Hematologic/immunologic disorders

Pathophysiology

Anaphylaxis (anaphylactic shock) is a potentially life-threatening condition resulting from an exaggerated or hypersensitive response to an antigen or allergen. The classic presentation occurs in a sensitized person (i.e., someone who has been exposed previously to the same antigen), within 1 to 20 minutes of exposure to the antigenic substance, most often drugs, foods, insect stings or bites, antisera, and blood products. The hypersensitive response results in airway inflammation that causes obstruction and respiratory distress, which can lead to respiratory arrest, with a relative hypovolemia caused by massive vasodilation. Fluids shift from the vasculature into interstitial spaces, creating a false hypovolemia or vasogenic (vasodilated) shock, which progresses to end-organ dysfunction secondary to tissue hypoxia from poor perfusion.

The hypersensitivity response occurs primarily on the surface of the mast cells of the lungs, small blood vessels, and connective tissue. The antigen combines with sensitized antibodies from previous exposure (usually immunoglobulin E [IgE] type) and attaches to basophils circulating in the blood. Inflammatory mediators are then released from the granules within the cells, including histamine, serotonin, kinins, and eosinophil and neutrophil chemotactic factors. Histamine is the primary mediator of an anaphylactic response. Activation of histamine receptors causes increased capillary permeability, increased pulmonary secretions, bronchoconstriction, and systemic vasodilation.

The antigen-antibody complexes activate production of prostaglandins and leukotrienes, which are termed slow-reacting substances of anaphylaxis (SRSA)—chemical mediators that produce systemic effects with potentially deleterious results, including profound shock. The leukotrienes produce severe bronchoconstriction and cause venule dilation and increased vascular permeability. The prostaglandins exaggerate bronchoconstriction and potentiate the effects of histamine on vascular permeability and pulmonary secretions. Kinins contribute to bronchoconstriction, vasodilation, and increased vascular permeability. Eosinophilic chemotactic factor of anaphylaxis (ECFA) is then released to attract eosinophils, which work to neutralize mediators such as histamine, but the amount of neutralization is ineffective in reversing the anaphylaxis. (See Figure 10-1 for a depiction of the pathophysiologic process of anaphylaxis.)

Figure 10-1 Pathophysiologic process of anaphylaxis. (Major chemical mediators are in boldface print.) SRS-A, Slow-reacting substance of anaphylaxis.

Researchers have made a distinction between “true anaphylaxis” and “pseudo-anaphylaxis” or an “anaphylactoid reaction.” The symptoms, treatment, and mortality risk are identical, but “true” anaphylaxis results directly from degranulation of mast cells or basophils mediated by immunoglobulin E (IgE). Pseudo-anaphylaxis results from the other causes. Differential diagnosis is based on studying the allergic reaction.

Assessment: anaphylactic shock

Collaborative management (see figure 10-2)

Figure 10-2 Algorithm for the treatment of acute anaphylaxis.

(From Nicklas RA, et al: The diagnosis and management of anaphylaxis. J Allergy Clin Immunol 101(6 Pt 2):S465–S528, 1998.)

Additional nursing diagnoses

Also see nursing diagnoses and interventions in Hemodynamic Monitoring (p. 75), Emotional and Spiritual Support of the Patient and Significant Others (p. 200), and Mechanical Ventilation (p. 99).

Pathophysiology

Assessment

Collaborative management: anemias

Collaborative management: hemolytic crisis

Additional nursing diagnoses

Uncontrolled pain, bleeding, and complications of hemolysis can be terrifying to the patient and significant others, who may fear that the patient will die. Chronic illness with episodic acute exacerbations may require more individualized intervention when handling long-term illness and its sequelae. See Emotional Support of Patient and Significant Others, p. 200.

