Exam 1 Flashcards
What are nursing implications for the administration of all blood components, including donation, processing, and administration, and complications?
DONATION
American Red Cross donation requirements
Type and Cross
A, B, O, AB
Rh+ & Rh –
FFP requires ABO but not Rh compatibility
Platelets are not typically cross-matched for ABO compatibility
Testing
Autologous donation
Intraoperative blood salvage- cannot be stored
TRANSFUSION
Blood Administration
Only with NS, Never medications or other fluids through blood tubing
Never medications or other fluids through blood tubing
Only through appropriate filter tubing, change tubing after 2 units (check hospital policy)
Administration time per unit should not exceed 3 ½ hours
Platelets or FFP:
Infuse each unit over 30-60 minutes
FFP requires ABO but not Rh compatibility testing
Platelets typically not cross-matched
steps:
verify Dr order- hgb of 10- anemic, below 8- needs blood transfusion
Obtain consent
Assess IV site & patency
Obtain blood from blood bank
Check accuracy of blood label and pts ID
Baseline VS & assessment
Start the infusion
VS & assessment recheck
Monitor transfusion reactions
complications: occurs in the first 10-15 minutes or first 50cc of blood
Febrile nonhemolytic reaction- chills, fever, HA, flushing tachycardia, anxiety
Acute hemolytic reaction- low back pain, hypotension, tachycardia, fever & chills, chest pain, tachypnea, hemoglobinuria, can be immediate
Allergic reaction- hives, pruritus, facial flushing, SOA, brochospasm, anxiety
Circulation overload-
Bacterial contamination-
Disease acquisition- Hepatitis, AIDS
implications
stop transfusion (maintain line with normal NS) & notify DR
change IV tubing
treat symptoms
recheck crossmatch record with unit
hemolytic reactions-
obtain 2 blood samples distal to infusion site
obtain first UA- test for hemoglobinuria
monitor F & E
serum calcium levels
bleeding disorders
Thrombocythemia- high platelet count resulting from stem cell disorder within BM
Thrombocytopenia- low platelet due to decreased production in BM, increased destruction and increased consumption
Immune Thrombocytopenic Purpura (ITP)- a decreased number of circulating platelets manifests as a bleeding tendency, easy bruising (purpura), or extravasation of blood from capillaries into skin and mucous membranes (petechiae).
Acquired Coagulation Disorders- including vitamin K deficiency and warfarin therapy, liver disease, Disseminated Intravascular Coagulation, platelet disorders and vascular disorders
Most important Labs-rhythm disturbances
Potassium: Normal: 3.5-5. mEq/L
Hypokalemia: irregular rate/rhythm, increased ectopy, PVC’s/V. Tach/ V Fib
<2.5
Hyperkalemia: peaked T wave/wide QRS, irregular rate/rhythm, increased ectopy, PVC’s/ V. Tach/heart block, asystole, v tach
>6
Magnesium: Normal: 1.8-3 mg/dL
Hypomagnesemia: tachycardia, atrial or ventricular
<1.2
Hypermagnesemia: bradycardia, decreases contractility, heart blck, asystole
>6.1
Calcium: Normal: 8.5-10.5 mg/dL
Hypocalcemia: dysrhythmias
<7
Hypercalcemia: dysrhythmias
>12
Atrial fibrillation/Atrial flutter
Thyroid, hepatic, and renal function
hyper
Clinical Manifestations-Rhythm Disturbances
Atrial fibrillation May be asymptomatic Palpitations, SOA, hypotension, dyspnea with exertion, fatigue Pulse deficit Angina
Atrial flutter
Chest pain, SOA, hypotension
Ventricular tachycardia (V. tach) Nearly always unresponsive/pulseless
Ventricular fibrillation (V. fib)
Absence of audible heartbeat
No palpable pulse
No respirations
Medical management/Medications- rhythm disturbances
Atrial fibrillation
Anticoagulants/antiplatelets, Class II and IV antiarrhythmics; Pharmacologic cardioversion
Electrical cardioversion, catheter ablation therapy, Maze/Mini-Maze Procedures
blood pools in atrial, beta blockers & calcium channel blockers (rate control),
Inititate anticoagulants prior to restoring sinus rhythm
Atrial flutter
Adenosine
Antithrombotic drugs, rate and rhythm control similar to atrial fibrillation
Electrical cardioversion
Ventricular Tachycardia
Immediate defibrillation for pulseless VT!
