Nursing: Sepsis and Therapeutic Effects Essay

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CLINICAL CARE PLAN

NURSING HISTORY
Client's Initials: FT Informant: Gwen RN
Age: 75 Sex: F
Admitting Diagnosis: Sepsis
Allergies: morphine
Chief Complaint: bacterial sepsis
History of Present Illness:
Pathophysiology: Sepsis can occur as a result of infection at any body site, including the lungs, abdomen, skin or soft tissue, or urinary tract and as a result of a primary blood stream infection, such as in meningococcemia. Bacteria are the pathogens most commonly associated with the development of sepsis, although fungi, viruses, and parasites can cause sepsis. The pathophysiology of sepsis can be initiated by the outer membrane component of gram (-) organisms (e.g., lipopolysaccharide [LPS], lipid A, endotoxin) or gram (+) organisms (e.g., lipoteichoic acid, peptidoglycan), as well as fungal, viral, and parasitic components. Signaling by these mediators occurs via a family of transmembrane receptors known as Toll-like receptors. Within the monocyte, nuclear factor-κB (NF-κB), is activated, which leads to the production of pro-inflammatory cytokines, tumor necrosis factor α, and interleukin 1. TNF-α and IL-1 lead to the production of toxic downstream mediators, including prostaglandins, leukotrienes, platelet-activating factor, and phospholipase A2. These mediators damage the endothelial lining, leading to increased capillary leakage. Furthermore, these cytokines lead to the production of adhesion molecules on endothelial cells and neutrophils. Neutrophilic endothelial interaction leads to further endothelial injury through the release of the neutrophil components. Finally, activated neutrophils release nitric oxide, a potent vasodilator that leads to septic shock.
Past Medical & Surgical History: paraplegic since fall in 2006; spinal cord injury: C6 C7 fracture; paralysis; pressure ulcer on coccyx; glaucoma, hypertension, menopausal, genitourinary disorders: urinary tract infection, urinary incontinence; musculoskeletal disorders, orthopedic surgery: spinal shunt x3, musculoskeletal trauma; drug resistent clostridium difficile
Medications:
Medication|Dose/Route|Classification|Indications|Action/Mechanism|Side Effects/Adverse Effects|
Metronidazole|500 mg Tab Q6H PO|Therapeutic: anti-infective, antiprotozoal, antiulcer agent|Treatment of anaerobic infections|disrupts DNA & protein synthesis in susceptible organisms (anaerobic bacteria & Clostridium difficile); Therapeutic Effects: bactericidal, trichomonacidal, or amebicidal action|CNS: seizures, dizziness, headache; EENT: optic neuropathy; GI: abdominal pain, anorexia, nausea, diarrhea, dry mouth, furry tongue, glossitis, unpleasant taste, vomiting; Derm: Stevens-Johnson Syndrome, rash uticaria; Hemat: leukopenia; Neuro: peripheral neuropathy; Misc: super-infection|
Amino Acid Protein (Pro-Stat Awc Liquid)|30 mL BID PO|nutrition supplement for advanced wound healing|Naturally rich in Arginine, Glycine, Proline and Hydroxyproline, high nitrogen donor amino acids that are a critical factor in replenishing depleted protein stores and accelerating tissue healing in pts with pressure ulcers.|free amino acid peptides increase absorption & assimilation by the body to promote tissue healing|N/A|
Acetaminophen (Tylenol)|650 mg Q4H PRN PO|Therapeutic: antipyretic, nonopioid analgesic|Treatment of: mild pain, fever|Inhibits synthesis of prostaglandins that serve as mediators of pain & fever, primarily in CNS; Therapeutic Effects: analgesia, antipyresis|GI: hepatotoxicity, increased liver enzymes; GU: renal failure (w/ high doses/chronic use); Hemat: neutropenia, pancytopenia; Derm: rash, uticaria|
Gabapentin (Neurotin)|300 mg Cap TID PO|Therapeutic: analgesic adjunct, anticonvulsant, mood stabilizer|partial seizures (adjunct tx), post-herpetic neuralgia; neuropathic pain|not known; may affect transport of amino acids across & stabilize neuronal membranes; Therapeutic Effects: decrease incidence of seizures, decreased post-herpetic pain, decreased
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