Week 2; Acute Care of Hematologic Alterations Flashcards
Congenital heart disease primarily includes anatomic abnormalities present at birth. Two broad categories include:
Heart failure and hypoxemia
Assessment of a child; heart rates for 1-3 y/o
80-120
Assessment of a child; heart rates for 2-9 y/o
70-115
Assessment of a child; heart rates for 9-14 y/o
65-109
Assessment of a pediatric patient
HR higher, RR higher
Failure to thrive or poor weight gain in a child is associated with
Heart disease, chest deformities, or enlarged heart.
Cardiac cath has been become a routine dx and therapeutic procedure, especially in
neonates and children
Teaching when caring for pediatric patients with HF
Important to teach developmental stage of patient, check families knowledge of illness-defining characteristics, understands definition of HF, states four characteristics, describes meds, expresses fears and concerns, shows appropriate rxn to illness
Perfusion
Total arterial blood flow through the tissues (peripheral perfusion) and blood that is pumped by the heart (central perfusion)
Perfusion
Total arterial blood flow through the tissues (peripheral perfusion) and blood that is pumped by the heart (central perfusion)
Clotting
Complex, multi-step process by which blood forms a protein-based structure (clot)
Bone marrow –
Produces RBC, WBC, and platelets. Also involved in immune response
Blood components
Plasma proteins, RBC, white blood cells, platelets
Plasma proteins include
albumin, globulins, fibrinogen
Red blood cells (erythrocytes) –
Carry oxygen and carbon dioxide
Accessory organs of blood formation
spleen and liver
Leukocytes r/t inflammation
Neutrophils, macrophages, monocytes, eosinophils, basophils
Intrinsic factors
Conditions such as circulating debris or venous stains within the blood itself that can activate platelets and trigger the clotting cascade
Extrinsic factors
Trauma, inflammation, toxins, or foreign proteins
Hematologic changes associated with aging
Decreased blood volume with lower levels of plasma proteins, bone marrow produces fewer blood cells, lower WBC count, lymphocytes have less rxn to antigens, loss of immune fxn, hemoglobin levels fall after middle-age
Fibrinolysis
Process that dissolves the clot
Hematologic assessment
•Age
•Gender
• Liver fxn
• Drug use (PRESCRIBED, OTC, ILLICIT)
• Dietary patterns
• Socioeconomic status
• Previous radiation therapy
• Occupation, hobbies
• Location of home
• Use of blood thinners, NSAIDS
• Nutrition status
• Family hx
• Current health problems
Hematologic physical assessment
• SKIN – color, jaundice, bruising, petechiae,
turgor, itching
• Head and neck – pallor, palpate lymph nodes, oral mucosa ulceration
• Cardiovascular – JVD, edema, phlebitis, BP (lower w anemia)
• Kidney and urinary - Hematauria
• Musculoskeletal – ROM, pain
• ABD– distended, enlarged liver or spleen
• CNS– B12 deficiency causes nerve degeneration, parasthesia
BP is lower with what condition?
Anemia
B12 deficiency causes
nerve degeneration, parasthesia
Hematology dx assessments
• PERIPHERAL BLOOD SMEAR
• CBC
• RETICULOCYTE COUNT – BONE MARROW FUNCTION
• PLATELET COUNT – NORMAL 150,00 TO 400,000
• HEMOGLOBIN ELECTROPHORESIS – DETECTS ABNORMAL
FORMS OF HEMOGLOBIN
• COOMBS’ TESTS (DIRECT AND INDIRECT) – BLOOD TYPING
• SERUM FERRITIN, TRANSFERRIN, AND TOTAL IRON BINDING
CAPACITY (TIBC)
Platelet count range
150,00 TO 400,000
Lab tests measuring bleeding and coagulation
Prothrombin time (PT), INR, PTT, anti-factor XA test, platelet aggregation
INR
An INR (international normalized ratio) is a type of calculation based on PT test results. Prothrombin is a protein made by the liver. Range 2-3
Hematologic imaging assessment
Radioisotopic imagine, standard x-ray
Bone marrow aspiration and biopsy is used when
When other tests show abnormal findings that indicate a possible problem in blood cell production
Bone marrow aspiration is usually done in
Iliac crest with a large bore needle, also can be done in sternum
Bone marrow aspiration; prepping the patient
Explain steps and procedure, as this causes anxiety, educate pt
Follow up care of bone marrow aspiration–
Apply pressure dressing, observe for 24 hrs for signs of bleeding, mild analgesic (NO ASPRIN), apply ice, inspect q 2 hrs, light activity for 48 hrs
UPON ASSESSMENT, THE NURSE NOTICES THAT A PATIENT
HAS BLEEDING GUMS. THE PATIENT REPORTS INCREASED
FATIGUE, MALAISE, AND “CHILLS.” WHAT IS THE PRIORITY
NURSING INTERVENTION?