CPR
Cardioversion, antiarrhythmic medications, antitachycardia pacing
ICD
Catheter ablation
Torsades de pointes: polymorphic, prolonged QT interval
Correct magnesium imbalance
Ventricular fibrillation
CPR
Defibrillation
Amiodarone, epinephrine
Defibrillate v fib and v flutter
Assess pt
Call code
Initiate cpr
Sinus brady- not a big deal unless they have symtoms
A fib- blood pools- anticoagulants first
A flutter- rare, same as a fib
Most Important lab values for CAD
Total Cholesterol <200 mg/dL
LDL (bad) Cholesterol <100 mg/dL
HDL (good) Cholesterol > 40 mg/dL (males) >50 mg/dL (females)
Triglycerides <150 mg/dL
increased = increased risk for coronary artery disease
most important labs for Acute Coronary Syndrome (ACS)/MI
Cardiac enzymes/biomarkers
Troponin <0.05 ng/mL- q6h x3
Creatine Kinase (total) Males 50-204 units/L;
Females 36-160 units/L
Creatine Kinase CK-MB 0-5 ng/mL
Myogobin Males 28-72 ng/mL Females 25-58 ng/mL
CORONARY VASCULAR DISORDERS CM, PRIORITY ASSESSMENTS, DIAGNOSTIC TESTS
CLINICAL MANIFESTATIONS
Angina
Chest pain, indigestion, choking or heavy sensation
Feeling of impending death/apprehension
MI
Often cannot be distinguished from unstable angina
PRIORITY ASSESSMENTS Pain Difficulty breathing Palpitations Unusual fatigue Syncope
DIAGNOSTIC TEST
12-lead ECG
Echocardiogram
Lab Tests (see previous slide)
medical management/medications for coronary vascular diseases
CAD Diet Physical activity Medications Tobacco cessation HTN management Diabetes control
Angina
Medications
Oxygen therapy
PCIs/CABG
Medications: Dual antiplatelet therapy: aspirin, clopidogrel (Plavix) or other antiplatelets STEMI-Emergent PCI Thrombolytics Inpatient management CICU with invasive monitoring Continuous cardiac monitoring ASA, beta-blocker, ACE Inhibitor BP, Urine output, Na, K, Creatinine Cardiac Rehab
percutaneous coronary interventions/complications
Percutaneous transluminal coronary angioplasty (PCTA)
Coronary artery stent
Coronary artery bypass graft (CABG) Blood vessel is grafted to an occluded coronary artery so blood can flow beyond the occlusion Indications Traditional CABG Alternative Techniques
priorities Pain management-Oxygen, morphine Bed rest with elevated HOB Fluid volume status Adequate tissue perfusion Anxiety Monitor for complications
complications hypovolemia bleeding cardiac tamponade fluid overload hypothermia hypertension tachydysrhythmias bradycardia cardiac failure MI
PCI Coronary artery dissection, perforation, abrupt closure, vasospasm Acute MI Dysrhythmias Cardiac arrest
education Prevention Non-modifiable/Modifiable risk factors Medication education Post-procedure education
structural, infectious, and inflammatory cardiac disorders
medications Antidysrhythmics CCB, Beta-blockers ACE Inhibitors, ARBs Anticoagulation Valvuloplasty Valve Replacement
priorities Assess for s/s heart failure and emboli Heart sounds Hemodynamic stability post valve replacement Neuro, resp, CV are priority assessments Wound care
complications
Heart failure
Infective endocarditis with mechanical valve prosthesis
education Prevention Medication education Infection prophylaxis Diet, activity, self-care
cardiomyopathy
diagnostic testing 12-lead ECG Echocardiogram Pulmonary artery systolic pressure, pulmonary artery wedge pressure Central venous pressure Cardiovascular MRI
clinical manifestations May be asymptomatic for years S/S of heart failure Cough Orthopnea Peripheral edema Nausea Chest pain, palpitations, dizziness, syncope
priority assessment Physical assessment focuses on s/s of heart failure VS Pulses Weight PMI palpation (shifted to left?) Murmurs, S3/S4 Crackles JVD Edema
medications Antidysrhythmics Anticoagulation Beta-blockers Pacemaker/ICD Alcohol septal ablation Surgical Management Left ventricular outflow surgery Heart transplantation Ventricular Assist Devices (VAD) Total artificial heart
priorities Improve CO and Peripheral blood flow Increase activity tolerance Improve gas exchange Reduce anxiety Decrease sense of powerlessness
complications
Severe heart failure
Lethal dysrhythmias
Death
education
aneurism
