Hemostasis Flashcards
Process of Hemostasis
- Start with vasospasm which causes vasoconstriction at the site of injury
- Von Willibrands factor is released which helps by binding to platelet receptors causing platelets to stick to the expressed collagen . vWF allows platelets to stick to the site of injury. Intrinsic pathway is activated by factor XII; extrinsic pathway is activated by tissue factors. These pathways lead to activation of factor X
- Need platelets to form the fibrin matrix and stick everything together. Prothrombin is converted to thrombin which is converted into fibrinogen which forms an insoluble fibrin thread around the platelets to hold it all together. In the clot itself, RBCs and neutrophils get trapped in which form a nice clot within the vessel
- t-PA is released when the process of hemostasis happens. If the clotting cascade were to start and nothing ever stopped it, the result would be massive clotting throughout the entire body. The fibrinolysis starts around the time the body is making the clot so that it breaks it down to prevent it from getting too big
The blood clotting cascade
The extrinsic pathway starts the clotting process with some type of trauma causing constriction which causes tissue factor to release in the form of a plug
The intrinsic pathway is starting with platelet aggregation itself. The platelets get called to vWF to begin sticking together.
Where meds are affected in the process: thrombin inhibitors (heparin, etc.) act in the extrinsic pathway (decrease the formation of the platelet plug), act at platelet aggregation (not calling as many platelets together and they aren’t sticking together), affecting thrombin and factor XII. Heparin acts in a lot of different places which makes it most effective. Aspirin platelet inhibitors only affect the ability of platelets to stick together. Vitamin-K dependent meds (Warfain, etc.) affect the conversion of prothrombin to thrombin. Tissue plasminogen activator (t-PA) interferes with the fibrin clot by introducing plasmin to assist with clot lysis.
Calcium role: low calcium levels= more inclined to bleeding
Clotting deficiencies: hemophilia is factor VII. Factor IXa needs factor VII to covert. We are halfway down the cascade is there is a Factor VII deficiency
Process of fibrinolysis
Plasminogen is released
Plasminogen activators and thrombin digest the fibrin clot into the fibrin degradation products
Lab- fibrin split products: the more clot that’s breaking down, the more split products there will be
Platelet labs
140-400,000
Lasts 7-10 days
Important when looking at effectiveness of platelet inhibitors (e.g., aspirin which lasts 7-10 days)
The platelets made under the effects of aspirin will have the same effect as the lifetime of the platelet
Bleeding time
3-10 minutes
Not typically done anymore
A cut is made on the forehead or earlobe and time it takes to clot without pressure is measured
Thrombin time
7-12 seconds
The time needed for blood to clot when thrombin is added
Fibrinogen defects, DIC (disseminated intravascular coagulation), streptokinase therapy are the reasons to measure this. Thrombin times need to be sent on ice because want to prevent them from clotting
PTT (aPTT)
21-35 seconds
Activated PTT (aPTT) is more sensitive to monitor Heparin; otherwise they are the same. If patient is on Heparin, their levels should be 1.5-2x the normal (want them higher). Anything greater than 70 seconds, the patient is at risk for spontaneous bleeding
Low levels of PTT occur after hemorrhages and very early in DIC- looking at using up those coagulation factors
PTT shows us a defect in intrinsic thromboplastin system and extrinsic coagulation mechanisms
PT
11-13 seconds
Measures a defect in the extrinsic system. Directly affected by Vitamin K levels and are decreased in alcohol abuse. Alcohol abusers are at an increased risk for bleeding because of the extrinsic pathway
PT & PTT are looking at normal within the same lab. INR looks across international standards. This is why INR is looked at more often that PT and PTT
INR (international normalized ratio)
0.7-1.8
For someone on Warfarin, levels will be 2-3x the normal for effective coagulation
Plasminogen
Males: 76-124% normal or 0.76-1.24 fraction
Females: 65-153%
Infants: 27-59%
In a normal clot, plasminogen is absorbed in the clot, turns to plasmin which gradually dissolved the clot. It’s the dissolving part of the clot. Antiplasmin in the plasma deactivates the plasmin. When abnormal clotting occurs, excessive plasmin is present in the plasma and antiplasmin is depleted causing bleeding. The more plasminogen we have, the higher our risk for clotting is
D-dimer
<250 ug/l or <1.37 nmol/l
Not a common lab; will be drawn in patients with pulmonary embolisms and confirming diagnosis of DIC
It confirms that thrombin and plasmin have been made
Fibrinogen
200-400 mg/dl
The enzyme action needed to convert fibrin (part of the normal clot)
