Anemia & Shock TOPIC Iggy 34 Iggy 36 Iggy37 SLIDES CLASS MODE LECTURE (RO) Reviewed? Property WEEK WEEK 2 Lecture Outcomes: Anemia, Sickle Cell, Disseminated Intravascular Coagulation Review the structure and functions of red blood cells. Describe general clinical manifestations and interventions for anemia Clinical manifestations Pallor, cool skin Increased fatigue Brittle nails Headache Murmurs/ Gallops (sounds like horse) Tachycardia- to compensate due to the low iron and oxygen circulating in the blood Orthostatic hypotension Low 02 sat Dyspnea on exertion Interventions Iron replacements and supplements (PO, IM z-track, or IVPB- Iron only) Anemia & Shock 1 Teach about iron-rich foods to incorporate in diet more ex. spinach, red meats, beans, raisins, etc Assess labs to find out what is causing the anemia What is a common cause for anemia in adults? GI bleeding Describe causes, specific clinical manifestations, diagnostic findings, and therapeutic management for the following anemias related to impaired RBC production Iron Deficiency Anemia Cause Inadequate iron intake caused by iron-deficient diet, chronic alcoholism, malabsorption syndromes, partial gastrectomy, or blood loss. aka may result from blood loss, poor diet, or poor intestinal absorptions More common in women, older adults, and clients with poor diets How many grams of iron do adults have? 2-6g 2/3 of iron is in Hemoglobin & other 1/3 in in bone marrow, spleen, liver, muscle Clinical manifestions Mild symptoms of anemia Weakness/ Fatigue Pallor Reduced exercise tolerance Fissures at the corners of the mouth Diagnostic findings Anemia & Shock 2 Serum ferritin values less than 10 ng/mL (Normal range is 10-300 ng/mL) Ferritin: a protein inside cells that store iron RBCs are small (Mircocytic) Management Iron replacements- PO, IM z-track, IVPB PO Iron supplements Pt’s can be noncompliant bc GI upset can occur ~ so teach patients to take between meals for better absorption IM z-track is used in severe treatment. It can be irritating to the mucosa and very painful. Teach about incorporating more food high in iron EX. Red meat, leafy green vegetables, kidney beans, egg yolks, raisins, etc. Only 5 % of dietary iron is absorbed ~ thats why patients are put on supplements Vitamin B12 deficiency/ Pernicious Anemia Cause B12 deficiency is caused by poor intake of foods containing B-12 (Vegetarian diets or protein deficient diets) Alcoholics have poor dietary intake* Caused by conditions that fail to activate enzymes needed to move folic acid into precursor RBCs for cell division and growth into functional RBCs B12 helps move folic acid into the cells where DNA synthesis occurs These precursor cells then undergo improper DNA synthesis and increase in size. This anemia is also called → Anemia & Shock 3 Megaloblastic or macrocytic anemia bc of the large size of the abnormal cells. Precursor cells are stem cells that have committed to developing into a new blood cell. Clinical manifestations Pallor, fatigue, weakness Jaundice- bc lack of RBCs Glossitis (red beefy tongue) Weight loss Vitamin B12 is needed for nerve function, so deficiency causes paresthesias (hands/feet) and poor balance Management Increase food high in B12 EX. Animal protein, eggs, nuts, dairy products, citrus, leafy green vegetables Vitamin supplements Pernicious Anemia A type of Megaloblastic anemia Is a type of autoimmune disorder. All autoimmune problems may have a genetic predisposition and may be present in other family members. Under the umbrella of B12 deficiency but caused by a different reason Failure to absorb vitamin B12 caused by an intrinsic factor which is a substance secreted by the gastric mucosa that is needed for intestinal absorption on B12. Caused by some damage to the gastric mucosa from a gastrectomy or gastro by-pass that disrupted the parietal cells which no longer allows the absorption of B12 Anemia & Shock 4 Is more common among older adults who may have reduced gastric absorption of many nutrients Treatment Weekly injections of vit. B-12 injections will be given then monthly there after Folic Acid Deficiency Cause Common causes of folic acid deficiency are poor nutrition, malabsorption, and certain medications Ex. of malabsorption syndromes - Crohn’s disease or Celiac disease Pts on anticonvulsants (Ex. Phenobarbital) Clinical manifestations Develops slowly Anemia & Shock 5 Same manifestations as other anemias Folic acid deficiency does not affect nerve function, so nervous system remains normal Folic acid is also required for DNA synthesis. Management Increase B12 rich foods like green leafy vegetables, liver, yeast, citrus fruits, dried beans, and nuts. Aplastic Anemia Cause Most RARE type- a deficiency of circulating RBCs bc of impaired cellular regulation of the bone marrow, which then fails to produce these cells. (aka damage to bone marrow stem cells) caused by an injury to the immature precursor cell for RBCs Clinical manifestation Presents with Pancytopenia → deficiency