Urosepsis With Subsequent Bacteremia Nursing Essay

3145 words (13 pages) Essay

1st Jan 1970 Nursing Reference this

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Sepsis is a clinical syndrome defined by a systemic, dysregulated inflammatory response to infection. Clinical features include either a culture-proven or visually identified infection along with two or more abnormalities in temperature, heart rate, respiration, or white blood count in the response to an infection. This case study will discuss the clinical presentation, diagnosis, and medical management of a patient with urosepsis and subsequent bacteremia in a 78-year-old male.

KEY WORDS:

Sepsis, abdominal pain, urinary tract infection, bacteremia

INTRODUCTION:

Sepsis is the clinical syndrome that results from a dysregulated inflammatory response to an infection. The definition of sepsis involves either a culture-proven or visually identified infection, along with two or more of the following:

Temperature > 38.3°C or <36°C

Heart rate >90 beats/min

Respiratory Rate >20 breaths/min or PaCO2 <32 mmHg

WBC >12,000 cells/mm3, <4000 cells/mm3, or >10 percent immature (band) forms (UPTODATE ARTICLE)

Common sites of origin of sepsis include the following:

Central nervous system: meningitis

Lungs: pneumonia, empyema

Abdomen: peritonitis, intraabdominal abscess, appendicitis, pancreatitis

Genitourinary tract: indwelling catheters

Skin and soft tissue: cellulitis, trauma, catheters (AM Journal of medicine: sepsis)

Common bacteria causing sepsis are gram positive bacteria including staphylococci, streptococci, and enterococci, and gram negative bacteria including Escherichia coli, Proteus species, Pseudomonas, and Klebsiella species. (The American journal of medicine: SEPSIS)

Predisposing factors of sepsis include trauma, burns, surgery (especially abdominal procedures), diabetes mellitus type 1 or type 2, chronic renal failure, immunosuppression (as with patients with AIDS, chronic steroid use, chemotherapy, neutropenia, post organ transplant), indwelling intravascular and urinary catheters, old age, infancy, and malnutrition. (first consult)

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To initiate appropriate supportive measures, it is important to identify the severity of the sepsis syndrome. The severity can be classified along a continuum of Systemic Inflammatory Response Syndrome (SIRS), sepsis, severe sepsis, or septic shock.

Systemic Inflammatory Response Syndrome (SIRS) criteria involve a dysregulated inflammatory response to a noninfectious etiology. Possible noninfectious insults include autoimmune disorders, pancreatitis, thromboembolisms, or surgeries. These noninfectious processes must be present along with two or more of the abnormalities in temperature, heart rate, respiratory rate, and white blood count listed above. UPTODATE

Sepsis, as mentioned above, is SIRS due to a suspected or confirmed infection (Sepsis The American journal of medicine). Two or more of the abnormalities mentioned above along with either a culture-proven or visually identified infection defines sepsis. UPTODATE

Severe sepsis is sepsis with atleast one of the following signs of hypoperfusion, hypotension, or end organ dysfunction. Signs of end organ dysfunction include areas of mottled skin, delayed capillary refill of greater than 3 seconds, urine output of <0.5 ml/kg for atleast one hour, lactate > 2 mmol, change in mental status, abnormal electroencephalographic findings, platelet count <100,000 platelets/mL, disseminated intravascular coagulation, acute respiratory distress syndrome, and cardiac dysfunction. (UPTODATE). With accurate blood pressure readings, the mean arterial pressure (MAP) can be calculated using the following formula:

MAP ~ 2/3 (Diastolic pressure) + 1/3 (SP).

The mean arterial pressure usually falls between 70 to 110 mmHg. If the mean arterial pressure falls below 70, this is a sign of hypoperfusion and thus results in end organ dysfunction.

Septic shock exists is defined as severe sepsis with hypotension despite adequate fluid resuscitation(American journal or medicine). Septic shock involves severe sepsis plus atleast one of the following: Systemic mean blood pressure is <60 mmHg (or <80 mmHg in a patient with baseline hypertension) despite adequate fluid resuscitation, and/or maintaining the systemic mean blood pressure >60 mmHg (or >80 mmHg in patients with baseline hypertension) requires vasopressors such as dopamine > 5mcg/kg per min, norepinephrine <0.25 mcg/kg per minutes, or epinephrine <0.25 mcg/kg per min despite adequate fluid resuscitation. (UP TODATE)

Empiric broad spectrum antibiotic coverage is indicated in cases of suspected sepsis. Early initiation of appropriate antibiotic therapy is the cornerstone of therapy.

CASE REPORT:

A 78-year-old Caucasian male presented to the emergency department with moderate and diffuse lower abdominal pain, fevers and chills that began earlier in the day. Two weeks prior to admission, he underwent lithotripsy and after lithotripsy he was given antibiotics (unknown which kind) that he just finished taking. Patient denies having abdominal pain like this before. Review of systems was remarkable for fevers and chills, dyspnea, and abdominal pain. Patient has chronic diarrhea for which he takes medication, and this is nothing new. Patient denied headache, chest pain, palpitations, nausea, and vomiting. Patient has an extensive past medical history of bladder cancer, hypertension, COPD for which he uses 2 L of oxygen at home as needed, hypercholesterolemia, pancreatitis, and cholelithiasis. Patient is unsure of family history. Surgical history includes a resection of bladder and placement of urinary diversion stoma in 1998. Patient had a 60 pack year history of smoking, he quit smoking 7 years ago, denied alcohol or drug use. He was a retired business man who lives at home with his wife. Home medications of patient include loperamide, hydrochlorothiazide 12.5 mg, and Tylenol arthritis. Patient was not on any medications for his COPD, just the home oxygen he used as needed. Patient had no known drug allergies.

