Sepsis is an inflammatory systemic response to infection. The symptoms are produced by the host’s defense systems rather than by the invading pathogens (Schouten et al. , 2008). Sepsis is a frequent cause of admission to intensive care units (ICUs) and it is one of the leading causes of death among hospitalized patients (Alberti et al. , 2003). It is a public health concern and it continues to be a burden on the healthcare system (Ely, Kleinpell and Goyette, 2003). Despite advancing medical technology, the rate of patients in intensive care units diagnosed with sepsis is continually increasing.
According to Schmidt and Mandel (2009), even when optimal treatment is provided, morbidity due to severe sepsis or septic shock is approximately 40 percent and can exceed 50 percent in the most critically ill patients. Early recognition of sepsis and sepsis-associated infections is essential to treating and controlling it from escalating to advanced stages that are associated with higher mortality rates (Lukaszewski et al. , 2008). Unlike other diseases or trauma, the initial signs and symptoms of sepsis are subtle and can easily be missed by health care practitioners.
Sepsis involves the activation of the coagulation cascade along with downregulation of anticoagulant systems and fibrinolysis (Schouten et al. , 2008). This cycle becomes exaggerated because inflammation induced coagulation produces further inflammation. Sepsis is associated with hypovolemia, hypotension and endothelial dysfunction. The following report will examine a patient’s course of illness during her stay in the ICU at XXXX. This paper will provide a discussion on the patient and her past Running Head: Sepsis
medical history, the pathophysiology of sepsis, the clinical manifestations of sepsis, the patient’s clinical course, and finally, a summary and critique of the case management. Patient Information Mrs. E is a 73 year old female with an extensive past medical history. According to her medical chart, her history includes type II diabetes mellitus, obesity, hypothyroidism, dyslipidemia, hypoglycemia, chronic kidney disease (due to hypertension and diabetic nephropathy), hyperuricemia and gastritis. She has a history of breast and uterine cancer.
As a result, she has undergone a left lumpectomy and she has had a hysterectomy. Mrs. E. is an ex-smoker and she has been diagnosed with chronic obstructive pulmonary disease (COPD). In June 2009, Mrs. E. was being investigated for transaminitis, and an MRI in the same month suggested a periampullary mass. She underwent Endoscopic Retrograde Cholangio Pancreatography (ERCP) on August 26, 2009 at Trillium Health Centre in Mississauga. The ERCP results indicated papillary fibrosis and stenosis; however no masses or stones were discovered. Mrs. E.
presented to the emergency department at Trillium Health Centre on August 27, 2009 in septic shock due to an intra-abdominal source. She was then taken to the operating room for a laprotomy for cholecystitis. It was discovered during surgery that Mrs. E. had a gangrenous gallbladder. The surgery team drained a supraphrenic abscess, sutured the intestine and repaired a ventral hernia. She was then admitted to the intensive care unit (ICU) at Trillium Health Centre. During her stay in the ICU, cultures were taken on successive days that confirmed Klebsiella, pneumonia, and sepsis. She was treated with ceftriaxone and flagyl.
Mrs. E’s renal function progressively worsened and her creatinine steadily rose. She developed thrombocytopenia due to sepsis. Mrs. E. began to become less responsive to furosemide treatments and was diagnosed with acute renal failure. As a result she was transferred to xxxxxx for hemodialysis. Upon arrival to xxxxxxx, Mrs. E was intubated, ventilated and sedated. On initial examination, her heart rate (HR) was 88 BPM, blood pressure (BP) was 189/59 mmHg, temperature was 36. 7 degrees celsius, her respiratory rate (RR) was approximately 22 bpm, and her oxygen saturation was 97%.
Mrs. E. had generalized pitting edema throughout her entire body. She also presented with periods of paroxysmal atrial fibrillation and as a result was given amiodarone. The amiodarone infusion helped to bring Mrs. E back to normal sinus rhythm. On assessment, Mrs. E. had inspiratory crackles with decreased breath sounds to the left lower lobe of her lung, and ecchymosis of her upper extremities. Based on the evidence she presented with, including laboratory evidence, Mrs. E. was diagnosed by the renal physician at The Credit Valley Hospital with acute on chronic renal failure.