Pathophysiology

Bleeding can result from qualitative (dysfunctional) or quantitative (lack of) abnormalities of platelets and/or coagulation factors, including proteins, in the plasma. Thrombocytopenia is common in the critically ill and, like anemia, necessitates differential diagnosis. The cause of thrombocytopenia, rather than simply the decreased numbers of platelets, poses the greatest threat to the critically ill patient. The four main causes of thrombocytopenia are as follows:

Platelet destruction may be mediated by congenital autoimmune or alloimmune disorders, or by acquired immunologic or nonimmunologic mechanisms. Causative or related factors include septicemia, systemic inflammatory response syndrome (SIRS), pulmonary hypertension, extracorporeal circulation, thrombotic disorders, acute transplant rejection, severe allergic reactions, rheumatic disorders, intravascular catheters and prosthetics, fat emboli, acute respiratory distress syndrome (ARDS), and HIV infection. The most significant diagnostic finding associated with severe thrombocytopenia is presence of petechiae in dependent areas (i.e., back, ankles, posterior thighs of bedridden patients). Larger purpura such as ecchymoses and hematomas may also be present but are nonspecific for diagnosis of platelet disorders. Patients must be assessed for risk of bleeding with thrombocytopenia, considering the severity and cause as well as comorbid factors.

Coagulopathies leading to bleeding (with/without associated thrombi) may be caused by liver disease, vitamin K deficiency, pregnancy-induced hypertension associated with HELLP syndrome, or other defects of blood coagulation factors, such as hemophilia, von Willebrand disease, and DIC.

Patients prone to thromboembolic conditions include those with platelet abnormalities, including thrombocytosis, diabetes mellitus, hyperlipidemia, heparin-induced thrombocytopenia, systemic lupus erythematosus; blood vessel defects including venous disease/stasis, roughened surface of vascular endothelium (seen with arteriosclerosis, trauma, severe sepsis, SIRS, or infection), atrial fibrillation, grafts or other devices in place, hyperviscosity, TTP, hemolytic uremic syndrome, vasculitis; and those with systemic illness and conditions, including long bone fractures, orthopedic surgery, abdominal surgery, malignancy, pregnancy or postpartum (risk of venous thromboembolism is five times higher than for nonpregnant women), oral contraceptives, nephrotic syndrome, inflammatory bowel disease, slow/stagnant blood flow through the vessels (e.g., shock states, severe peripheral vascular disease), infusion of prothrombin complex, and sickle cell disease.

When patients are evaluated for a bleeding disorder, the process should include evaluation of platelets, deficiency of a single coagulation factor (factors VII, VIII, IX, X, or XI) or multiple coagulation factors, for endogenous or exogenous antibiotics in the circulation, and consumptive coagulopathy (e.g., ITP, TTP, vasculitis, hemolytic uremic syndrome, paroxysmal nocturnal hematuria, obstetric complication, trauma, liver disease). Adequate levels of calcium and vitamin K are also needed for adequate function of the clotting cascade.

Those suspected of having thromboembolic disease may require evaluation of coagulation factors, circulating antibodies, abnormal proteins (deficient protein C or S), and other endogenous chemicals.

Normal blood coagulation is activated most often as a result of injury to blood vessels, causing the following series of events:

Figure 10-3 Coagulation pathway.

(From Janz TG, Hamilton GC: Disorders of hemostatis. In Marx J, Hockberger R, Walls R, editors: Rosen’s Emergency medicine: concepts and clinical practice, ed. 7. St. Louis, 2009, Mosby.)

Pathophysiology

Heparin is the most widely used IV anticoagulant and one of the most frequently prescribed drugs in the United States. Heparin prevents the conversion of fibrinogen to fibrin. Heparin-induced thrombocytopenia (HIT), also called heparin-induced thrombocytopenic thrombosis (HITT), white clot syndrome, or heparin-associated thrombocytopenia (HAT), types I and II, occurs when heparin therapy causes either a mild to moderate (i.e., HAT type I) or severe (i.e., HAT type II) decrease in the number of freely circulating platelets. Platelets in affected patients exhibit unusual aggregation and can result in heparin resistance, arterial and venous thrombosis, and subsequent emboli in extreme cases (Figure 10-4). Depending on the source of the heparin received, HIT is reported in about 5% of all patients receiving heparin. Bovine (beef-based) heparin has been associated with HIT more frequently than other heparins. It is estimated that as many as 50% of patients on heparin may be asymptomatic but generate antibodies to heparin-platelet factor 4 (H-PF4), which increases the risk of HIT on their next exposure to heparin. HIT is not related to the heparin dosage and has been seen in patients receiving low-dose subcutaneous heparin, as well as in patients receiving simple heparin “flushes” to maintain patency of IV lines.