A. DOCUMENT ASSESSMENT FINDINGS.
B. NOTIFY THE HEALTH CARE PROVIDER OF THE
PATIENT’S SYMPTOMS.
C. OBTAIN VITAL SIGNS AND ADMINISTER ANTIPYRETIC
MEDICATIONS.
D. REVIEW LABORATORY ANALYSIS FOR SIGNS AND
SYMPTOMS OF BONE MARROW SUPPRESSION.
ANSWER D
• THE NURSE SHOULD INITIALLY REVIEW THE PATIENT’S
LABORATORY ANALYSIS FOR COLLECTIVE SIGNS OF
PANCYTOPENIA RELATED TO THE PATIENT’S REPORT AND
ASSESSMENT FINDINGS OF FATIGUE (ANEMIA), BLEEDING
GUMS (THROMBOCYTOPENIA), AND CHILLS
(NEUTROPENIA).
• LABORATORY DATA ARE NEEDED BEFORE INFORMING
THE HEATH CARE PROVIDER AND DECIDING WHETHER TO
ADMINISTER AN ANTIBIOTIC.
• OBTAINING BLOOD CULTURES PRIOR TO ANTIBIOTIC
ADMINISTRATION IS AN IMPORTANT INTERVENTION.
ANTIPYRETIC MEDICATIONS MAY BE PRESCRIBED TO
TREAT THE PATIENT’S SYMPTOMS (“CHILLS”).
A PATIENT IS TRANSITIONING FROM IV HEPARIN THERAPY
TO ORAL WARFARIN. WHICH LABORATORY FINDING DOES
THE NURSE IDENTIFY THAT CONFIRMS WARFARIN
TREATMENT EFFICACY?
A. BLEEDING TIME OF 5 MINUTES
B. PROTHROMBIN TIME (PT) OF 18 SECONDS
C. INTERNATIONAL NORMALIZED RATIO (INR) OF 2.5
D. PARTIAL THROMBOPLASTIN TIME (PTT) OF 24.3
SECONDS
ANSWER C
• INR IS A MORE ACCURATE MEASURE OF
ANTICOAGULATION THERAPY BECAUSE OF VARIATIONS IN
PT VALUES ACROSS DIFFERENT LABORATORIES.
• THE GOAL OF WARFARIN THERAPY IS USUALLY TO
MAINTAIN THE PATIENT’S INR BETWEEN 2.0 AND 3.0
REGARDLESS OF THE ACTUAL PT IN SECONDS.
WHAT IS THE MOST IMPORTANT PRECAUTION FOR THE
NURSE TO TEACH A CLIENT WHOSE PLATELET COUNTS
USUALLY RANGE BETWEEN 50,000 TO 60,000/MM3?
• A. DRINK AT LEAST 3 LITERS OF FLUIDS PER DAY
• B. TAKE A MULTIPLE VITAMIN THAT CONTAINS IRON
• C. AVOID ASPIRIN AND ASPIRIN-CONTAINING DRUGS
• D. INCREASE INTAKE OF DARK GREEN, LEAFY
VEGETABLES
ANSWER C
• AVOID ASPIRIN CONTAINING SUBSTANCES WHICH WILL
FURTHER AFFECT CLOTTING PARTICULARLY IN A PATIENT
WITH AN ALREADY LOW PLATELET COUNT
What is the antidote for warfarin?