clinical manifestations Pain most prominent symptom Dyspnea Cough Hoarseness, stridor Feel heart beating in abdomen Low back pain
assessment
Dilated veins of chest, neck, arms
Edematous areas on chest wall and cyanosis
Pulsatile mass in middle and upper abdomen
Systolic bruit
tests Chest X-ray CTA MRA TEE Duplex ultrasonography
medications
Blood pressure control
Beta-blockers, ACEs, ARBs, diuretics, CCBs
Endovascular repair with graft
priorities
Assessments of baseline prior to surgical repair
Functional capacity of all organ systems
Post operative considerations
complications Hemorrhage Shock Arterial occlusion Infection Ischemic bowel Kidney injury Impotence
education
Medications
Diet/activity
Fluid intake
dissecting aorta
Poorly controlled HTN
Blunt chest trauma
Cocaine use
Sudden and severe Persistent pain-tearing or ripping Pale Sweating Tachycardia Elevated BP/may vary greatly from one arm to the other
diagnostics/management
Pericardial Effusion & Tamponade
Accumulation of fluid in the pericardial sac Heart failure, pericarditis, metastatic carcinoma, surgery/trauma Acute (cardiac tamponade) vs chronic S/S: Tamponade Chest pain Tachypnea SOA JVD Low CO/hypotension Tachycardia Pulsus Paradoxus
management Pericardiocentesis Peri and post procedure monitoring Possible complications Puncture, dysrhythmias, plural laceration, gastric puncture Reaccumulating Pericardial window
steps in blood transfusion
verify Dr order- hgb of 10- anemic, below 8- needs blood transfusion Obtain consent Assess IV site & patency Obtain blood from blood bank Check accuracy of blood label and pts ID Baseline VS & assessment Start the infusion VS & assessment recheck Monitor transfusion reactions
Get a new set of tubing and start NS after a reaction – document & notify Dr.
Disseminated Intravascular Coagulation
A sign of an underlying condition
Initiated by: an infection or a malignancy
May be triggered by: sepsis, trauma, cancer, shock, abruption placentae, toxins, allergic reactions
Clinical Manifestations: bleeding from mucous membranes, venipuncture sites, GI and urinary tracts; multiple organ dysfunction syndrome (MODS) (Chart 33-10, pg. 957).
Diagnostic test: platelet, D-dimer, PT, aPTT, fibrinogen level
STOP THE BLOOD
management
Assess for risks (“triggers”)
Monitor signs and symptoms of thrombi and bleeding
Monitor lab value
Prepare to administer plasma and Platelets
common symptoms of leukemia
A- anemia
N- neutropenia
T- thrombocytopenia
Weight loss, fever, infection Shortness of breath Weakness Pain and tenderness in bones or joint Fatigue Loss of appetite Swollen lymph nodes Liver, spleen enlargement Bleeding and bruising, petechiai
acute myeloid leukemia
over 50 years
Pathophysiology- start in immature forms of myeloid cells – white blood cells (other than lymphocytes), red blood cells, or platelet-making cells (megakaryocytes).
Clinical Manifestations
insufficient prod of normal BC
Low neutrophil count- fever and infection
Anemia- weakness, fatigue, dyspnea, pale
Thrombocytopenia- petechia, ecchymosis, bleeding tendency
diagnostic
Diagnostic- decrease in erythrocytes or platelets
Bone marrow analysis- shows blast cells
Assessment
Prevention/Risk Factors
Smoking, Chemical/Radiation exposures,
Chemotherapy drugs
Certain blood disorders
Management- Chemotherapy
snapshot Fatigue, weight loss, pallor, bleeding , infection Labs: blast cells > 20%, anemia, thrombocytopenic Tx: Chemotherapy Complications: bleeding/infection Nursing Infection prevention Assess for bleeding Prevent bleeding
snapshot
Chronic phase few s/s
leukocytosis on CBC performed for other reason
Acute phase: hepatomegaly, splenomegaly, weight loss, bleeding, fatigue
Tx:
TKI’s
chronic myeloid leukemia
Increases with age – 65 average
See it rarely under 20
Men more likely to get it
Pathophysiology- a genetic change takes place in an early (immature) version of myeloid cells - the cells that make red blood cells, platelets, and most types of white blood cells (except lymphocytes). The leukemia cells grow and divide, building up in the bone marrow and spilling over into the blood. In time, the cells can also settle in other part of the body, including the spleen.
