Sepsis is a systemic response to infection; it may occur after a burn, surgery, or a serious illness and is manifested by two or more clinical symptoms: temperature of more than 38°C or less than 36°C, heart rate of more than 90 beats per minute, respiratory rate of more than 20 breaths per minute, PaCO2 of below 32 mmHg, white blood cell count of more than 12,000 cells/mm3, less than 4,000 cells/mm3 or greater than 10% of bands or immature cells, hyperglycemia, bleeding, and abnormal clotting.
The nursing care plan for clients with sepsis involves eliminating infection, maintaining adequate tissue perfusion or circulatory volume, preventing complications, and providing information about disease process, prognosis, and treatment needs.
Here are six (6) nursing care plans (NCP) and nursing diagnosis for patients with sepsis and septicemia:
- Risk For Infection
- Risk For Shock
- Risk For Impaired Gas Exchange
- Risk For Deficient Fluid Volume
- Deficient Knowledge
Risk For Shock
Shock: is a life-threatening condition that occurs when the body is not getting enough blood flow. This can lead to damage to multiple organs.
- Reduction of arterial/venous blood flow: selective vasoconstriction, vascular occlusion–intimal damage, microemboli.
- Relative or actual hypovolemia.
Possibly evidenced by
- [not applicable].
- Client will display adequate perfusion as evidenced by stable vital signs, palpable peripheral pulses, skin warm and dry, usual level of mentation, individually appropriate urinary output, and active bowel sounds.
|Monitor trends in blood pressure (BP), especially noting progressive hypotension and widening pulse pressure.||Hypotension develops as circulating microorganisms stimulate release and activation of chemical and hormonal substances. These endotoxins initially cause peripheral vasodilation, decreased systemic vascular resistance (SVR), and relative hypovolemia. As shock progress, the cardiac output becomes severely depressed due to major alterations in contractility, preload, and/or afterload, thus producing profound hypotension.|
|Monitor heart rate and rhythm. Note dysrhythmias.||Tachycardia occurs because of sympathetic nervous system stimulation secondary to stress response and to compensate for the relative hypovolemia and hypotension. Cardiac dysrhythmias can occur because of hypoxia, acid-base and electrolyte imbalance, and/or low-flow perfusion state.|
|Note quality and strength of peripheral pulses.||Initially, the pulse is strong and bounding because of increased cardiac output. Pulse may become weak and thready because of sustained hypotension, decreased cardiac output, and peripheral vasoconstriction if the shock state progresses.|
|Assess respiratory rate, depth, and quality. Note onset of severe dyspnea.||Increased respirations occur in response to direct effects of endotoxins on the respiratory center in the brain, as well as developing hypoxia, stress, and fever. Respirations become shallow as respiratory insufficiency develops, creating the risk of acute respiratory failure.|
|Assess skin for changes in color, temperature, and moisture.||Vasodilation results in the warm, dry, pink skin characteristic of hyperperfusion in the hyperdynamic phase of early septic shock. If shock state progresses, compensatory vasoconstriction occurs, shunting blood to vital organs, reducing peripheral blood flow, and creating a cool, clammy, pale and dusky skin.|
|Assess for changes in sensorium (confusion, lethargy, personality changes, stupor, delirium, and coma).||Changes in mentation reflect alterations in cerebral perfusion, hypoxemia, and/or acidosis.|
|Auscultate bowel sound.||Reduce blood flow to the mesentery (splanchnic vasoconstriction) decrease peristalsis and may lead to paralytic ileus or possibly trigger multiple organ failure syndrome.|
|Measure hourly urine output; record urine specific gravity.||Decreasing urinary output with high specific gravity indicates diminished renal perfusion related to fluid shifts and selective vasoconstriction. There may be transient polyuria during the hyperdynamic phase, while cardiac output is elevated, but this may progress to oliguria.|
|Hematest gastric secretions and stools for occult blood.||Stress of illness and use of steroids increases the risk of gastric mucosal erosion and bleeding.|
|Monitor for signs of bleeding; oozing from puncture sites or suture lines, petechiae, ecchymoses, hematuria, epistaxis, hemoptysis, and hematemesis.||Coagulopathies such as DIC may occur, related to accelerated clotting in the microcirculation reflecting activation of chemical mediators, vascular insufficiency, and cell destruction creating a life-threatening hemorrhagic situation and multiple emboli.|
|Evaluate lower extremities for local tissue swelling, erythema, and positive Homan’s sign (calf pain at dorsiflexion of the foot).||Venous stasis, changes in the coagulation processes, and infection may result in the development of thrombosis.|
|Maintain bedrest and assist with care activities.||Preventing overexertion decreases myocardial workload and oxygen consumption, thus maximizing the effectiveness of tissue perfusion.|
|Maintain sequential compression devices (SCDs), as indicated.||These preventive measures for a bedfast client to reduce lower extremity stasis complications.|
|Administer parenteral fluids.||Parenteral fluid therapy helps maintain tissue perfusion and expand circulating volume.|
|Administer medications, as indicated:|
|Low-dose steroids may be given for the potential advantages of decreasing capillary permeability, increasing renal perfusion, and inhibiting microemboli formation.|
|Histamine receptor blockers prevent or treat stress ulcers.|
|Inotropic agents and vasopressors may be needed to improve organ perfusion and to maintain blood pressure during and after fluid treatment.|
|Low-molecular-weight-heparin prevents or treats deep vein thrombosis (DVT).|
|Note drug effects, and monitor for toxicity.||Massive doses of antibiotics have potentially toxic effects in clients with compromised renal and/or hepatic function.|
|Monitor laboratory studies, such as ABGs and lactate levels.||Circulatory collapse reduces tissue perfusion. Inadequate renal perfusion alters filtration, reabsorption, and secretion of various substances resulting in fluid and electrolyte imbalance and anaerobic metabolism. Respiratory or metabolic acidosis indicates weakened compensatory mechanism. Lactic acid accumulation is due to inadequate oxygenation and thus accumulation of anaerobic by-products or lactate.|
|Maintain stable body temperature, using adjunctive aids as necessary.||Temperature elevations increase metabolic and oxygen demands beyond cellular resources, hastening tissue ischemia, and cellular destruction.|
|Provide supplemental oxygen.||Supplemental oxygen improves cellular oxygenation.|
|Prepare for and transfer to critical care setting, as indicated.||Progressive deterioration requires more aggressive therapy including hemodynamic monitoring and vasoactive drug infusions.|
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Hematologic and Lymphatic Care Plans
Care plans related to the hematologic and lymphatic system:
- Anaphylactic Shock | 4 Care Plans
- Anemia | 4 Care Plans
- Aortic Aneurysm | 4 Care Plans
- Deep Vein Thrombosis | 5 Care Plans
- Disseminated Intravascular Coagulation | 4 Care Plans
- Hemophilia | 5 Care Plans
- Leukemia | 5 Care Plans
- Lymphoma | 3 Care Plans
- Sepsis and Septicemia | 6 Care Plans
- Sickle Cell Anemia Crisis | 6 Care Plans