The acute component was determined to be secondary to sepsis and hypertension perioperatively. Disease Process Pathophysiology Sepsis is a clinical condition that complicates a severe infection and is characterized by systemic inflammation and widespread tissue injury (Neviere, 2009). When coupled with acute organ dysfunction, sepsis can lead to severe life-threatening complications, including death (Lukaszewski, 2008). Individuals suffering from sepsis display signs of inflammation at tissue sites remote from the original insult such as vasodilation, increased
microvascular permeability and leukocyte accumulation. During sepsis, the inflammatory response causes extensive damage to an individual’s microcirculation (Neligan, 2006). According to Schouten et al (2008), sepsis involves the activation of the coagulation cascade coupled with down-regulation of anticoagulation and fibrinolysis. An intricate link between inflammation and coagulation exists within the body (Neligan, 2006). When a pathogen is present in the bloodstream or when tissue injury occurs, an inflammatory response occurs.
The response causes a stimulation of the immune system to produce interleukin-1 (IL-1), interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF? ) (Neligan, 2006). These cytokines are the main catalysts of the inflammatory response and cause the release of several agents including, interleukin-8, histamine, kinins, serotonin, selectins, and neutrophils. When the above compounds are activated, local vasodilation occurs, cytotoxic chemicals are released and the invading pathogen is destroyed (Neligan, 2006). The inflammatory response can be excessive at times and causes local cellular destruction (Neligan, 2006).
In septic patients, damage to their own tissues occurs throughout the body in the vasculature and endothelium. The release of the proinflammatory cytokines, specifically IL-6, causes activation of the coagulation cascade (Neligan, 2006). Coagulation can be activated by either the intrinsic or extrinsic pathway following a particular tissue damaging event (Neligan, 2006). The intrinsic pathway is the slower of the two pathways and it requires that all factors are present within the blood for clotting to occur (Marieb & Hoehn, 2007).
However, when blood is exposed to a factor that resides under the damaged endothelium, called tissue factor (TF), the extrinsic pathway is activated (Marieb & Hoehn, 2007). The extrinsic pathway is shorter than the intrinsic pathway as it bypasses several steps of the intrinsic pathway. Each clotting pathway 6 requires ionic calcium and involves a series of procoagulants, and eventually forms a common factor X (Marieb & Hoehn, 2007). Within the extrinsic pathway, tissue factor binds to activated factor VII. The complex that results activates factors IX and X (Marieb & Hoehn, 2007).
When factor X has been activated, it complexes with calcium ions, PF3 and factor V to form prothrombin activator (Marieb & Hoehn, 2007). Prothrombin activator catalyzes the transformation of the plasma protein prothrombin to the thrombin, an active enzyme. Thrombin catalyzes the formation of fibrinogen and eventually into fibrin (Marieb & Hoehn, 2007). Thrombin, in the presence of calcium ions, activates factor III in order to bind the fibrin strands closely together (Marieb & Hoehn, 2007). The last step in the normal clotting cascade is fibrinolysis.
Fibrinolysis is responsible for removing clots once the healing process is complete (Marieb & Hoehn, 2007). Without fibrinolysis, vessels have the potential to become completely blocked because clotting occurs continuously (Marieb & Hoehn, 2007). Plasmin, a digesting enzyme, is responsible for breaking clots (Marieb & Hoehn, 2007). It is produced when the plasma protein plasminogen is activated. Plasminogen is incorporated into a forming clot, however it remains dormant until it is activated by an appropriate signal or tissue plasminogen activator (tPA) (Marieb & Hoehn, 2007).
Activated factor XII and thrombin can also activate plasminogen. In a septic patient, the fibrolytic system is inhibited (Neligan, 2006). Cytokines and thrombin stimulate the release of plasminogen-activator inhibitor-1 (PAI-1), from platelets and the endothelium (Marieb & Hoehn, 2007). Thrombin is an activator of inflammation and an inhibitor of fibrinolysis. Thrombomodulin, a modulator of fibrinolysis that activates protein C, is also impaired by inflammation and endothelial injury.