of all blood cell types (RBCs, PLTs, and WBCs) Due to the damage in bone marrow stem cells, body does not make enough Bleeding gums or bleeding of the nose Infection is common. Diagnostic findings Pancytopenia: Deficiency in all 3 cell types in the blood (RBCs, PLTs, WBCs) CBC will show severe macrocytic anemia, leukopenia, and thrombocytopenia Bone marrow biopsy- May show replacement of the red, cellforming marrow with fat Management/ TX Anemia & Shock 6 Repetitive blood transfusions- short term management Prednisone Stem cell transplant Most succesful method of treatment that does not respond to other therapies Sometimes a Splenectomy- bc the spleen is responsible for destroying PLTs by the immune system so a splenectomy would prevent the damage or reduction of PLTs What is the difference between vitamin B12 deficiency and folic acid deficiency? Vitamin B12 deficiency has to do with nerve function and can result in paresthesias. Folic acid deficiency has NOTHING to do with nerve function but is required for DNA synthesis. ((B12 moves folic acid into the cell where DNA synthesis.)) So you’ll see nervous system changes with B12 deficiency but not with folic acid deficiency What type of anemia sometimes follows with a viral infection? Aplastic anemia because it causes pancytopenia (deficiency in all 3 blood cells types) Low WBCs makes the patient more susceptible for infection to follow. Describe causes, specific clinical manifestations, diagnostic findings, and therapeutic management for Sickle Cell Anemia. What is sickle cell anemia? It is a genetic disorder with an autosomal- recessive pattern of inheritance Causes It is a genetic disorder in which a mutation in the gene for the beta chains of hemoglobin causes chronic anemia, pain, disability, organ Anemia & Shock 7 damage, increased risk for infection, and early death as a result of of poor blood perfusion. Results in the formation of abnormal hemoglobin chains Specific clinical manifestations Clumped masses of sickled RBCs block blood flow and perfusion, known as a vaso-occlusive event (VOE) Pain is the most common symptom of SCD crisis!! Top priority SOB General fatigue/ weakness Murmurs Increased jugular- venous distention Ulcers or sores on lower legs due to poor perfusion Cool to touch extremities that are distal to the blood vessel occlusion, pallor or cyanotic skin Abdominal changes due to organ damage to the spleen and liver Slow cap refill Pulmonary hypertension Anemia & Shock 8 What is “Sickling” and what can cause it? Clumped masses of sickled RBCs block blood flow and perfusion, known as a vaso-occlusive event (VOE) VOE leads to further tissue hypoxia and more sickled shaped cells, which leads to more blood vessel obstruction, inadequate perfusion, Anemia & Shock 9 and ischemia in the affected a tissues ~ aka Sickling aka sickle cell crisis Sickling can be caused by hypoxia, dehydration, infection, venous stasis, pregnancy, alcohol consumption, high altitudes, low or high environments or body temperature, acidosis, stress, strenuous exercise, etc. Sickled cells usually go back to normal shape when the precipitating condition is removed and the blood O2 level is normalized, but some of the hemoglobin remains twisted decreasing cell flexibility and more fragile RBCs containing 40% or more of HbS is about 10-20 days , much less than the 120-day life span of normal RBCs with HbA. Diagnostic findings In SCD at least 40% and more of the total hemoglobin is composed of two normal alpha chains and two abnormal beta chains creating (HbS) that fold poorly While normal human hemoglobin molecule (HbA) has two normal alpha chains and two normal beta chains of amino acids Normal RBCs usually contain 98-99% HbA with a small % of a fetal form of hemoglobin (HbF) not HbS HbS is sensitive to low O2 content of RBCs, which causes them to fold even more, distorting the cells into sickle shapes Therapeutic management ~First always try to PREVENT the crisis!!~ Drug therapy Hydroxyurea (Droxia)- stimulates fetal hemoglobin production (HbF) → reducing the number of sickling and pain episodes Oral hydration Assess circulation Q hour Anemia & Shock 10 Pain management Oxygen therapy Patient education on prevention of crisis and identifying external factors that cause crisis What to do during a sickling crisis? Remove restrictive clothing to prevent ulcers on LE Keep extremities extended to promote venous return Assess circulation every hour Obtain pulse ox of fingers and toes Checking cap refill, peripheral pulses and toe temperatures Administer hydroxyurea (antimetabolites) Which two anemias are genetic? Aplastic & Sickle Cell Which anemia is an autoimmune disorder? Pernicious Describe the etiology, pathophysiology, diagnostic tests and treatment for disseminated intravascular coagulation (DIC). Etiology Is a rare condition affecting the blood’s ability to clot and stop bleeding In DIC abnormal clumps of thickened blood clots form inside blood vessels. → These abnormal