Vitamin K
Antidote for heparin
protamine sulphate (PS)
Sickle cell disease
Genetic hemoglobin disorder that causes RBC to be sickle shaped, rather than a round biconcave cell
Sickle cell disease results in
• Chronic anemia
• Pain
• Disability
• Organ damage
• Increased risk for infxn
• Early death d/t poor perfusion
• Formation of abnormal hemoglobin chains
• Periodic episodes of sickle cell crisis
Sickle cell disease is most common in
African Americans in US
Sickle cell disease assessment: noticing
PAIN IS THE MOST COMMON SCD SYMPTOM
• CARDIOVASCULAR CHANGES
• RESPIRATORY CHANGES
• SKIN CHANGES
• ABDOMINAL CHANGES
• KIDNEY AND URINARY CHANGES
• MUSCULOSKELETAL CHANGES
• CENTRAL NERVOUS SYSTEM CHANGES
Priority problems for pt with SCD
Pain d/t poor tissue oxygenation and joint destruction and potential for infxn, sepsis, multi-organ dysfunction and death
Nursing interventions when caring for patient with SCD
Oxygen, pain meds, fluids, remove constrictive clothing, do not raise knee position of bed, elevate HOB no more than 30 degrees to decrease pressure on diaphragm, keep room at or above 72 degrees (warmth is soothing and cold promotes sickling), avoid taking BP with external cuff, check extremity circulating Q hr
Check circulation by:
Pulse ox, cap refill, peripheral pulses, toe temp
Planning and implementation for SCD
• MANAGE OXYGEN AND PAIN
• PREVENT SEPSIS
• CONTINUAL ASSESSMENT
• PREVENTION AND EARLY DETECTION STRATEGY
• DRUG THERAPY
• CARE COORDINATION AND TRANSITION MANAGEMENT
Pain meds
• ONCE IV PAIN MEDS HAVE CAUSED RELIEF, PATIENT CAN GO
BACK TO ORAL PAIN MEDS.
• CONCERNS ABOUT SUBSTANCE ABUSE CAN LEAD TO
INADEQUATE PAIN TREATMENT IN THESE PATIENTS. OPIOID
ADDICTION IS RARE IN PATIENTS WITH SCD
• PATIENTS LABELED “DRUG SEEKING”
• BE AWARE OF YOUR OWN ATTITUDES.
• THIS IS A VERY PAINFUL DISEASE. ADDICTED PATIENTS IN
ACUTE PAIN CRISIS STILL NEED OPIOIDS.
Hydroxyurea
SCD treatment, reduces sickling and pain episodes. Increases risk for leukemia, is teratogenic, and suppresses bone marrow fxn, including immunity.
Preventing a sickle cell crisis
• DRINK 3-4 LITERS WATER EVERY DAY
• AVOID ALCOHOL
• AVOID CIGARETTES
• CONTACT PCP AT FIRST SIGN OF INFECTION
• FLU SHOT ANNUALLY
• AVOID EXTREME TEMPERATURES
• AVID PLANES WITH UNPRESSURIZED CABINS
• AVOID TRAVEL TO HIGH ALTITUDES
• AVOID STRENUOUS ACTIVITIES, ENGAGE IN LOW IMPACT
EXERCISE WHEN NOT IN CRISIS
Anemia
Reduction of RBC, hemoglobin, or hematocrit. It is a clinical indicator of abnormal conditions, not a specific disease.
Common causes of anemia
SCD, glucose 6-phosphate dehydrogenase, iron deficiency, vitamin b 12 deficiency, folic acid deficiency
Polycythemia vera
Chronic disorder characterized by excessive production of RBC’s. As volume increases, blood viscosity and HGB concentration increases causing excessive workload on heart and congestion of organs. Poses risk for hemorrhage, stroke, HF, MI
Polycythemia interventions
• PAIN MEDS
• HYDRATION
• PHLEBOTOMY TO MAINTAIN HEMATOCRIT OF LESS THAN
42% IN WOMEN AND 45% IN MEN
• ANTICOAGULANTS OR LOW DOSE ASPIRIN
Lukemia
CANCER THAT RESULTS FROM A LOSS OF
NORMAL CELLULAR REGULATION LEADING TO
UNCONTROLLED PRODUCTION OF IMMATURE WBCS
(“BLAST” CELLS) IN THE BONE MARROW.
Lukemia dx
Exam of cells obtained from bone marrow aspiration and biopsy.