Clinical Manifestations Bone pain!!!! Pale skin Anemia Fever Bruising Lethargic/fatigue Unusual bleeding from nose/gums Get infection easy
Assessment Prevention/Risk Factors- Radiation exposures, age, gender Management- Imatinib therapy Tyrosine Kinase Inhibitor (TKI) DO NOT MISS THE DOSE
acute lymphoid leukemia
children- 4 year old peak
Pathophysiology- start in immature forms of lymphocytes. Lymphoid leukemia develops from cells in the bone marrow, lymphomas develop from cells in lymph nodes or other organs.
Clinical Manifestations
Pain from enlarged liver or spleen or pain at the bone area
CNS symptoms- cranial nerve pulses or HA, V
Assessment
Prevention/Risk Factors
Radiation/chemical exposure
Certain viral infections
Inherited syndromes
Management- Chemotherapy, Stem cell transplant
Corticosteroids and vinca alkaloids
snapshot
Usually dx before 15 yr and incidence rises again > 50 yr
Splenomegaly, splenic pain, bone pain, HA, emesis, elevated blast cells
Tx:
Chemotherapy,
Stem cell transplant,
Targeted therapy
chronic lymphoid leukemia
Pathophysiology- In chronic leukemia, the cells can mature partly but not completely. They generally do not fight infection as well as normal white blood cells do. The leukemia cells survive longer than normal cells, and build up, crowding out normal cells in the bone marrow.
Clinical Manifestations- Fatigue, Increase sensitivity to insets bites A lot of time asymptomatic Swollen lymph nodes Enlarged spleen Dying from infection
Assessment Prevention/ Risk Factors Chemical exposure Family history Race (North America and Europe) Management- Chemotherapy, Stem cell transplant
Progress very slowly (years)
Hard to treat because it could be too late
snapshot
Asymptomatic and dx on assessment for something else
Lymphadenopathy, splenomegaly, lymphocytosis
Tx:
Chemotherapy,
Stem cell transplant
lymphoma
Pathophysiology- a cancer starts in cells that are part of the body’s immune system,
Lymphoid tissue in spleen, GI, liver or bone marrow
Clinical Manifestations swollen lymph nodes night sweats fatigue red spots fever vomiting weight loss backache shortness of breath nausea radiation therapy chemotherapy
Assessment
sx
Prevention/Risk Factors prevent infection Epstein-Barr virus, autoimmune diseases, HIV/AIDS, smoking
Management
Chemotherapy/ Radiation therapy (skin)
Targeted therapy
Surgery
Nursing Management Help patient with side effects of treatments Educate to minimize infection risk Educate to ID s/s of infection Educate when to call provider
non-hodgkins lymphoma
Lymphadenopathy, may be asymptomatic Lymphoid tissue becomes infiltrated with malignant cells (B cells)- unpredictable multiple lymph nodes involved Increases with age, 65 Common in US Incidence rate has doubled 5 year survival rate -70% Increased autoimmune problems- organ transplant, viral infection or prior treatment for cancers
can occur in children & adults
Hodgkins lymphoma
painless, firm, enlarged lymph node, Reed-Sternberg cells present Anemia & altered WBC count Pruritus Frequent viral infections Rare High cure rate More common in men Fever Weightless Night sweats Chemo, radiation Stem cell for advanced disease Can start with a single lymph node and then develop other places Cad, dysrhythmia, cardiomyopathy seen in later stages
Educate about secondary malignancy- stop smoking, drinking, check breast, yearly skin check
young adulthood and >55
most patients have a good prognosis
multiple myeloma
A malignant disease of the plasma cells
Most common symptom is bone pain
Most common areas- Back & ribs
Increased with movement and decreased with rest
No cure;
treatment depends on age and includes:
corticosteroids
chemotherapy