Increased in tissue damage and inflammation
A patient is transitioning from IV Heparin therapy to oral Warfarin. Therapeutic anticoagulation of the patient is best assessed by:
A- partial thromboplastin time of 24.3 seconds
B- Prothrombin time of 18 seconds
C- INR of 2.5
D- bleeding time of 5 minutes
C
INR is more accurate because of variations that occur with PT values across different labs. The goal of warfarin is to maintain INR between 2.0-3.0 regardless of the actual PT in seconds
Assessment
History: chronic diseases (GERD, ulcers, Chrons, etc.), meds (aspirin, Coumadin, etc.), is the problem r/t bleeding or anemia (anemia’s can be caused by bleeding)
Diet- great consumption of alcohol decreased clotting factors, high in Vit K (e.g., green leafy vegetables) increases clotting, low calcium decreases clotting
Skin- pallor, cyanosis (extreme bleeding or anemia can cause decreased oxygenation), do their gums bleed after brushing teeth, petechiae (pinpoint red dots that do not Blanche when pushed on), ecchymosis (bruising)
HEENT- nosebleeds or epistaxis
Respiratory- dyspnea and fatigue may be a possible pulmonary embolism
Cardiac- history of MI, pulmonary embolism, A-fib (or other cardiac dyrhythmias) may increase the risk for clot
Abdomen- GI assessment
MS- calf measurements (if one is bigger than the other, a clot is suspected), positive Homens sign (pain with dorsiflexion of the foot)- negative sign does not mean there is not a clot
Renal- hematuria, history of chronic diseases with anemia’s
Hemophilia
X-linked recessive- all X’s must be affected; boys are more at risk
Deficiency of Factor VIII or IX necessary for formation of thromboplastin
Hemophilia A: factor VIII disorder
Hemophilia B: Factor IX disorder
Bleeding into the joint spaces are most common because they have the most stress on them with daily activities: nosebleeds, knee bleeds; kids may need to be hospitalized to have their knees drained
Have a humidifier on furnace to help prevent nosebleeds
If they bleed, apply pressure and elevate until can give them whatever Factor they are missing via IV. Teach parents how to start peripheral IVs and give Factor at home. Teach them to reconstitute with normal saline and pull IV out after factor is given
DDAVP (Demopressin) to help concentrate clotting factors
Prevent bleeding: no contact sports; encourage activities that are not stressful on joints and things that will not increase risk for bleeding, bruising, or head injuries
Von Willebrand Disease
Autosomal inherited
Risk is equal in male and females
Control bleeding and replace missing factors
DDAVP (Desmopressin) to help concentrate. Typically do not give vWF as injections
vWF sticks the platelets to the site of bleeding. Typically not as bad as in Hemophilia. They can have joint bleeds, nose bleeds, etc.
Ice packs for minor cuts or bruises. Typically do not need to do anything.
Often not diagnosed in women until first menses where the bleeding does not stop. vWF will be drawn and labs will be lower in these patients. Some aren’t diagnosed until they get pregnant and have a postpartum hemorrhage
Immune Thrombocytopenia Purpura (ITP)
Platelet count less than 150
Acute or chronic
Autoantibody destruction of the platelets
Steroids, IVIG
Not genetic
Example: child has normal flu/cold, small fever, feels crummy, 5 days later, they feel great, up and running around. Petechiae are noticed. Scratching causes petechiae in the skin to form due to capillary bleeds
Immune system kicks into overdrive during flu/cold and begins to destroy platelets. This makes them high risk for bleeding.
Give immune factors (IVIG, IV immunoglobulins) which is an artificial immune system that stops the body from needing to produce its own. If we stop producing our own, we stop destroying the platelets and eventually normalizes. Also may be started on a course of steroids until platelets come back up.
For most kids, platelets begin to rise, immune system normalizes, and problems go away after 5 days. There are a small amount of kids that will end up with chronic ITP
Chronic ITP
Normal platelets of 50-100
Bleeding risk is very high. No contact sports
If less than 50, may need periodic IVIG injections or infusions. Girls may need to be put on Depo-Provera shots to prevent menses
Can become very anemic from losing blood
If we have autoantibody destruction of the platelets, they will not get a platelet bump from infusing platelets. Platelet infusions do not work. Someone with acute bleeding like a subdermal hematoma, platelets will be helpful. Platelet infusions themselves do not work with ITP because they are automatically destroyed
Supportive care and bleeding prevention until able to raise platelet counts go back up. Kids with chronic ITP may need to wear a helmet (r/t falling down a lot) to prevent any injuries
Regularly monitor platelets to see if need IVIG
Splenectomy may be done to cause less platelet destruction.