Priority problems for pts with acute myelogenous leukemia (AML)
Potential for infxn, possible injury d/t poor clotting from thrombocytopenia from chemo, fatigue d/t decreased gas exchange and increased energy demands.
Most common type of leukemia in adults
ACUTE MYELOGENOUS LEUKEMIA (AML)
Lukemia; infection prevention
Drug therapy, induction therapy, consolidation therapy, maintenance therapy, hematopoietic stem cell transplantation, minimize injury
Care coordination for the patient with leukemia
HOME CARE MANAGEMENT
• INFUSION NURSES – TEACHING!
• SELF-MANAGEMENT EDUCATION
• PSYCHOSOCIAL PREPARATION
• HEALTH CARE RESOURCES – ONCOLOGISTS, ONCOLOGY
NURSES, SOCIAL WORKERS, PHYSICAL OR
OCCUPATIONAL THERAPISTS, SUPPORT GROUPS
Malignant lymphomas include
• HODGKIN’S LYMPHOMA
• NON-HODGKIN’S LYMPHOMA
Signs and sx of lymphoma
• LARGE BUT PAINLESS LYMPH NODE OR NODES
• FEVERS
• NIGHT SWEATS
• UNPLANNED WEIGHT LOSS
• MANY PATIENTS HAVE NO SYMPTOMS AT TIME OF
DIAGNOSIS
Lymphoma treatment
•RADIATION OR CHEMO OR COMBO
• TEACHING ABOUT EFFECTS OF RADIATION AND/OR
CHEMO
• SYMPTOM MANAGEMENT AND LIFESTYLE MODIFICATIONS
• SPERM DONATION FOR YOUNG MALES
What is one of the most treatable cancers?
HODGKIN’S LYMPHOMA
Multiple myeloma
Cancer of WBC. B-lymphocyte called a plasma cell secretes antibodies, which are overgrown in bone marrow. Excessive antibodies are produced (gamma globulins) as well as excessive cytokines that destroy bone.
Multiple myeloma risk factors
EXPOSURE TO RADIATION, TOXINS
Multiple myeloma s/s
MANY TIMES NO SYMPTOMS WHEN DIAGNOSED
• FIRST SIGNS: FATIGUE, BRUISING, BONE PAIN
Multiple myeloma dx
ELEVATED SERUM TOTAL PROTEIN OR DETECTION OF A
MONOCLONAL PROTEIN IN THE BLOOD OR URINE
Multiple myeloma treatment
CHEMO, STEM CELL TRANSPLANT
Multiple myeloma nursing implications
ASSESSMENT, TEACHING, PAIN
MANAGEMENT
Thrombocytopenia
Low platelets, coagulation disorder
Autoimmune thrombocytopenia purpura
Autoimmune disease with unknown trigger; clotting disorder
THROMBOTIC THROMBOCYTOPENIA PURPURA
PLATELETS CLUMP TOGETHER N THE CAPILLARIES AND TOO FEW REMAIN IN
CIRCULATION, BLOOD FAILS TO CLOT WHEN TRAUMA OCCURS
Management of coagulation disorders
PREVENTING CLUMPING AND STOPPING AUTOIMMUNE RESPONSE, ADMINISTERING FROZEN PLASMA TO REDUCE CLUMPING, ASPIRIN, IMMUNOSUPPRESSIVE
Hemophilia
CLOTTING FACTOR DEFICIENCIES
HEPARIN-INDUCED THROMBOCYTOPENIA (HIT)
• EXCESSIVE BLEEDING FROM MINOR CUTS, BRUISES OR
ABRASIONS, JOINT AND MUSCLE HEMORRHAGES
• MANAGED BY INFUSIONS OF SYNTHETIC FACTOR VIII
• HIT MANAGED BY A DIRECT THROMBIN INHIBITOR
Disseminating intravascular clotting
DISRUPTION OF HEMOSTASIS CHARACTERIZED BY
WIDESPREAD INTRAVASCULAR CLOTTING AND BLEEDING. TRAUMATIC INJURY OR CAUSATIVE AGENT STARTS THE
CASCADE.