Figure 10-4 Heparin-induced thrombocytopenia. IgG, Immunoglobulin G.

Two types of HIT have been described:

Assessment

Collaborative management

Additional nursing diagnoses

Uncontrolled bleeding or thrombotic complications can be terrifying for the patient and significant others, who may fear that the patient will die. See nursing diagnoses and interventions in Emotional and Spiritual Support of the Patient and Significant Others,p. 200.

Pathophysiology

Immune (often idiopathic) ITP is a disorder characterized by premature platelet destruction as well as impaired platelet production, resulting in a decrease in the platelet count to below 100,000/mm³. Normal platelet life span averages 1 to 3 weeks, whereas in ITP the platelet life span averages 1 to 3 days because of the presence of antiplatelet IgG and IgM antibodies, which destroy platelets in the reticuloendothelial system of the spleen. The coagulopathy is believed to be an autoimmune response and manifests as both an acute and a chronic problem.

Acute ITP is primarily a childhood disease, characterized by an abrupt onset of severe thrombocytopenia with evident purpura. Usually it occurs within 21 days following a viral infection. At the onset, platelets decrease to less than 20,000/mm³. The chronic form is typically a disease of adults ages 20 to 50 years, but it has occurred in a small percentage of children and elders. The chronic disease rarely resolves spontaneously, sometimes responds to treatment of the underlying disorder, and usually is not associated with infection but can be related to autoimmune disorders (e.g., systemic lupus erythematosus, rheumatoid arthritis) and neoplastic disorders (e.g., chronic lymphocytic leukemia, lymphoma). Women are affected three times more often than men. Petechiae and purpura are commonly seen on the distal upper and lower extremities. Patients may feel symptom-free until actual bleeding begins. Intracranial hemorrhage is a potential complication. Platelet counts decrease to as low as 5,000/mm³ in some patients but may be as high as 75,000/mm³ in others.

Assessment

Collaborative management: immune thrombocytopenic purpura

Additional nursing diagnoses

Uncontrolled bleeding can be terrifying for the patient and significant others, who may fear that the patient will die. Refer to nursing diagnoses in Emotional and Spiritual Support of the Patient and Significant Others, p. 200, for appropriate interventions.

Pathophysiology

DIC is a syndrome characterized by overstimulation of the normal coagulation cascade, often related to severe sepsis or shock. DIC is a coagulopathy with potential to cause both profuse bleeding and widespread thrombosis leading to MODS. Inherent bodily control of bleeding requires a balance between procoagulants and thrombus formation, along with anticoagulants, inhibitors, and thrombolysis (see Figure 10-3, Table 10-4). The delicate balance may be upset by disease processes (Table 10-5), resulting in a cascade of uncontrolled coagulation and fibrinolysis. The abnormal clotting cascade that develops during DIC is as follows:

A predisposing event that damages the vascular endothelium initiates the clotting cascade. Studies reflect that both the intrinsic and extrinsic pathways are activated initially, resulting in an abnormal acceleration of the clotting process. Thrombocytopenia occurs because of thrombin production and microvascular thrombus formation.

Assessment

Collaborative management: disseminated intravascular coagulation

Care priorities

1. Treat the primary cause of the disease:

Aggressively treat the underlying cause. A primary disease promotes the development of DIC. If treatment of the disease fails, the mortality rate of DIC is high. When DIC occurs without apparent cause, the possibility of undiagnosed malignancy (e.g., prostate cancer or APL), a large abdominal aortic aneurysm, a progressive gram-negative bacterial infection, or hepatic cirrhosis should be explored. If the diagnosis is by laboratory tests alone, conservative management is appropriate. Other conditions and medication side effects should be considered (see Table 10-5).