Post-op complications: very high risk of bleeding due to removal of a highly vascular organ
Bleeding disorders in women
Von Willebrand Disease (vWD): most common bleeding disorder in women; effects 1-2% of the general population; if the patient has menorrhagia, incidence of vWD is 20-25%
Menorrhagia can lead to chronic pain, anemia, hospitalizations, blood transfusions, limitations in activities,
Symptomatic carriers of hemophilia: mucotaneous- nose bleeding, mouth bleeding, easy bruising; 2 categories: inherited a gene from father and mother; or she is a genotype carrier who has experienced extreme lyonization of the hemophilia gene causing factor VIII or IX to be turned off . Lyonization is X-inactivation where one copy of the X chromosome in each female cell is inactivated to prevent female cells from having twice as many gene products from the X chromosomes as males
Rare bleeding disorders in women: factor XI deficiency (very rare; autosomal inheritance pattern-males and females equally affected); common in Jewish, European, eastern, Israeli heritages
Gynecological and OB Bleeding
Dysmenorrhea- painful menstruation
Menorrhagia- exceeding 80mL per cycle; alkaline technique to test for this where feminine hygiene products go to the lab; need women to record the number of days menstruated, number of feminine products used, level of saturation of products each day or each hour. Treat with hormone therapy, desmopressin, acetate or DDAVP, antifibrinolytics, and replacement of clotting factors
Estrogen raises the levels of clotting factors II, VII, VIII, X, and vWF. Avoid excessive fluid intake with DDAVP because hyponatremia may develop
Amicar and lysteda are antifibrinolytics may be used
Surgical interventions: endometrial ablation or hysterectomy. Ablation is preferred because it is not as invasive and some can be done chemically in the office. This can render a patient sterile and reproductive plans should be considered
Women with dysmenorrhea experience endometriosis which is where endometrial tissue has migrated outside the uterus. The extra tissue in the abdominal cavity will bleed each month with menstruation. Free blood in the abdomen can cause severe pain. Usually treated with NSAIDs but can worsen the bleeding because can cause platelet dysfunction so other pain meds should be considered.
OB complications: amniocentesis, chronic sampling, and cordocentesis can be done but are invasive and risk for bleeding and miscarriage should be weighed. Recommended to have vaginal delivery unless there is fetal distress. Suction and forceps should be avoided. Late PPH (5-14 days after birth) is frequent
Start around age 6; not usually diagnosed until 23-25. Can cause anger, fear, depression. Affects QOL, lethargy, reproductive affects, absenteeism
Early pregnancy spontaneous abortion
Cause: congenital anomalies, maternal infection, immune response, bleeding anomalies
Threatening when vaginal bleeding is followed by uterine cramp, backache, pelvic pressure
Inevitable with membrane rupture, cervix dilate
Manage by notifying immediately, look for history of symptoms, ultrasound
Natural expulsion (body expels the pregnancy), D&C (dilation and curtage) to remove the products from the uterine cavity
VIP- planned abortion
SAB- spontaneous abortion
Ectopic pregnancy
Implant outside the uterus most often in the Fallopian tubes
Missed menses with abdominal pain and vaginal spotting
Needs to be removed with meds (like methotrexate) or surgically
May have positive beta-hCG or pregnancy test but no gestational sac present in ultrasound
Manage-inhibit cell division with surgery
Notify provider, IV access, pain treatment, ready for surgery. May cause infertility related to damage of the tube
If tubal pregnancy continues, can be life-threatening
Offer support and utilize resources to help mom
Early pregnancy/ bleeding gestational trophoblastic disease
Trophoblasts develop abnormally
Placenta develop not fetus
Can be malignant
About 90% of women who have abnormal cells in the uterus experience increased bleeding; fibroids are a common cause of increased bleeding as well in pregnant and non-pregnant
Ask about history of uterine fibroids, cancers, uterine known anomalies, IUD currently or in the past, tubal pregnancy, tubal ligation, etc.