PAIN medication is the most important
Plasma & pain
Bone damage – pelvic, rib cage (prevent falls)
Blood issues – anemia, clotting problem, infection
Kidney problems – decreased kidney function, monitor UO, blood workhypercalcemia
management Pain Management NSAIDS and possible opioids monitor renal function (NSAIDS) Education of activity restrictions Education of manifestations of hypercalcemia Maintain mobility Hydration- to prevent hypercalcemia Infection prevention- Wear a mask Hand hygiene
Type I Diabetes
Destruction of pancreatic beta cells
Decreased insulin production,
Increased glucose production by liver
Fasting hyperglycemia
Glucose derived from food cannot be stored in liver but instead remains in bloodstream = post-parandial (after meals) hyperglycemia
Type II Diabetes
Insulin resistance = decreased tissue sensitivity to insulin
Intracellular reactions are diminished – making insulin less effective at stimulating glucose uptake by the tissue
Impaired insulin secretion
Usually a slow progression and can go undetected for many years
Diabetic Ketoacidosis (DKA)
- Hyperglycemia: There is no insulin, so no glucose entering the cells, All the glucose is in the bloodstream , And production and release of glucose by the liver is increased
- Dehydration and electrolyte loss: The kidneys attempt to rid the body of the excess glucose , Glucose – along with water and electrolytes – are excreted
- Metabolic acidosis: Breakdown of fat (lipolysis) to free fatty acids and glycerol occur The free fatty acids are then converted into ketone bodies by the liver Ketone bodies accumulate leading to metabolic acidosis
occurs with type 1 diabetes
clinical manifestations Clinical Manifestations Polyuria Polydipsia Marked fatigue Blurred vision Weakness Headache Orthostatic hypotension GI symptoms (nausea, vomiting, abdominal pain) Acetone breath (fruity odor) Hyperventilation w/ very deep (not labored) respirations - Kussmaul Mental status changes
Assessment and Diagnostic Findings
High blood glucose (300-800 mg/dL)
Low serum bicarbonate (0-15 mEq/L)
Low serum pH (6.8-7.3)
Presence of ketone bodies in blood and urine
Depending on amount of water loss:
Sodium and Potassium may be low, normal, or high
Creatinine, BUN, and hematocrit may be high
Decreased or missed dose of insulin
Illness or infection
Undiagnosed/untreated diabetes
Management
Rehydration: (Fluid loss from polyuria, hyperventilation, diarrhea, and vomiting)
GIVE IV FLUIDS!!!
May need as much as 6-10 L
Start with NS at rapid rate – 0.5-1L per hour for 2-3 hours
Then ½NS for continued rehydration for several more hours
When blood glucose reaches 300 or less – switch to D5W to prevent decline in blood glucose level
MONITOR FLUID VOLUME STATUS!!!
Frequent vital signs
Lung assessments
Monitoring intake and output
Monitor for signs/symptoms of fluid overload
Restoring Electrolytes: IV potassium slowly
POTASSIUM REPLACEMENT!!!!
As much as 40 mEq/hour may be needed for several hours to avoid dysrhythmias that occur with hypokalemia
Frequent ECG and lab monitoring
Reversing Acidosis
GIVE INSULIN!!!!
IV Regular insulin is given at a slow, continuous rate
Hourly blood glucose measurements
Blood glucose levels are usually corrected before acidosis is corrected IV insulin may be continued for 12-24 H until serum bicarbonate levels increase to at least 15-18 mEq/L
SICK DAY RULES
Never eliminate insulin doses when nausea and vomiting
Take insulin dose and then attempt to consume frequent small portions of carbs
Drink fluids every hour to prevent dehydration
Assess blood glucose and urine ketones every 3-4 hours
If patient cannot take fluids without vomiting, or if elevated glucose or ketone levels persist – call provider!
