Overview
The patient is a 72-year-old Hispanic male. The patient is retired, obese, legally separated, has one child, and lives with his sister. They have a history of E. coli Extended Spectrum Beta Lactamase (ESBL) bacteria, Type II Diabetes Mellitus, hyperlipidemia, hypertension, endocrine problems, benign prostatic hyperplasia, and smoking up until 1990. The chief complaint upon admission was weakness and dizziness, and the medical diagnosis was a UTI, AKI, and later bacteremia and sepsis. Medications included Merrem (meropenem), Invanz (ertapenem), Flomax (Tamsulosin), Metformin, Invokana (canagliflozin), Amaryl (glimepiride), Pepcid (famotidine), Lipitor (atorvastatin) and Tricor (fenofibrate), and aspirin.
Assessment of the patient at 0955 on November 5th was as follows:
Vital Signs:
• Temperature: 38.3°C (100.94°F)
• Pulse: 99
• Respirations: 24
• Blood Pressure: 136/66
• SpO2: 98 on room air
• Pain: 0/10
Neurological:
• Pupils equal, round, reactive to light
• Clear and appropriate speech
• No noticeable abnormalities
Cardiovascular:
• Clear S1/S2, sinus rhythm
• Capillary refill <2 on all extremities
• No noticeable abnormalities
Respiratory:
• Symmetrical chest expansion, no use of accessory muscles
• Clear lung sounds on both sides and all areas
• Fast, shallow breathing with a respiratory rate of 24
o No other noticeable abnormalities
GI/GU:
• Bowel sounds active and present in all four quadrants
• Round, soft, non-tender abdomen
• Patient reports nausea
o No other noticeable abnormalities
Musculoskeletal:
• Moderate-strong grips, pushes, and pulls
o Feeling of weakness despite actual strength
• Good range of motion and gait (as stated by patient)
• No edema
• No noticeable abnormalities
General
• Three IV lines (in preparation for the possibility of sepsis)
o IV solution running: 150mL/hour potassium chloride in NS
• No stated anxiety
Pathophysiology
The major pathophysiology affecting this patient was an untreated urinary tract infection (UTI) that was complicated by diabetes and lead to sepsis. The patient presented to the Emergency Department complaining of weakness and dizziness and was tested for and diagnosed with a UTI and acute kidney injury (AKI). Later diagnoses included acute tubular necrosis, bacteremia, and sepsis.
The most common cause of UTI is Escherichia coli (E. coli) (Lewis, Bucher, Heitkemper, and Harding, 2017), and (referencing Table 2) this patient was indeed positive for Extended Spectrum Beta Lactamase (ESBL) E. coli. ESBL bacteria are Gram-negative bacteria that excrete beta-lactamase, an enzyme which makes infection hard to treat because it destroys penicillins and other commonly used antibiotics (PIC-NL, 2011). In healthy patients, the bladder and urinary tract are normally free of bacteria, however when bacteria enter the urinary tract or bladder they can proliferate and cause further damage to the kidneys, causing an AKI. An AKI is an all-encompassing term describing deterioration and impairment of kidney function (Lewis, Bucher, Heitkemper, and Harding, 2017). According to a study done in 2016 in Bangladesh by a team of doctors, an AKI is classified as at least one of the following occurrences: an increase of absolute serum creatinine of over 0.3mg/dL in 48 hours, serum creatinine being at least one and a half times the baseline in a week, or urine production of <0.5ml/kg/hour for over 6 hours (Rahim et al. 2017). The study looked at patients with Type II Diabetes with an ESBL UTI and concluded that because they had poor glycemic control, they were at higher risk for developing an AKI. Other risk factors included age and previous infection.
The patient was a Type II diabetic, geriatric, had benign prostatic hyperplasia, a history of ESBL UTI and, referencing Table 1, maintained poor glycemic control—making them prone to developing an AKI. Diabetics are prone to kidney injury and disease because poor glycemic damages the blood vessels and nerves in the body (National Kidney Foundation, 2017). Elevated glucose levels reduce levels of nitric oxide, a vasodilator (Bai, 2011), and chronically constricted blood vessels cause hypertension and ischemic damage to the vessels, including those in the kidneys. Elevated glucose also causes the blood to become thick, sugary, and viscous which not only is harder for the kidneys to filter but increases risk of bacteria proliferation because bacteria feed and thrive off of sugar-rich environments (Irace et al., 2013). In addition to that, nerve damage can impede the emptying of the bladder which causes urinary retention, pressure buildup, and heightened risk for infection (National Kidney Foundation, 2017). Urinary problems are also associated with benign prostatic hyperplasia (BPH) which is the enlargement of the prostate, which can block the flow of urine (Mayo Clinic, 2018).
