk for autonomic dysreflexia
- Instruct patient in prevention and management

51
Orthopedics

52
Dislocations → Bone separates from joint Soft tissue injuries
Causes : MVA, Falls a. Sprains → Injury to ligament around joint
S/S: deformity to the limb, shorter or rotated, pt will feel pain, edema, vascular injury b. Strains → ´Excessive stretching of muscle
- We want to assess for vascular injury: check blood supply, pulse, and color of Manifestations
extremity distal to dislocation because it can be an ORTHO EMERGENCY is it is - Edema, pain, bruising, decrease function
blocking a vessel or is on a nerve - ´Self limiting 3-6 wks
Diagnostics: X Ray for FX
Treatment
a. Closed reduction → bone is put back into place without use of surgery using
countertraction; the pt will be put in a sling or splint to keep it in place because
dislocation can reoccur
Tractions
1. Buck traction → pulling force or weights
- used to reduce pain which as a result reduces muscle spasms; Immobilize
joint & reduce the fracture until surgery; We want to check for skin
breakdown

2. Skeletal traction → for long term use to align the bone, wt is attached to pins in the
bone
- Interprofessional care → a splint or sling is given to prevent dislocation
b. Open reduction→ Interprofessional care → surgical fixation & screws, pins, plates,
rods, & nails are placed so that bone can heal

53
Fractures → A break in bone Manifestations
Classifications of fractures - Bruising; Edema
1. Open (bone is sticking out of skin) or closed (bone is broken but is inside of skin) - Crepitation → crunching of bone fragments when multiple fragments of bone are
2. Complete → bone is completely broken involved
3. Incomplete → bone is partially broken - Deformity → caused by displacement of bone, it can make extremity seem shorter
4. Displaced → complete fracture of the bone and it is not in alignment (this can cause
- Loss of function; Muscle spasms → a lot of pain can cause muscle spasms
shortening of the extremity)
- Pain; Tenderness; Inability to bear weight on the fractured extremity
5. Nondisplaced → a crack in the bone but is still in alignment
Fracture Immobilization
Types of fractures
a. Casts are usually done after closed reduction → will immobilize/ stabilize Fx above
a. Traverse; Linear
or below the fracture
b. Oblique non-displaced; Oblique displaced
b. External Fixation Device → Wires in bone attached to rods to stabilize Fx to heal
c. Spiral
- Pin care → Use clean swab for each pin site, remove any drainage/debris
d. Greenstick (common in pediatrics)
- Infection and Loose pins
e. Comminuted (caused by compression fractures usually from falls)
c. Internal Fixation Device → Pins, rods surgically inserted to align and stabilize Fx

Drug therapy for fractures Nursing Interventions Fractures

a. Pain medication / Robaxin muscle spasms a. Immobility can cause constipation → Increase activity, fluids & Stool softeners
b. Tetanus: open fracture b. Renal stones
Nutrition for Fractures c. Orthostatic hypotension → Turn, position
a. Nutrition is important to promote tissue and bone healing; and lots of fluids d. DVT/ VTE → Occurs usually in hip or pelvic fracture; Give lovenox & use
- Protein, Calcium, Vitamin D, Vitamin B12, Fruits and veggies compression device; ROM exercises
The 5 P’s e. Traction; Monitor for Skin breakdown; Pin care; Frequent position changes; ROM
Pain; Pulse; Pallor (white); Paresthesia (can you feel it?);Paralysis (can you move it?) exercises; Cough/ deep breath
Nursing Assessment f. Casts → Check 5 Ps; Neurovascular checks; Edema; Elevate / ice extremity; Do not
1. Thorough history and physical place anything in cast, take padding out, get it wet
2. Immobilize extremity and Limit movement of extremity g. Ambulation→ PT mobility training; Wt bearing, non weight bearing
3. Neurovascular assessment → used to detect nerve and vascular injury a. Exercise joints wiggle fingers, toes
4. Compare both extrem w/ ALL OF THE FOLLOWING → Pulse, color, temp, cap b. Use of cane, crutch, walker 54
refill, edema, sensation, motor function, pain, numbness, tingling, loss of sensation
Types of Fractures Hip fracture → Commonly occurs in older adults because of falls
Pelvic fractures S/S → severe pain, bruising, swelling, unable to bear weight on leg, ext rotation
- can be life threatening of leg, muscle spasms/pain, shortened leg
- Can be caused by abdominal injuries, vascular injuries or compartment syndrome
Interprofessional Care
- Assessment → Abd assessments and Neurovascular lower extremities
- Surgery; Bucks' traction; Closed reduction- pins; ORIF;Hip replacement
- Diagnostics → Xray/CT scan
Post Op Care Hip Fracture
- Treatment → May need external fixation
- Incision for bleeding, infection; PT transfers & ambulation; OT dressing self
Femoral Fracture
- Neuro stat→ Color, temp, refill, pulse, edema, sensation, motor function, pain
- Direct force that causes tissue damage, nerve, vascular; this can lead to a lot of blood
- Elevate leg; Pillow in between legs – abduction; Overhead trapeze
loss, pain, deformity / shortening of the extremity
Post Op Complications
- It is important to stabilize and Immobilize extremity
- Pulmonary Emboli; DVT; Pneumonia; Muscle atrophy (wasting of muscle
- Treatment
tissue); Post-op infection; Non-union or improper union of the bone; bedsores
a. Surgery – rod placement
b/c of min movement; Mental deterioration following surgery in older patients
b. External fixation for open fractures
Home care
- Complication compartment syndrome
- May need rehab facility; PT/OT at home; Pain management; Prevent DVT;
Prevent infection; Anticoagulation treatment – teaching; Exercise per PT