2. Manage abnormal clotting with continuous IV heparin therapy:

There are three conditions associated with DIC in which heparin may be effective:

• Underlying malignancy/carcinoma

• Acute Promyelocytic Leukemia (APL): a leukemia most often seen in young adults with acute myelocytic anemia, which may also be linked to patients who received radiotherapy for prostate cancer.

• Purpura fulminans/extreme purpura, often seen with severe sepsis

If used, the patient should have clinically obvious thrombosis. Low-dose therapy (5 to 10 units/kg/hr) is considered. Heparin binds to antithrombin, resulting in a strong anticoagulant effect. Use of higher-dose heparin in DIC is associated with a high risk of bleeding, and greater efficacy has not been documented. Heparin may be considered for serious bleeding or clotting when the condition underlying the DIC is not rapidly reversible and the patient’s vascular system is surgically intact.

APL patients with DIC often experience accelerated symptoms of fibrinolysis (declotting) when receiving chemotherapy. If these individuals receive heparin, an antifibrinolytic agent such as epsilon- (ε-) aminocaproic acid (Amicar) may be added to decrease bleeding.

3. Manage abnormal bleeding due to fibrinolysis with antifibrinolytics:

ε-Aminocaproic acid (Amicar) and tranexamic acid (Cyklokapron) are used to inhibit fibrinolysis in patients who are bleeding as a result of a variety of causes. In patients with DIC, these agents should be used with extreme caution because they may convert a bleeding disorder into a thrombotic problem. When used in DIC, these agents are used in combination with heparin to minimize the potential for thrombosis. Failure rates with use are high.

4. Consider use of thrombolytic agents for abnormal clotting:

Use of streptokinase, urokinase, and tissue plasminogen activator (rtPA) is not indicated for patients with thrombosis because these agents may facilitate excessive bleeding.

5. Provide replacement of necessary blood components:

Clotting factors and inhibitors are replaced in the form of fresh-frozen plasma. The PT/INR may be the most accurate parameter(s) for guiding plasma replacement. Patients with markedly decreased fibrinogen levels may be given cryoprecipitate, which contains 5 to 10 times more fibrinogen than plasma contains. Thrombocytopenia in DIC may not be severe. The platelet count is usually more than 50,000/mm³. General replacement therapy guidelines indicate approximately 10 units of cryoprecipitate should be given for every 2 to 3 units of plasma. Platelet transfusions are used if the patient has impaired platelet production and profuse bleeding. AT-III concentrate has been used on a limited basis (see Table 10-3). More recently, DIC is being managed with antithrombin concentrate, activated protein C (APC) (drotrecogin alfa), tissue factor pathway inhibitor (TFPI), and synthetic serine protease inhibitors (e.g., aprotinin).

• RBC replacement: Packed RBCs may be administered to increase oxygen-carrying capacity to maintain a Hgb value 7 to 9 mg/dl or greater than 20% below the patient’s baseline if the patient is chronically anemic and symptomatic.

6. Supplement vitamin k₁ (phytonadione) and folate:

Patients with DIC are at high risk for deficiency of these substances, and administration of both vitamins is recommended for most patients.

7. Prevent viral infections resulting from immunosuppression with protease inhibitors:

Gabexate, nafamostat, and trasylol have been used.

8. Manage hypotension related to heart failure, as appropriate:

If patient becomes severely hypotensive due to heart failure, the following drugs may be considered: milrinone, dobutamine, dopamine, epinephrine, and nitroprusside (see Appendix 6).

CARE PLANS: DISSEMINATED INTRAVASCULAR COAGULATION

Ineffective protection

related to bleeding resulting from overstimulation of the clotting cascade and rapid consumption of clotting factors

Goals/outcomes

Within 48 to 72 hours of initiation of treatment, patient is free of symptoms of bleeding as evidenced by absence of frank bleeding from invasive procedure sites and mucosal surfaces; secretions and excretions that are negative for blood; absence of large or increasing ecchymoses; decreasing purpura; and HR, RR, and BP within 10% of patient’s baseline (or HR 60 to 100 bpm, RR 12 to 20 breaths/min, systolic BP greater than 90 mm Hg).