DIC s/s
•TACHYCARDIA, HYPOTENSION, CIRCULATORY COLLAPSE
• TACHYPNEA
• ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)
• OLIGURIA, ANURIA
• GI BLEEDING
• BRUISING, CYANOSIS
DIC treatment
TREATMENT IS GEARED TOWARD UNDERLYING CAUSE
• IF BLEEDING IS MAJOR MANIFESTATION – FRESH FROZEN
PLASMA OR PLATELETS TO RESTORE CLOTTING FACTORS.
HEPARIN MAY BE ADMINISTERED BUT IS CONTROVERSIAL
BECAUSE IT DISRUPTS CLOTTING BUT MAY BE NECESSARY IF
CLOTTING IS A MAIN CONCERN. PATIENTS WITH CHRONIC DIC
MAY BE PUT ON LONG TERM HEPARIN.
• FLUIDS, I&O
• MONITOR RESPIRATOR STATUS, O2 OR OTHER RESPIRATORY
SUPPORT
• NEURO ASSESSMENTS
• MONITOR OUTPUT, MAINTAIN CATHETER
• MONITOR FOR OCCULT BLOOD
• MEASURE ABDOMINAL GIRTH
• MONITOR SKILLS FOR EVIDENCE OF BLEEDING
RBC TRANSFUSIONS—
GIVEN TO REPLACE CELLS LOST FROM TRAUMA OR SURGERY
PLATELET TRANSFUSIONS—
GIVEN FOR LOW PLATELET COUNTS, ACTIVE BLEEDING, SCHEDULED FOR INVASIVE
PROCEDURE
PLASMA TRANSFUSIONS—
GIVEN TO REPLACE BLOOD VOLUME AND CLOTTING FACTORS
GRANULOCYTE (WBC) TRANSFUSIONS—
GIVEN (RARELY)
TO NEUTROPENIC PATIENTS
UNIVERSAL DONOR IS TYPE __
O
UNIVERSAL RECIPIENT IS TYPE __
AB
Pre-transfusion therapy care
• VERIFY PRESCRIPTION WITH ANOTHER RN
• TEST DONOR’S/RECIPIENT’S BLOOD FOR COMPATIBILITY
(TYPE AND CROSS MATCH)
• VERIFY PATIENT’S IDENTITY WITH ANOTHER RN
• EXAMINE BLOOD BAG LABEL, ATTACHED TAG, AND
REQUISITION SLIP FOR ABO AND RH COMPATIBILITY WITH
THE PATIENT WITH ANOTHER RN
• CHECK EXPIRATION DATE WITH ANOTHER RN
• INSPECT BLOOD FOR DISCOLORATION, GAS BUBBLES,
CLOUDINESS
During transfusion care
• PROVIDE PATIENT EDUCATION
• ASSESS VITAL SIGNS IMMEDIATELY BEFORE STARTING
INFUSION
• BEGIN TRANSFUSION SLOWLY, STAY WITH PATIENT FIRST 15
TO 30 MINUTES
• ASK PATIENT TO REPORT UNUSUAL SENSATIONS (FOR
EXAMPLE, CHILLS, SHORTNESS OF BREATH, HIVES, ITCHING)
• ADMINISTER BLOOD PRODUCT PER PROTOCOL
• ASSESS FOR HYPERKALEMIA
• BLOOD MUST BE STARTED WITHIN 30 MIN OF ARRIVAL FROM
BLOOD BANK AND COMPLETED WITHIN 4 HOURS. **CHECK
FACILITY POLICY
Transfusion reactions
•FEBRILE
•HEMOLYTIC
•ALLERGIC
•BACTERIAL
•CIRCULATORY OVERLOAD
•TRANSFUSION-ASSOCIATED GRAFT-VERSUS-HOST
DISEASE (GVHD) – CAN OCCUR SEVERAL WEEKS LATER
• THE EARLIER A TRANSFUSION REACTION OCCURS, THE
MORE SEVERE IT TENDS TO BE. PROMPT IDENTIFICATION
MINIMIZES CONSEQUENCES.
Care for a patient experiencing an infusion reaction
STOP TRANSFUSION, REMOVE BLOOD TUBING
• INFUSE NORMAL SALINE KVO – DO NOT FLUSH BLOOD TUBING!