The specific type of AKI that this patient was diagnosed with was acute tubular necrosis, which is when ischemia and/or nephrotoxic agents cause the necrosis (death) of the renal tubules (Lewis, Bucher, Heitkemper, and Harding, 2017). This patient was taking metformin to control his diabetes, which on its own is not nephrotoxic (Chen, Liu, Ye, 2016), however when compounded with Type II diabetes and decreased renal function can be harmful to the kidneys and cause further damage (Hsu et al., 2017). This coupled with the rest of his comorbidities (age, history, etc.) caused the perfect storm— blocked urine flow and kidney damage lead to the stasis of urine, leading to UTI, which left untreated caused further damage to the kidneys. Because this infection was untreated, it not only further damaged his kidneys but became systemic and lead to sepsis.
Upon admission, the patient was suspected to have bacteremia (bacteria in the blood) and, referencing Table 1, the suspicion was confirmed when blood cultures came back positive for ESBL E. coli (the same bacteria causing the UTI). The infection in his urinary tract spread to the kidneys and became systemic by infecting the blood stream. Because the infection was systemic, the patient’s body responded to it systemically—however, the response was dysregulated and caused sepsis. In 2016 The Third International Sepsis Consensus Definitions Task Force defined sepsis as, “A life-threatening organ dysfunction due to dysregulated host response to infection” (Hostetter-Lewis, 2018). When monitoring for sepsis, health care providers check for two or more of the following SIRS (Systemic Inflammatory Response Syndrome, a precursor to sepsis) criteria—a temperature greater than 38°C (100.4°F) or less than 36°C (96.8°F), a heart rate over 90 beats/minute, a respiratory rate of over 20 breaths/minute or a PaCO2 of less than 32mmHg, and a white blood cell count of either over 12 or under 4 (Hostetter-Lewis, 2018). Because this patient fit three of the SIRS criteria (temperature, heart rate, and respirations) and had a confirmed infection, they were diagnosed and treated for sepsis. Untreated, sepsis can progress to septic shock and eventually to severe sepsis (Hostetter-Lewis, 2018). Because this patient’s disease process was accurately identified and treated, they did not progress to septic shock or severe sepsis and were able to be discharged within five days.
Medications
The patient was taking several medications—the ones pertinent to their diagnosis being Merrem (meropenem), Invanz (ertapenem), Flomax (Tamsulosin), Metformin, Invokana (canagliflozin), and Amaryl (glimepiride). Other medications included Pepcid (famotidine) for stomach ulcer prophylaxis, Lipitor (atorvastatin) and Tricor (fenofibrate) for cholesterol control, and aspirin for MI/stroke prophylaxis (Davis's Drug Guide for Nurses).
The patient was taking two antibiotics to control and eliminate their infection as well as prevent further progression of sepsis—meropenem and ertapenem. Meropenem and ertapenem are both carbapenem antibiotics which kill bacteria by binding to the cell wall (Davis's Drug Guide for Nurses). They were used to treat this infection because they are immune to beta lactamase and thus would be effective against ESBL E. coli (Davis's Drug Guide for Nurses).
The patient was taking Tamsulosin for benign prostatic hyperplasia, which binds to alpha1-adrenergic receptors and causes a decrease in the contraction of smooth muscle around the prostate (Davis's Drug Guide for Nurses). Although it does not shrink the prostate, the relaxation of smooth muscle makes it easier for urine to pass through the urinary tract (Davis's Drug Guide for Nurses). Allowing urine to pass through easier decreases risk for UTI and a repeat infection. An important side effect of Tamsulosin is dizziness because the patient was already dizzy and weak from the UTI (Davis's Drug Guide for Nurses).
For diabetes management the patient was taking Metformin, canagliflozin, and glimepiride. Metformin and canagliflozin are expected to be used alongside management of diet and adequate exercise, while Glimepiride is used when diet therapy is ineffective (Davis's Drug Guide for Nurses).