Monitoring and Managing Potential Complications
Fluid Overload
Hypokalemia
Cerebral Edema
Hyperglycemic Hyperosmolar Syndrome (HHS)
- Hyperglycemia: Lack of effective insulin to prevent hyperglycemia , but enough insulin is present to prevent the breakdown of fat , So no ketosis and acidosis occur
- Hyperosmolarity: Persistent hyperglycemia causes osmotic diuresis , results in loss of water and electrolytes
Clinical Manifestations Hypotension Dehydration Tachycardia Variable neurologic signs
Assessment and Diagnostic Findings
High blood glucose (600-1200 mg/dL)
Osmolality (>320 mOsm/kg)
High BUN and Creatinine
Causes
Infection or acute illness
Medications that exacerbate hyperglycemia
Treatments such as dialysis
Management
Rehydration
Restoring Electrolytes
Insulin Administration
Rehydration
Very similar to management in DKA
Restoring Electrolytes
Very similar to management in DKA
Insulin Administration
Less of important role because not needed for reversal of acidosis
Insulin is given at a continuous low rate
Monitoring and Managing Potential Complications
Fluid Overload
Hypokalemia
Cerebral Edema
DKA VS HHS
DKA
More common Type 1
Rapid onset (<24 H)
Blood Glucose >250
Arterial pH Level < 7.3
Serum and urine ketones present
Serum osmolality 300-350 mOsm/L
Plasma bicarbonate level <15 mEq/L
BUN and creatinine elevated
HHS
More common in Type 2
Slower onset (over several days)
Blood Glucose > 600
Arterial pH Level is normal
Serum and urine ketones absent
Serum osmolality >350 mOsm/L
Plasma bicarbonate level is normal
BUN and creatinine elevated
Long Term Complications of DM
Macrovascular Complications Results from changes in the medium-large blood vessels Coronary artery disease Myocardial infarction Cerebrovascular disease Transient ischemic attacks Strokes Peripheral vascular disease Occlusive peripheral arterial disease Prevention and treatment of atherosclerosis Nutrition therapy and exercise to manage obesity, HTN, HLD Medications to control HTN and HLD Smoking cessation Control of blood glucose levels MORE COMMON IN TYPE 2
Microvascular Complications
Results from changes in the capillary basement membrane (thickening)
Diabetic Retinopathy
Nephropathy
Routine eye exams Annual urine analysis for albumin Annual serum creatinine and BUN Control of HTN Prevention/Treatment of UTIs Avoidance of nephrotoxic Rx and contrast dye Low-sodium and Low-protein diet Smoking cessation Control of blood glucose levels MORE COMMON IN TYPE 1
Diabetic Neuropathies Results from changes in the nerves Peripheral Neuropathy Distal portion of the nerves, especially in lower extremities, affects both sides symmetrically Autonomic Neuropathy Broad range of dysfunction affecting almost every organ system COMMON IN BOTH TYPES parathesia burning decreased sensation of light touch decrease proprioception decrease pain & temperature Intensive insulin therapy FALL PRECAUTIONS! Pharmacologic treatment Foot checks and care
AUTONOMIC NEUROPATHY
Ranges from tachycardia, orthostatic hypotension, to MI
Urinary retention, decreased sensation of bladder fullness, neurogenic bladder
Delayed gastric emptying “diabetic gastroparesis”, bloating, N/V, constipation or diarrhea
Discontinue meds that interfere with autonomic nervous system responses
Use sympathomeimetic meds that stimulate an autonomic response
Low-fat diet, frequent small meals
Use meds that increase gastric motility
Frequent glucose monitoring
Meds to help treat constipation/diarrhea
Intermittent straight caths
Foot and Leg Problems and Infections
Results from neuropathy, peripheral vascular disease, and immunocompromised
Neuropathy = loss of pain and pressure sensation
PVD = poor circulation contributes to poor wound healing
Immunocompromise = lowers resistance to infections
FOOT CARE!!!!