Complication of Fractures
Infection → An open fracture/injury to tissues, blood vessels can cause infection
- Surg debridement may need to be done to muscle, bone, tissue, or fat
- Clean with saline irrigation and antibiotic solution; Give pt IV antibiotics/skin graft
Compartment Syndrome→ Swelling in compartment of muscle causing pressure
on nerves & blood vessels; the cut off blood supply can cause ischemia, necrosis
- Usually in long bone fractures; Casts, splints, restrictive dsgs; Check “P”s;
neuro checks; DO NOT ELEVATE EXTREMITY; no ice constrict blood vessels;
Cut cast, loosen dgs; Fasciotomy- surgical decompression; Amputation severe
cases
- S/S → Pain, pallor, paresthesia, pulse, pressure
Fat embolism syndrome → Fat released from bone marrow; Usually in long
bones, pelvis and can lead to ARDS, Pulm edema
S/S → Chest pain, cyanosis, dyspnea, tachycardia, change in LOC
Treatment → Manage symptoms; Resp support; Fluids
Prevention careful handling long bone fxs;decrease risk fat droplets dislodgment
Rhabdomyolysis →breakdown of muscle causes release of myoglobin which can
obstruct the renal tubules; as a result it can lead to AKI S/S → low UO & red
Emergency Management for Fractures
1. Immobilize the body part ; Splint joints distal & proximal to the suspected fx
2. Assess neurovascular status before and after splinting
3. Open fracture → cover w/ sterile dressing to prevent contamination 55
4. DO NOT ATTEMPT TO REDUCE FRACTURES
Amputation Home Care
Causes: PVD, DM, trauma 1. Keep your incisions clean and dry and Inspect incision site
Health promotion 2. Do not put any creams, lotions, powders or ointments on your surgical incision
- Manage DM; Foot Care; Prevent foot infections, skin breakdown; Smoking 3. Do not shave the skin on your residual limb as this may cause irritation.
- Pt education; Balanced diet; HTN management 4. Keep your incision away from sunlight for 6 months to promote optimal
Interprofessional Care healing.
Goals of surgery: 5. Once incision heals, you may be asked to do gentle massage to reduce scar
1. Preserve greatest extremity length tissue tightness.
2. Preserve function of extremity 6. Wear your shrinker sock as directed to help reduce swelling in your residual
3. Disarticulation – amputation through joint limb. It also helps to shape the limb to fit your prosthetic.
post-OP care 7. Do not soak in a bathtub/hot tub/ swim in a pool/lake until cleared by
a. V/Ss provider.
b. Hemorrhage, Infection 8. Do not prop your residual limb on pillow or blankets when you sit or lie down.
c. Sterile dsg change; Surgical tourniquet available 9. Keep your residual limb straight and flat when you are sitting.
10. You doctor will order effective medications to keep your post-surgical pain
11. Neurontin can help with phantom limb pain as well as non-medication
therapies such as massage of the residual limb.

Phantom Limb Pain→ Phantom pain may be partially explained as a response to

mixed signals from the brain. After an amputation, areas of the spinal cord and
brain lose input from the missing limb
Therapies → Mirror therapy does this by tricking the brain: it gives the illusion
that the missing limb is moving, as the person looks at the real, remaining limb in
a mirror

Prostheses → an artificial devices that replaces the part of the body that is
missing (like a arm or leg) 56
Osteomyelitis → Infection of bone, bone marrow and tissues which can cause bone Osteomalacia → Bone loss, soft bones because of Vit D deficiency
death to occur S/S → Bone pain, Muscle weakness, Pain worse at night, Decreased serum Calcium,
Causes: open wound, foreign body (joint replacement, diabetic ulcers Vitamin D
S/S → Bone pain, swelling, tenderness, warmth, deceased movement, Fever, chills, Treatment → give Vit D, Calcium, Phosphorus supplements
Nausea, can ead to septicemia, septic arthritis, pathological fractures Osteoporosis → Chronic and progressive metabolic bone disease that causes low
Diagnostics bone mass and fragile bones
- Bone biopsy / culture At Risk
- Blood C&S; Wound C&S - More common in women; Pregnancy and Breastfeeding; Menopause
- CBC Diagnostics
- C reactive protein - Bone scan to screen for bone loss
- Bone scan; X ray a. More common in hips, spine, wrists
Care b. Weak bones lead to spontaneous fractures
-IV antibiotics X 4-6 wks
- Surgical removal of dead bone, tissues Management
-Proper nutrition

- Hyperbaric O2 → Hyperbaric Oxygen Therapy or HBOT is a medical treatment that - Calcium, Vit D supplements
enhances the body’s natural healing process by providing 100% pure oxygen to a - Exercise, wts build muscle strength
patient in a chamber where atmospheric pressure is increased and controlled. Every - Prevent falls, fractures
cell of the body is dependent upon oxygen for the - No smoking and Decrease ETOH
Drug therapy
- Fosamax – daily or weekly pill
- Reclast – IV yearly
- Evista – estrogen therapy

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