Blood Coagulation

Bleeding precautions

1. Discuss bleeding history with patient or significant others. Assess prior incidences of bleeding from gums, skin, or urine; tarry/bloody stools; bleeding from muscles or into joints; hemoptysis, vomiting of blood, epistaxis, or prolonged bleeding from small wounds or after tooth extraction; or unusual bruising or tendency to bruise easily. Provide soft tooth brush.

2. Question patients about current medications, including over-the-counter (OTC) preparations, since many medications promote bleeding (Table 10-6).

3. Monitor coagulation tests daily. Consult physician or midlevel practitioner for abnormal values (Table 10-7).

4. Monitor closely for increased bleeding, bruising, petechiae, and purpura. Assess for internal bleeding by testing suspicious secretions (i.e., sputum, urine, stool, emesis, gastric drainage) for the presence of blood. Monitor for hemorrhage.

5. Monitor neurologic status (see Glasgow Coma Scale, Appendix 2) every 2 hours by assessing LOC, orientation, pupillary reaction, and movement and strength of extremities. Changes in status can indicate intracranial bleeding.

6. Use alcohol-free mouthwash and swabs for oral care to minimize gingival/gum injury. Use normal saline solution (NSS) or solution of NSS and sodium bicarbonate (500 ml NSS with 15 ml bicarbonate) to irrigate the oral cavity if irritated. Massage gums gently with a sponge-tipped applicator to help remove debris. Do not attempt to remove large clots from the mouth, to avoid profuse bleeding.

7. Use electric rather than safety razor for shaving patient.

8. Refrain from inserting objects into a bleeding orifice. Avoid taking rectal temperatures.

9. Protect the patient from trauma. Avoid unnecessary venipunctures and IM injections.

10. If patient undergoes an invasive procedure, manually hold pressure over the insertion site for 3 to 5 minutes for IV catheters and 10 to 15 minutes for arterial catheters or until bleeding subsides.

11. Instruct the patient and/or family on signs of bleeding and appropriate actions.

12. Teach patient the importance of avoiding vitamin K–inhibiting and platelet aggregation–inhibiting medications or vitamin and dietary supplements (see Table 10-6), which promote bleeding.

Table 10-6 MEDICATIONS THAT MAY PROMOTE BLEEDING

Medications that Inhibit Platelets or Cause Thrombocytopenia
Analgesics Nonsteroidal anti-inflammatory agents (NSAIDs) Aspirin (acetylsalicylic acid) Acetaminophen Antipyrine Ibuprofen Indomethacin Fenoprofen Sodium salicylate Antirheumatic agents Oxyphenbutazone Phenylbutazone Hydroxychloroquine Gold salts Antimicrobials Ampicillin Cephalothin Methicillin Penicillin Pentamidine Streptomycin Sulfonamides (antibiotics) Chloramphenicol Isoniazid Nitrofurantoin Rifampin Trimethoprim Anticoagulants Heparin Enoxaparin Dalteparin Thrombolytics Alteplase Reteplase Streptokinase Urokinase Anisoylated plasminogen streptokinase Tenecteplase	Diuretic Agents Sulfonamide derivatives Acetazolamide Chlorpropamide Chlorothiazide Chlorthalidone Clopamide Diazoxide Furosemide Bumetanide Hydrochlorothiazide Tolbutamide Spironolactone Mercurial diuretics Glycoprotein IIb/IIIa inhibitors Abciximab Eptifibatide Tirofiban Phenothiazines Chlorpromazine Promethazine Trifluoperazine Phosphodiesterase inhibitors Caffeine Dipyridamole Theophyllines Antiplatelet drugs Aspirin (acetylsalicylic acid) Ticlopidine Clopidogrel Prostaglandins I2 D2 E Sedative-hypnotics Benzodiazepines Clonazepam Diazepam Vasodilators Nitroglycerin Nitroprusside	Other Antihistamines Ethanol Heparin Beta adrenergic blocking agents General anesthetics Local anesthetics Chemotherapeutic agents Vitamin E Estrogens Digitoxin Cimetidine Levodopa Propylthiouracil
Medications that Inhibit Vitamin K
Salicylates Aspirin and aspirin-combination drugs Other salicylates Coumarins Anisindione Dicumarol Warfarin	Broad-Spectrum Antibiotics Sulfonamides Triple sulfa Sulfamethoxazole Sulfasalazine Sulfisoxazole Sulfamethoxazole-trimethoprim Clindamycin Gentamicin Neomycin Tobramycin Vancomycin Imipenem Cefamandole Cefoxitin	Vitamins A E