Inspect feet daily
Do not allow moisture to accumulate between toes
Wear closed-toed shoes that fit well
Trim toenails frequently
Protect feet from hot/cold
Keep blood flowing to feet
DO NOT – walk barefoot, use heating pads, wear open-toed shoes, soak the feet, shave calluses
diabetes in the hospital
Blood glucose levels tend to increase due to stress
Management of glucose control very important during perioperative period
Frequent blood glucose monitoring
May need to use IV insulin
Monitor closely post-operative for cardiovascular complications, wound infections, and skin breakdown
change in diets
NPO
Usual dosage of rapid or intermediate acting insulin must be changed
Continue to give basal dose insulin
Frequent blood glucose monitoring
Clear Liquids
A lot of clear liquids contain simple carbohydrates – try to use diet types
Glucose tests and insulin administration should match mealtimes
Enteral Tube Feeding
Often results in increased levels of glucose
If continuous tube feeding, regularly scheduled intervals of insulin given
Must be cautious if tube feeding is temporarily discontinued or paused
HYPERGLYCEMIA DURING HOSPITALIZATION
Reasons:
Changes in usual treatment regimen
New medications introduced or routine medications changed
Use of IV dextrose in fluids
Overly vigorous treatments for hypoglycemia
Inappropriate withholding of insulin
Inappropriate use of “sliding scales”
Mismatched timing of meals and insulin
NURSING INTERVENTIONS
Nursing Interventions:
Assess patient’s usual home routine and try to mimic
Monitor blood glucose levels
Test blood glucose before a meal served and administer insulin at that time
Use NS as much as possible, and not IV fluids with dextrose
Avoid overly vigorous treatment of hypoglycemia
HYPOGLYCEMIA DURING HOSPITALIZATION
Reasons:
Overuse of “sliding scale” insulin
Not changing insulin dosage when dietary intake is decreased
Overly vigorous treatment of hyperglycemia
Delayed meal after administration of insulin
NURSING INTERVENTIONS
Nursing Interventions:
Follow hospital protocol
Assess patient’s pattern of glucose levels
Avoid giving doses of insulin repeatedly
Arrange for snacks to be giving if meals are going to be delayed
osmolality
high osmolality > High concentration of particles
Low concentration of water > high adh > KIDNEYS KEEP WATER
URINE MORE CONCENTRATED
low osmolality > Low concentration of particles
High concentration of water > low adh > KIDNEYS EXCRETE WATER
URINE LESS CONCENTRATED
1.005-1.030- normal specific gravity
Urine Osmolality 100-900
Diabetes Insipidus
DEFICIENCY OF ADH
CAUSES Head Trauma Brain Tumor Surgical/Irradiation of pituitary gland Infections of CNS Failure of renal tubules to respond to ADH
Diagnosis:
Urine specific gravity
Urine osmolality
Fluid deprivation test
Treatment:
Replace ADH
Desmopressin (DDAVP) – synthetic vasopressin, intranasally once to twice daily
Ensure adequate fluid replacement
Identify and correct underlying pathology
LARGE VOLUMES OF DILUTE URINE: Greater than 250 mL per hour Low urine specific gravity(1.001-1.005) POLYDIPSIA: Intense thirst Drinking 2-20 L daily Craves cold water
OSMOLALITY <100 for DI
DRY INSIDE
Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)
EXCESS OF ADH
Causes: Non-endocrine origin Disorders of the lungs (pneumonia, pneumothorax) Head injury Brain surgery/tumor CNS infection Some medications
Treatment: Identify and correct underlying pathology Restrict fluid intake Use of hypertonic IV solution Diuretics may be used
CANNOT EXCRETE A DILUTE URINE: Urine is very concentrated
Elevated urine specific gravity
RETAIN FLUIDS
Euvolemic
No edema present
DILUTIONAL HYPONATREMIA Nausea Vomiting Headache Weakness Fatigue Confusion
Sticky and stinky pee
Not going to see edema, see body holding water in intravascular space- hypertension
Watch for seizures – seizure precautions
SIADH- soaked inside
3% NS
DI VS SIADH
DI low ADH, low water in body High UO, polyuria high sodium high h&h and serum osmolality from dehydration risk: hypovolemic shock tx: DDVAP (ADH)
SIADH high ADH, water intoxication low UO, oliguria low sodium (dilution) weight gain risk: seizures tx: hypertonic saline
hypovolemic shock
drink plenty of fluids when exercising or in hot weather
obtain early medical attention with illness or trauma and with any evidence of dehydration or bleeding
educate about manifestations of dehydration, including thirst, decreased UO, and dizziness
chest pain lethargy somnolence restlessness anxiety dyspnea diaphoresis thirst muscle weakness nausea constipation
cariogenic shock
educate about ways to reduce the risk of a MI, such as exercise, diet, stress, reduction, and smoking cessation
chest pain lethargy somnolence restlessness anxiety dyspnea diaphoresis thirst muscle weakness nausea constipation
hemoglobin & hematocrit
hgb: men: 13.5 to 17.5 women: 12.0 to 15.5
hct: men: 41% to 50% women: 36% to 48%