• SAVE TUBING AND BLOOD – THIS WILL BE RETURNED TO BLOOD
BANK
• OXYGEN
• CONTACT MD WITH ASSESSMENT, CALL RAPID ACCESS TEAM IF
MODERATE TO SEVERE
• ANTIHISTAMINE – BENADRYL
• ANTIPYRETIC - ACETAMINOPHEN
• CORTICOSTEROIDS
• MEPERIDINE FOR RIGORS
A 27-YEAR-OLD FEMALE WITH A HISTORY OF SICKLE CELL DISEASE
(SCD) COMES TO THE ED WITH ABDOMINAL PAIN THAT IS RATED AS A
“9” ON A 0-TO-10 SCALE. PHYSICAL ASSESSMENT SHOWS THAT SHE IS
GRIMACING AND GUARDING HER ABDOMEN AND HAS A FEVER OF 103º
F, A PALE YELLOW HARD PALATE, AND SEVERAL VERY SMALL ULCERS
ON HER LOWER EXTREMITIES.
WHAT IS THE PRIORITY PROBLEM THAT THE NURSE MUST
IMMEDIATELY ADDRESS?
A. ACUTE PAIN
B. HYPERTHERMIA
C. POTENTIAL FOR INFECTION
D. DECREASED TISSUE PERFUSION
ANS: A
THE PATIENT’S PAIN MUST BE CONTROLLED FIRST AND
FOREMOST. ALL OTHER PROBLEMS CAN BE ADDRESSED
AFTER THE ACUTE PAIN IS MANAGED.
THIRTY MINUTES LATER, THE PATIENT IS DIAGNOSED
WITH ACUTE SICKLE CELL CRISIS. SHE CONTINUES TO
HAVE PAIN.
WHICH DRUGS DOES THE NURSE ANTICIPATE WOULD
BE PRESCRIBED FOR PAIN CONTROL AT THIS TIME?
(SELECT ALL THAT APPLY.)
A. MEPERIDINE IV PUSH PRN
B. ACETAMINOPHEN ORALLY OR RECTALLY
C. HYDROMORPHONE IV PUSH SCHEDULED DOSES
D. MORPHINE SULFATE IV PUSH SCHEDULED DOSES
E. MORPHINE SULFATE SR ORALLY OR IM SCHEDULED DOSES
ANSWER: C, D
A PATIENT IN SICKLE CELL CRISIS OFTEN STARTS WITH AT
LEAST 48 HOURS OF IV ANALGESIA. MORPHINE AND
HYDROMORPHONE (DILAUDID) ARE GIVEN IV ON A REGULAR
SCHEDULE, OR USING A PATIENT-CONTROLLED ANALGESIA
(PCA) PUMP.
ONCE RELIEF IS OBTAINED, THE IV DOSE CAN BE TAPERED
AND ORAL DRUGS MAY BE GIVEN. PRN DOSAGES SHOULD
BE AVOIDED BECAUSE THEY DO NOT PROVIDE ADEQUATE
PAIN RELIEF. IM INJECTIONS SHOULD BE AVOIDED BECAUSE
ABSORPTION IS IMPAIRED BY POOR PERFUSION AND
SCLEROSED SKIN.
QUESTION 1
WHAT IS THE PRIORITY NURSING INTERVENTION
IN THE CARE OF AN OLDER PATIENT WITH A
HISTORY OF DIVERTICULAR DISEASE AND
PERNICIOUS ANEMIA?
A. PREVENTING FALLS
B. MONITORING INTAKE AND OUTPUT
C. TURNING THE PATIENT EVERY 2 HOURS
D. ENCOURAGING A DIET HIGH IN VITAMIN B12
ANSWER A
THE PATIENT WILL HAVE DIFFICULTY ABSORBING VITAMIN
B12 BECAUSE OF HIS OR HER DIVERTICULAR DISEASE AND
MAY HAVE DEVELOPED PARESTHESIA IN THE FEET,
INCREASING THE RISK FOR FALLS.
ANEMIA MAY ALSO INCREASE THE PATIENT’S SYMPTOM OF
WEAKNESS, THEREBY INCREASING FALL RISK. PREVENTING
FALLS IS A PRIORITY INTERVENTION IN THE CARE OF
OLDER PATIENTS.
QUESTION 2
A PATIENT WITH POLYCYTHEMIA VERA IS
ADMITTED WITH REPORTS OF SHORTNESS OF
BREATH, HYPERTENSION, AND LOSS OF PULSES
IN HER RIGHT FOOT. WHICH IS THE PRIORITY
NURSING INTERVENTION?