Table 10-7 DISSEMINATED INTRAVASCULAR COAGULATION (DIC): LAB VALUES

Infection Control; Infection Protection; Surveillance: Safety

Risk for deficient fluid volume

related to bleeding/hemorrhage

Goals/outcomes

Patient remains normovolemic as evidenced by HR and RR within 10% of patient’s baseline (or HR 60 to 100 bpm and RR 12 to 20 breaths/min with normal depth and pattern; BP within patient’s baseline (or systolic BP more than 90 mm Hg), warm extremities, distal pulses at least 2+ on a 0 to 4+ scale, urinary output more than 0.5 ml/kg/hr, and capillary refill less than 2 seconds. Within 24 hours of initiating treatment, patient verbalizes orientation to time, place, person, and self.

Fluid Balance

Fluid monitoring

1. Monitor every 2 hours for increases in HR and RR, decreased BP, and decreasing pulse pressure.

2. Measure urinary output every 2 to 4 hours. Consult physician or midlevel practitioner for output less than 0.5 ml/kg/hr.

3. Maintain accurate I&O record. Weigh daily, and monitor trends.

4. Increase measurement of vital signs and urine output to at least every 30 minutes for active bleeding. For profuse bleeding, check vital signs at least every 15 minutes. Inspect invasive procedure sites and dressings for bleeding.

5. Monitor CBC daily for significant alterations in Hct, Hgb, and platelets (Table 10-8).

6. Ensure that patient has typed and cross-matched blood available for transfusion.

7. Monitor coagulation studies (PT, PTT, fibrinogen, FDP/FSP, platelet counts), as appropriate.

8. Assess for signs of impending shock if the following signs are noted: increased HR and RR; decreased BP; or pallor, diaphoresis, cool extremities, delayed capillary refill, decreased pulse amplitude, restlessness, or disorientation.

9. Maintain at least one 18-gauge or larger IV catheter for use during shock management, at which time rapid infusion of blood products or IV fluids may be necessary.

10. Evaluate the effects of fluid therapy.

Table 10-8 COMPLETE BLOOD COUNT (CBC) VALUES

Parameters	Common Measurement Value	Population
Red blood cells (RBCs)	4–5.5 million/mm3 4.5–6.2 million/mm3	Adult females Adult males
Hemoglobin (Hgb)	12–16 g/dl 14–18 g/dl	Adult females Adult males
Hematocrit (Hct) Mean corpuscular volume (MCV) Mean cell hemoglobin (MCH) Mean cell hemoglobin concentration (MCHC) White blood cells (WBCs)	37%–47% 83–93 mcg3 26–34 pg 31%–38% 4,500–11,000/mm3	Adult females Adults Adults Adults Adults
Differential White Blood Cells (Granulocytes)
Segmented neutrophils (Segs) Band neutrophils (Bands) Eosinophils (Eos) Basophils (Basos) Monocytes (Monos) Lymphocytes (Lymphs) Platelets	54%–62% 3%–5% 1%–3% 0–0.75% 3%–7% 25%–33% 150,000–400,000/mm3	Adults Adults Adults Adults Adults Adults Adults

Electrolyte Management; Fluid Management; Hypovolemia Management; Intravenous (IV) Therapy; Shock Management: Volume