Pregnancy: placenta previa
Implant in lower uterus
Marginal: >3cm from cervical os
Partial: <3cm; not completely cover cervical os
Total: covers cervical os
Sudden onset of painless uterine bleeding often when cervical changes disrupt placental attachment
Home care: bed rest, assess vag bleeding after each urination and BM, count fetal movement, assess uterine activity, no sex
Delay birth of mom CV stable and has adequate oxygenation and perfusion; deliver after 36 weeks if possible
If mom not stable, treat mom and remove baby so mother can survive
Can start with low-lying placenta, but as uterus grows, can grow to be not low-lying later in pregnancy
Low-lying placenta- more gravity pressure which can lead to more bleeding
Pregnancy: abruptio placenta
Separation before fetus is born
Bleed and hematoma on maternal side; fetal vessels can be disrupted resulting in fetal and maternal bleed
Risk: HTN, smoke, multigravida, abdominal trauma, cocaine
Manifestations: vaginal bleeding, abdominal and lower back pain, frequent low-intensity contraction, uterus tender on side of abruption, increased fundal height, hard abdomen, late decels
Treat: if no fetal distress ans minimal bleed- bed rest, decreased uterine activity with tocolytic (magnesium, nifedipine), prompt/emergency delivery
Bicordinate uterus: heart shaped
Concealed abruption is often fatal. Usually happens in shearing odd the uterine wall with slamming on breaks or getting in a car accident
Relatively concealed may have slight intermittent bleeding
Postpartum Hemorrhage: uterine atony
Failure of muscle fibers to contract around blood vessels
Soft/boggy; should feel like a grapefruit at umbilicus, fundus is higher than expected, excessive clots
Bright red lochia
Treat with massage, pitocin, oxytocin, hemabate for bleeding, support lower uterus
Caused by overdistention (multiples, large, hydramnios), precipitate delivery, long labor, forceps/ vacuum, c-section, uterine inversion, placenta previa, tocolytics
Greater than 1 pad in 15 minutes
Express clots by applying gentle pressure on the fundus in direction of the vagina; only push on contracted uterus to prevent inversion
Postpartum Hemorrhage: trauma
Laceration: perineum, vagina, cervix, urethral meatus: bright red blood
Hematoma- vulvar, vaginal, retroperitoneal: discolored bulging mass sensitive to touch, pain with pressure, small reabsorb, large incision and evacuate clot
Sometimes pulsatile bleeding of artery is affected
What intervention most effectively protects a client with thrombocytopenia?
Avoiding dentures
Encouraging electric shaver
Rectal temperatures
Warm compress on trauma sites
Electric shaver
A client with thrombocytopenia is being discharged. What info does the nurse incorporate into teaching plan?
Avoid large crowds
Drink at least 2L of fluid a day
Elevate lower legs when sitting
Use a soft-bristled toothbrush
Use a soft bristled toothbrush
2 hours after giving birth, a primiparous woman becomes anxious and complains of intense perineal pain with a strong urge to have a BM. Her fundus is firm at the umbilicus and midline. Her lochia is moderate rubra with no clots. The nurse would suspect:
Bladder distention
Uterine atony
Constipation
Hematoma formation
Hematoma formation
The nurse is preparing to discharge a 30y/o F who experienced a miscarriage at 10 weeks gestation. Which statement shows a correct understanding of discharge instructions?
I will not experience mood swings since I was only 10 weeks
I will avoid sex for 6 weeks and pregnancy for 6 months
I should eat foods high in iron and protein to help my body heal
I should expect the bleeding to be heavy and bright red for at least one week
Eat foods high in iron and protein
The school nurse is caring for a boy with hemophilia who fell on arm during recess. What supportive measure should the nurse do until factor replacement can be initiated?
Apply warm, moist compress
Apply pressure for at least one minute
Elevate area above the level of the heart
Begin passive ROM unless pain is severe
Pressure for at least one minute
What’s the most appropriate action for stopping an occasional episode of epistaxis (nosebleed)?