blood clots exhaust and deplete the blood’s clotting mechanisms, which can lead to massive bleeding to all other areas Pathophysiology Happens in response to some type of injury~ either severe trauma or surgery with lots of blood loss or a hemorrhage Overstimulation of clotting and anti-clotting processes in response to injury (severe, trauma, surgery, or hemorrhage) Anemia & Shock 11 Dx tests Low levels of fibrinogen Prolonged PT Decreased platelets Elevated d-dimer level Treatment Plasma transfusions Anti-coagulation medication; blood thinners to prevent blood clots Lecture Outcomes: Nursing Role In Management of Shock Define shock. Shock occurs when there are some types of insults to the body or the patient in which it starts a process where there is an inadequate tissue oxygenation which leads to poor perfusion~ it can put the patient in a state of anaerobic cellular metabolism. Anaerobic cellular metabolism is a mechanism to compensate or to maintain/restore tissue perfusion Identify factors that influence tissue perfusion. Tissue perfusion depends on how much oxygen from arterial blood perfuse tissues Organ perfusion is related to MAP (mean arterial pressure) Factors that influence MAP Total blood volume Cardiac output Size of the vascular bed Describe the clinical manifestations associated with the compensatory mechanisms for shock. Increased HR, RR, and vasoconstriction- To ensure blood flow and oxygen to vital organs Anemia & Shock 12 Shunting blood flow to less vital area e.g. skin and skeletal muscles; the body will bypass these areas to make sure theres enough O2 for the vital areas → Heart and brain If initiating event continues then MAP continues to drop and anaerobic metabolism starts→ Increase lactic acid → Causes electrolyte and acidbase imbalances which have tissue damaging effects → Leading to injured organs Describe the stages of shock. Initial (early shock) Decrease in mean arterial pressure (MAP) of 5-10mmHg from baseline value Increased sympathetic stimulation Mild vasoconstriction Increased heart rate Non-progressive/ Compensatory stage Decrease in MAP 10-15 mmHg from baseline value Continued sympathetic stimulation Moderate vasoconstriction Increased HR/ Decreased pulse pressure Chemical compensation Renin, aldosterone, and antidiuretic hormone secretion Increased vasoconstriction Decreased urine output Some anaerobic metabolism in non-vital organs Mild acidosis Mild hyperkalemia Progressive/ Intermediate Anemia & Shock 13 Decrease in MAP of >20 mmHg from baseline Anoxia of non-vital organs Hypoxia of vital organs Overall metabolism is anaerobic Moderate acidosis Moderate hyperkalemia Tissue ischemia Refractory/ Irreversible When too much cell death and tissue damage result from too little oxygen reaching the tissues Severe tissue hypoxia with ischemia and necrosis Release of myocardial depressant factor from the pancreas Build up of toxic metabolites Multiple organ dysfunction syndrome (MODS) Death Identify clients at risk for hypovolemic shock and discuss precipitating factors Common in elderly and ped. pts Hemorrhage # 1 cause to hypovolemic Trauma Surgery Vomiting/ Diarrhea Diaphoresis NGT Diuretic therapy Prioritize nursing care for a client with hypovolemic shock. Priority problem for patients in hypovolemic shock is perfusion!! Anemia & Shock 14 Best practice for a patient safety and quality care - pg. 739 red box Ensure a patent airway Insert an Iv catheter or maintain O2 saturation at 92-96%: supplemental oxygen in no longer recommended if saturation is normal Elevate the patient’s feet, keeping his or her head flat or elevated to no more more than 30-degree- angle Examine the patient for overt bleeding If overt bleeding is present, apply direct pressure to the site. Administer drugs as prescribed Increase the rate of IV fluid delivery Do not leave the patient Describe the pathophysiology, clinical manifestations and effects of shock on major body systems. Clinical manifestations of shock on major body systems Neuro: thirst, anxiety, restless Cardiac: decreased MAP (increased HR, dec BP) Resp: RR increases to perfuse organs Renal: saves water by decreasing filtration Skin: blood vessel constrictions, allows more blood to circulate to vital organs GI: decreased motility, absent bowel sounds Explain the basis for intravenous therapy for hypovolemic shock. Colloids- helps restore osmotic pressure; ex: albumin Crystalloid- Normal saline increases plasma volume; help maintain an adequate fluid and electrolyte balance ex. NS and Ringer’s lactate; Normal saline is a replacement solution used to increase plasma volume and can be infused with any blood product. Anemia & Shock 15 Blood products - Used when shock is blood loss Explain the role of the nurse in detecting and preventing shock. Assess for dehydration and early manifestations ALOC Changes in vital signs (increased HR, RR, Decreased BP) Dec I &O Thirsty Labs: H&H, RBC Consider PMH, look at meds, surgery (EBL), anemic Anemia & Shock 16