Ineffective tissue perfusion (or risk for same): peripheral, cardiopulmonary, cerebral, gastrointestinal, and renal

related to blood loss or presence of microthrombi

Goals/outcomes

Patient has adequate perfusion as evidenced by peripheral pulses more than 2+ on a scale of 0 to 4+, brisk capillary refill (less than 2 seconds), BP within patient’s normal range, CVP 2 to 6 mm Hg, and HR regular and less than 100 bpm. Patient is oriented to time, place, person, and self and has urinary output at least 30 ml/hr (0.5 ml/kg/hr) and oxygen saturation greater than 96%.

Circulation Status

Shock prevention

1. Assess and document peripheral perfusion every 2 hours, including temperature, sensation, pulses, and movement in extremities. Perform a comprehensive assessment of peripheral circulation (i.e., check peripheral pulses, edema, capillary refill, and color and temperature of extremities).

2. Monitor vital signs frequently. Evaluate chest pain. Document cardiac dysrhythmias.

3. Monitor BP and assess for early signs of perfusion deficit at least every 2 hours, including dizziness, confusion, and decreased urinary output.

4. Monitor for decreased myocardial or pulmonary perfusion as evidenced by chest pain, ST-segment depression or elevation, T-wave inversion, SOB, dyspnea, and decreased oxygen saturation using continuous pulse oximetry.

5. Monitor CVP, observing for both high and low readings. Decreased pressures are indicative of hypovolemia/hemorrhage. Anticipate vasoconstriction with hypovolemia: CO may increase or decrease from normal range of 4 to 7 L/min, depending on cardiac contractility.

6. Monitor GI status by observing tolerance to diet or tube feedings, bowel habits (e.g., constipation, diarrhea), character of stool (e.g., tarry, bloody), and presence or absence of bowel sounds.

Cardiac Care: Acute; Circulatory Care: Arterial Insufficiency; Circulatory Care: Venous Insufficiency; Respiratory Monitoring; Shock Management: Cardiac; Cerebral Perfusion Promotion; Neurologic Monitoring; Peripheral Sensation Management; Fluid/Electrolyte Management; Fluid Management; Vital Signs Monitoring

Impaired gas exchange (or risk for same)

related to loss of oxygen-carrying capacity through hemorrhage or pulmonary microembolus formation

Goals/outcomes

Patient’s gas exchange is adequate as evidenced by PaO₂ at least 80 mm Hg, PaCO₂ 35 to 45 mm Hg, pH 7.35 to 7.45, RR 12 to 20 breaths/min with normal depth and pattern, oxygen saturation at least 90%, HR 60 to 100 bpm, SVO₂ at least 60%, and orientation to time, place, and person.

Respiratory Status: Gas Exchange

Respiratory monitoring

1. Assess respiratory status every 2 hours, noting rate, rhythm, depth, and regularity of respirations. Provide supplemental oxygen as appropriate.

2. Monitor for signs of respiratory failure: restlessness, anxiety, and air hunger indicative of hypoxemia; ABG values for increased PaCO₂ and decreased pH indicative of hypoventilation; or oxygen saturation less than 95% via pulse oximetry indicative of decreased ventilation. Consult physician or midlevel practitioner if signs of respiratory insufficiency are present.

3. Monitor ScVO₂ or SVO₂: steady increase or decrease from patient’s normal level may indicate deterioration.

4. Assess lungs for bibasilar crackles (rales), indicative of pulmonary edema.

5. Monitor patient’s respiratory secretions. Institute respiratory therapy treatments as needed.

6. Monitor for pulmonary embolus, including sharp, stabbing chest pain, dyspnea, pallor, cyanosis, pupillary dilation, rapid or irregular pulse, profuse diaphoresis, and anxiety. Assess need for supplemental oxygen, and consult physician immediately. Patients with severe pulmonary emboli may require mechanical ventilation. See Pulmonary Embolus, p. 396.