Have child sit up and lean foreword
Apply ice under nose and above lip
Lie down with feet elevated
Apply continuous pressure to the nose with thumb and forefinger for at least 1 minute
Sit up and lean foreword
Thrombus
Collection of blood factors on vessel wall
Thrombophlebitis
Inflammatory response to thrombus
This is the inflammation where the venous thrombus is the clot itself
Embolus
Mass of thrombus or amniotic fluid released into the vasculature to obstruct capillary bed elsewhere
Pulmonary embolism
Pulmonary artery obstructed by a clot
Blockage by clot, air, or fat emboli or tumor tissue. Can be caused by amniotic fluid. Most originate in the calf, femoral popliteal, or iliac vein
Emboli can move from a smaller vessel to a larger vessel and obstruct circulation
Other sources of emboli include tumor, fat emboli, bone marrow, amniotic fluid, septic thrombi, and vegetations on heart valves that develop with endocarditis
Clotting risk factors
Bed rest, sitting, inactivity, incompetent valve, presence of catheters or wires in the vasculature, pregnancy, oral contraceptives that contain estrogen, lupus, and clotting disorders
Hip, knee, abdominal, and extensive pelvic procedures
Pregnancy, obesity, and cancer
Virchow triad
Venous stasis
Hypercoagulation
Vessel damage
If one is removed through prevention or drug therapy, we can help reduce the change of clots forming
Signs and symptoms of different clots
Pulmonary embolism: anxiety, sudden dyspnea, tachypnea, tachycardia, cough, significant pleural chest pain, hemoptysis, crackles, fever, pulmonic heart sound change, change in mental status
Major pulmonary embolism: pallor, shock, dyspnea, crushing chest pain, pulse that’s very rapid and weak, low BP, ECG indications of right ventricular straining; will lead to atelectasis and decreases CO
Medium sized embolism: pleuritic chest pain with breathing, dyspnea, slight fever, productive cough with blood-streaked sputum
Small emboli: pulmonary HTN, EKG and chest x-ray will indicate right ventricular hypertrophy. Arterioles will constrict because of platelet degradation accompanied by an increase in histamine, serotonin, catecholines, and prostaglandins
PE can lead to right sided heart failure from increased workload of the right side of the heart
Massive pulmonary embolus can result in pulmonary collapse, hypoxia, and acidosis
Factor V Leiden Thrombophilia
Protein C deficiency
Clot process is active longer- risk for DVT and PE
Common inherited form of thrombophilia
Mutation in Factor V gene increases risk for developing Factor V Leiden. The protein is involved in chemical reactions that hold clots together. Activated C protein prevents the clots from growing too large by inactivating Factor V. Unable to do this with this deficiency
S/S: DVT or PE before 50y/o, venous thrombus in unusual sites in body like brain or liver, DVT or PE after pregnancy, multiple pregnancy loses, unexplained pregnancy loss in second or third trimester, family history of embolism
Women with this who take oral contraceptives are 35x more likely to develop DVT or PE; postmenopausal women taking HRT (hormone replacement therapy) are 2-3x more likely to develop DVT or PE
Usually diagnosed with coagulation studies and DNA analysis of Factor V (F5 gene). This increases clot risk during pregnancy by 7x; require close monitoring with pregnancy
Inheriting one copy from a parent increases risk for clot by 4-8x; inheriting two copies may increase risk for thrombophilia by 80x
DVT
Vessel trauma leads to platelet aggregation (worse with stasis/immobility) leads to a clot from platelet and fibrin leading to RBC trapped in fibrin leads to clot growth in direction of blood flow which then leads to inflammation
Clot vessel damage is reversible but fibroblasts invade the thrombi and can permanently destroy valves (leads to persistent varicose veins after DVT)
80% begin in calf
DVT risk factors
Orthopedic surgery
Pregnancy
A-fib
MI/heart failure
Angina
Ischemic stroke
Anything that increases estrogen or estrogen-like pharmacological treatment will increase risk for clotting
DVT Manifestations
Calf pain
Positive Homens sign
Diagnosis with duplex venous ultrasound (US), MRI, Ascending contrast venography, D-dimer
DVT treatment
NSAIDs
Anticoagulant: heparin, LMWH, warfarin
Fibrinolytic- t-PA, streptokinase
Platelet inhibitors- aspirin
DVT nursing interventions
Prevent venous stasis- embolic stocking (make sure they fit properly), ensure adequate blood flow with casts, compression socks and foot pumps may be used to contract the valve muscles and help with circulation
Increase perfusion
Manage pain
Monitor labs
Diet
The nurse is teaching the young female client on how to prevent venous thromboembolism specific to her hospital stay after invasive orthopedic surgery. Which statement indicates the need for further teaching?
I must stop taking birth control pills
I should drink lots of water to prevent dehydration
I should exercise my legs when I have been standing or sitting for a long time
If I wear pantyhose, I won’t have to wear the stockings the hospital gives me
If I wear pantyhose I won’t have to wear the stockings the hospital gives me
When caring for a client who has received recombinant tissue plasminogen activator (t-PA) for a large DVT, the nurse would be most concerned if the client developed which of these?
Small amount of blood at IV insertion site
Heavy menstrual bleeding g
+1 pitting edema of the affected extremity
Client stating the year is 1967
Client stating the year is 1967