A. ASSESS CURRENT HYDRATION STATUS
B. ADMINISTER PAIN MEDICATION
C. ELEVATE HER LOWER EXTREMITIES ON PILLOWS
D. EVALUATE THE PATIENT FOR HYPERTENSIVE CRISIS
ANSWER: A
POLYCYTHEMIA VERA, A FORM OF MALIGNANT RBC
HYPERPRODUCTION AND CLOTTING FACTOR DYSFUNCTION,
REQUIRES EVALUATION OF INTRAVASCULAR HYDRATION,
PREPARATION OF LABORATORY TESTS FOR POSSIBLE
THERAPEUTIC PHLEBOTOMY, AND ANTICOAGULANT THERAPY TO
DECREASE CLOTS.
PATIENTS WITH THIS DISEASE ARE AT RISK OF HYPERTENSION
AND EXPERIENCE POOR TISSUE OXYGENATION AS WELL,
REQUIRING ASSESSMENT. RAISING LOWER EXTREMITIES MAY
ASSIST WITH PERFUSION AND SYMPTOMS BUT WOULD NOT BE A
PRIORITY IN THIS SCENARIO.
Sickle cell crisis: Vaso-occlusion (thrombotic)
Most common type of crisis. It may last for days or weeks.
Precipitated by dehydration, exposure to cold, acidosis, or localized hypoxia.
Caused by stasis of blood with clumping of cells in the microcirculation, ischemia, and infarction.
Thrombosis and infarction of local tissue may occur if the crisis is not reversed.
Cerebral occlusion can result in stroke, manifested by paralysis or other central nervous system complications. Extremely painful; symptoms include fever, tissue engorgement, painful swelling of joints in hands and feet, priapism, and severe abdominal pain.
Sickle cell crisis: splenic sequestration
Life-threatening crisis; death can occur within hours. Caused by pooling of blood in the spleen; because the spleen can hold much of the body’s blood supply, cardiovascular collapse can result. It is most commonly seen in children and adolescents and may be seen in young adults.
Clinical manifestations include profound anemia, hypovolemia, and shock.
Sickle cell crisis: aplastic crisis
Aplastic crisis is caused by diminished production and increased destruction of RBCs.
Often triggered by human parvovirus B19 viral infection.
Signs include profound anemia, pallor, and fatigue.
Sickle cell crisis: acute chest syndrome
Acute chest syndrome is a common cause of hospitalization for patients with SCD.
Associated with a pediatric mortality rate of 2% and an adult mortality rate of 4%.
Pulmonary infiltrate of abnormal blood cells leads to lower respiratory tract symptoms.
Clinical manifestations include fever, cough, chest and back pain, dyspnea, and hypoxemia.
Pulmonary infection, infarction, and fat embolism may occur and can lead to pulmonary failure and death.
SCD therapies
Bone marrow or hematopoietic stem cell transplantation, blood transfusion is the most common treatment, splenectomy, oxygenation, hydration, and analgesic administration, hydroxyurea
For children between 2 months and 5 years of age who are diagnosed with SCD, treatment often includes daily administration of prophylactic penicillin
SCD therapies
Bone marrow or hematopoietic stem cell transplantation, blood transfusion is the most common treatment,
Conditions That May Precipitate Disseminated Intravascular Coagulation Tissue Damage:
Trauma, such as:
burns, gunshot wounds, frostbite, head injury.
Conditions That May Precipitate Disseminated Intravascular Coagulation Tissue Damage:
Obstetric complications:
septic abortion, abruptio placentae, amniotic fluid embolus, retained dead fetus
Conditions That May Precipitate Disseminated Intravascular Coagulation Tissue Damage:
Neoplasms:
acute leukemia, adenocarcinomas, hemolysis, fat embolism
Conditions That May Precipitate Disseminated Intravascular Coagulation Tissue Damage:
Vessel Damage;
Aortic aneurysm, acute glomerulonephritis, hemolytic uremic syndrome
Conditions That May Precipitate Disseminated Intravascular Coagulation Tissue Damage:
Infections;
bacterial infection or sepsis, viral or mycotic infections, malaria