7. Assess patient for changes in sensorium (i.e., confusion, lethargy, somnolence), indicative of inadequate cerebral oxygenation or CO₂ retention (respiratory insufficiency).

Airway Management; Oxygen Therapy; Respiratory Monitoring

Risk for injury

related to blood product administration

Goals/outcomes

Throughout transfusion and up to 8 hours after transfusion, patient does not exhibit signs of a blood transfusion reaction as evidenced by stable mentation, absence of fever and chills, normal appearance of skin (i.e., no flushing, rash, lesions), and baseline RR, BP, and HR.

Risk Control

Surveillance: safety

1. Check blood to be transfused with another professional to ensure the patient receives the correct blood. Verify the following: patient’s name, patient’s birthday and hospital number, blood unit number, blood expiration date, blood group, and blood type.

2. Discuss signs and symptoms of potential reaction with patient and family. Premedicate if there is a history of reaction or antibodies are present.

3. When blood products are being infused, check vital signs every 15 minutes for the first hour. Check patient frequently throughout the first 15 minutes of the transfusion to observe for signs of an acute hemolytic transfusion reaction, including fever, chills, dyspnea, hypotension, flushing, tachycardia, back pain, hematuria, mentation changes, and shock.

4. Observe for transfusion reactions throughout the transfusion and during the 8-hour period afterward. If a transfusion reaction (Table 10-9) occurs, implement the following:

• If the transfusion is in progress, stop the infusion immediately.

• Maintain IV access with normal saline solution.

• Maintain BP with a combination of volume infusion and vasoactive drugs, if indicated.

• Monitor HR and ECG for changes. Treat symptomatic dysrhythmias as prescribed by a physician or midlevel practitioner.

• Administer ordered diuretics and fluids to promote diuresis (urine output approximately 100 ml/hr).

• Obtain blood and urine for a transfusion workup per institution blood bank protocol.

• Perform blood cultures if patient exhibits signs of sepsis.

5. If an intravascular hemolytic reaction is confirmed, implement the following:

• Monitor coagulation studies, including PT, PTT, and fibrinogen levels (see Table 10-7).

• Monitor renal status by measuring the following: blood urea nitrogen (BUN), creatinine, potassium, and phosphate levels.

• Monitor lab values for hemolysis: increased lactate dehydrogenase (LDH), bilirubin, and haptoglobin.

6. With massive transfusion for severe bleeding, manage hypocalcemia caused by citrated blood, hyperkalemia of uncertain etiology, hypothermia from refrigerated blood, ARDS, coagulopathy, and hemochromatosis (iron overload).

Table 10-9 ACUTE TRANSFUSION REACTIONS

Type	Symptoms	Time Frame
Acute intravascular hemolytic	Fever, chills, dyspnea, tachycardia, hypotension, back pain, flushing, hematuria, shock	After start of transfusion within 5–30 minutes
Acute extravascular hemolytic	Fever, elevated bilirubin, unusually low posttransfusion hematocrit and hemoglobin	Usually within 8 hours Delayed: 7–10 days
Allergic (mild)	Rash, hives pruritus	Within 1 hour
Anaphylactic	Dyspnea, shortness of breath, bronchospasms, tachycardia, flushing, hypotension, shock	Within 30 min–1 hour
Febrile	Fever, chills	Within 4 hours
Hypervolemic	Dyspnea, tachycardia, bibasilar crackles, jugular venous distention, possible hypertension, headache	Within 1–2 hours
Septic	Fever, chills, tachycardia, hypotension, vomiting, shock, muscle pain, cardiac arrest	Within 5 minutes–4 hours

Bleeding Precautions; Bleeding Reduction; Blood Products Administration

Additional nursing diagnoses

The uncontrolled bleeding related to DIC can be terrifying to the patient and significant others, who may fear that the patient will die. Refer to nursing diagnoses in Emotional and Spiritual Support of the Patient and Significant Others, p. 200. For patients who manifest activity intolerance, see that nursing diagnosis in Prolonged Immobility, p. 149. For patients with sepsis or septic shock, see SIRS, Sepsis and MODS, p. 924.