Sickle Cell Anemia Flashcards
Nursing interventions to reduce infection
- administer antibiotics as prescribed
- Take special care of leg ulcers & other wounds
- Observe Hand hygiene & Facility precautions
Acute Chest Syndrome
- Develops from either hypoxia/ increased blood viscosity
- Type of Sickle Cell crisis common in children w/ the disorder
S/S: fever, cough, chest & back pain, SOB, and hypoxemia
Can lead to pulmonary infection, infart, fat embolism which can lead to pulmonary failure & death
Sickling
When the % of hemoglobin is replaced by Hgb S increases
May be triggered by fever & an emotional/ physical stressor
Vaso-Occlusive Sickle cell crisis
When sickling develops, the cells tend to stick together; causes an obstruction of blood flow in the capillaries; triggers vessels to vasospasm and halt blood flow; leads to ischemia and infartion
s/s: fever, tissue engorement, painful swelling in joints (hands&feet), priapism (painful erection), severe abd. pain
Sickling test (Sickle cell prep)
O2 is removed from blood collection & the RBCs are observed for the sickling effect
Sickle dex
After the collecting of blood, Hgb S is known if the solution turns cloudy after they add a chemical agent to it.
-Sickle dex test verifies Hgb electrophoresis
Nursing Interventions to relieve pain (Sickle cell crisis)
- Ora & IV Hydration
- Carfully position & support painful areas
- Massages
- Music Therapy
[NO ICE] –> Vasoconstriction
Diagnostics (Sickle cell)
- Sickle cell prep (Sickling test)
- Sickle Dex
- Hgb electrophoresis
- Antenatal diagnosis (via aminocentesis & gene mapping)
Splenic Sequestration
- Pooling of blood in the spleen
- The spleen holds much of the body’s blood supply, and pooling of blood can cause a cardiovascular collaspe
S/S: anemia, hypovolemia, and shock
Decrease in spleen function increases the risk of infection
Pharmacological agents (Tx of Sickle cell anemia)
- IV hydration
- Analgesics (Morphine sulfate, hydromorphone
- Antibiotics
- Packed RBCs
Sickle Cell anemia
chrronic hemolytic anemia
Sickle Cell Disorder
What is it?
What happens?
How does one get it?
- The replacement of normal Hgb w/ abnormal Hgb S in the RBCs
- The Hgb S gene, changes the structure of the beta chains (valine instead of glutamic acid) causing Hgb molecules to form long chains
- This deforms the cell and turns it into an S shape.
- The disorder is transmitted as an autosomal revessive genetic defect
- If both parents have the trait, there’s a 25% the child will have the disease
Risk factors for Sickle Cell Disorder
- African descent
- If both parents carry the disease and/or trait
- Medditerranean descent
Sickle Cell Crisis
- Periods when the % of Hgb S increases
- Symptoms often marked by acute pain resulting from ischemia
- Precipitating Factors: Increased Blood Viscosity (Thickness of blood) & Hypoxia (low O2 tension)
[Any condition that increases the body’s need for O2 or alters the transportation of O2 may lead to sickle cell crisis]
-Sickle cells resume normal shape when rehydrated & reoxygenated. Shortens the lifespan of the RBC to 10-20 days, because is causes the membranes to be fragile
Nursing Interventions to increase tissue perfusion
- O2 therapy (Do whatever it takes to keep the pt’s O2 sat above 94%)
- Pt-controlled analgesic pump
- Administer blood when the anemia/ vaso-occlusion is severe