Metformin helps to control blood glucose by decreasing glucose production by the liver, absorption of glucose in the intestines, and increases the body’s sensitivity to insulin (Davis's Drug Guide for Nurses). However, as mentioned above, it can have adverse effects on the renal system in Type II diabetics and thus renal function should be monitored.
Canagliflozin is a sodium-glucose co-transporter 2 (SGLT2) inhibitor (Davis's Drug Guide for Nurses). SGLT2 refers to the co-transport of glucose and sodium in the proximal tubule of the nephron to reabsorb into the blood after filtration (Wright). Canagliflozin inhibits reabsorption of glucose back into the blood from the tubular lumen, causing lower levels of blood glucose (Davis's Drug Guide for Nurses).
Glimepiride is a sulfonylureas medication used to control blood sugar by stimulating the release of insulin, increasing insulin receptor sensitivity, and in some cases reducing glucose production by the liver (Davis's Drug Guide for Nurses).By assisting in glycemic control, the aforementioned medications attempt to make the blood less sugary and viscous—decreasing risk of organ damage and infection.
Laboratory/Treatments
The patient had several laboratory tests done, the ones pertinent to the diagnosis and treatment being a complete blood count (CBC), complete metabolic panel (CMP), urinalysis, and a blood culture. Referencing Table 1, the CBC showed abnormalities in creatinine kinase (CK) and glucose. Although the white blood cell count would be expected to be abnormal in a patient with this type of infection, it was within normal limits and thus not explored in this case study. It is worth mentioning, though, that while the white blood cell count was within normal limits it dropped by about 50% after the initiation of antibiotic therapy. The CMP showed a low level of CO2 in the blood, but other than that there were no other abnormalities. The urinalysis showed glucose, trace protein, and ESBL E. coli in the urine. The blood culture showed a presence of ESBL E. coli as well.
Creatinine kinase is metabolic waste created by the kidneys when filtering blood, and heightened levels in the blood indicated that the kidneys were not filtering the blood properly (Lewis, Bucher, Heitkemper, and Harding, 2017). A CK level of 1.6 indicated kidney damage and assisted in the diagnosis of AKI.
A heightened level of glucose in the blood meant that the patient was hyperglycemic and indicated that they were not able to appropriately control their blood sugar, exacerbating their infection and renal function. This indicated that the patient needed effective diabetes education and a review of the medications they were taking.
The patient also had a low blood CO2 level which was explained by their shallow and rapid respirations. By breathing rapidly, the patient was blowing off CO2 at a rapid rate, causing a decrease in the levels of it in the blood (Lewis, Bucher, Heitkemper, and Harding, 2017).
Glucose and protein in the urine also showed that the patient had an AKI and poor glycemic control. There was so much glucose in their blood that it was spilling over into their urine, and kidney damage caused proteins to slip into the urine (Lewis, Bucher, Heitkemper, and Harding, 2017). The urinalysis and blood culture both showed the presence of ESBL E. coli which confirmed the suspicion of infection.
Treatment included the administration of medication, placement of a peripheral inserted central catheter (PICC) for antibiotic administration after discharge, monitoring of vital signs, and a nursing care plan. The patient was already weak and dizzy from the UTI, and that coupled with the administration of Tamsulosin made them a fall risk. In order to reduce the risk of fall, a call bell and other necessary objects were placed close to them and they were alerted to not get out of bed alone. The care plan also included the monitoring of vital signs and labs in order to assess the effectiveness of treatment and detect a potential complication such as worsening of sepsis. The patient also needed to be educated about his disease and treatments.
Conclusion
The patient had an ESBL E. coli urinary tract infection which was complicated by comorbidities and unfortunately progressed to sepsis. They were treated by a combination of antibiotics and medications to control their diabetes. This patient was effectively treated and was able to be discharged in five days, however the outcome could have been morbid had the patient not received treatment in time. The patient needed to have extensive and effective education on the management of diabetes in order to control their blood sugar and prevent exacerbation of infection. They also needed education on their PICC line, medications, and hygiene in order to prevent another, more serious infection from developing. Education was a key part of this patient’s care in and out of the hospital—if the patient can be properly educated, then they can take care of themselves and reduce instances of hospitalization.