On physical exam, his blood pressure was 158/81, heart rate was tachycardic at 126, respiratory rate was elevated at 26, temperature was 98.4 F, and oxygen saturation was 95% on 2L of oxygen via nasal canula. Patient was alert and oriented to person, place and time, and was in mild distress. Patient was tachycardic, regular rhythm with no clicks, rubs, murmurs or gallops noted. There was no peripheral edema. Patient had increased work of breathing with mild accessory muscle use, lungs were clear to auscultation bilaterally without wheezing, rhonchi, or crackles. Abdominal exam showed right lower quadrant diversion stoma in proper place with yellow urine output and without redness or drainage from the site. Abdomen was soft and nondistended without rebound, guarding, organomegaly or masses noted. A osteopathic structural exam was not performed, but it can be expected that the patient would have increased tissue texture in the paraspinal musculature of the lower thoracics and upper lumbar spine (specifically T12-L2), and sacral dysfunction (S2-S4). This somatic dysfunction can be explained by the viscerosomatic reflex- this occurs when continued visceral dysfunction will transmit abnormal sensory input to the spinal cord, resulting in exaggerated response to the somatic structures of the brain. (REWORD AND LOOK AT SAVARESE)The rest of the physical exam was unremarkable.

The following labs and imaging were ordered: complete blood count (CBC) with differential, renal function panel, urinalysis, lipase, lactate, pro-calcitonin, urine culture, chest x-ray. CBC showed a leukocytosis of 16.01 with absolute neutrophil count of 14.26. Renal function panel showed elevation of BUN and creatinine of 30 and 1.40 respectively and a low GFR of 49. Moderate blood, positive nitrites, large leukocyte esterases, and urine WBC elevation of 74 was noted on urinalysis. Lipase, lactate, and pro-calcitonin were all negative. Urine culture was read after 3 days and showed 3 colony types, none predominant. Chest x-ray impressions showed COPD and granulomatous and fibrotic-type appearance, and no other superimposed acute process seen. Patient was started on ceftriaxone due to the findings on the urinalysis showing a urinary tract infection and given intravenous fluid hydration for the acute renal failure (with creatinine elevated at 1.40) and/or sepsis.

Although patient met sepsis criteria, with most likely source of infection being from urinary tract, he appeared stable and was admitted to ICU step down. That same night, a rapid response was called to the patient’s room and he was noted to be more tachypneic (respiratory rate of 34 from previous 26) and febrile (100.3 °F from 98.4 °F previously) requiring 5 L of oxygen from his previous 2 L to keep oxygen saturation at 95%, and with a drop of blood pressure to 116/69 from previous 158/81 and was transferred to ICU for closer observation. Blood cultures and blood gases were obtained. Blood cultures grew gram negative bacilli Enterbacter cloacae. Arterial blood gases showed an acidotic pH of 7.32, pCO2 of 36, and HCO3 of 18.3 representing a metabolic acidosis, there was no anion gap looking at CMP so this was a non anion gap metabolic acidosis that can most likely be contributed to patient’s chronic diarrhea. Patient was switched from third generation ceftriaxone to a fourth generation cephalosporin cefepime for broader coverage. The patient never required pressors or intubation and was transferred to ICU step down the following day.

The differential diagnosis included: Sepsis secondary to urinary tract infection, pneumonia, cellulitis, appendicitis, inflammatory bowel disease, urinary calculi, intestinal ischemia or intestinal obstruction, diverticulosis, or diverticulitis.

After 3 days in the hospital on intravenous cefepime, the patient began to feel much better without subjective fevers, chills or abdominal pain, his vitals stabilized and his white blood count trended down to 12.2. Patient was discharged from the hospital with a diagnosis of a lower urinary tract infection and was placed on Bactrim BID for 14 days. His serum creatinine was stable at 1.2 on discharge and the patient’s hydrochlorothiazide was changed to Norvasc 5 mg. Patient is to follow up with primary care physician regarding urinary tract infection progress, hypertensive medication switch, and to obtain pulmonary function tests as the patient has never had these tests done and is a COPD patient without any medications.

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As the patient met 4 out of 4 sepsis criteria upon admission to the hospital, urine culture showed 3 colony types- none predominant, and a blood culture that grew gram negative bacilli Enterobacter cloacae, it can be said that the patient has a diagnosis of urosepsis with subsequent bacteremia. Enterobacteriaceae is a commonly isolated organism in patients with community-acquired primary urosepsis. In such cases a third generation cephalosporin, piperacillin in combination with a beta-lactamase inhibitor or a fluoroquinolone with propensity to achieve high urinary concentration (e.g. ciprofloxacin, levofloxacin) should be used for empirical therapy. (approach to a patient website)

Alternative treatments- vitamin A study?

DISCUSSION:

This patient’s clinical presentation, laboratory data, urine and blood cultures were consistent with urosepsis with subsequent bacteremia. Urosepsis is defined as a clinically proven infection of the urinary tract (evidenced as positive urinalysis and/or urine culture) and/or the male genital tract (prostate) with features consistent with a dysregulated inflammatory response. (DEFINITION in that article of approach to a patient). In this case, the urosepsis led to subsequent bacteremia as evidenced by the patient’s positive blood culture growing Enterbacter cloacae.

In the late 1970s, it was estimated that 164,000 cases of sepsis occurred in the United States each year. Due to the advancing age (60% of severe sepsis episodes have been reported amongst patients older than 65 years old), immunosuppression, and multi-drug resistant infections, this trend has increased with a recent estimate of 750,000 cases of sepsis cases diagnosed annually. (American journal of medicines). Sepsis has a high mortality rate, with estimates ranging from 20-50%, depending on the severity of sepsis. In one study, the mortality rate of SIRS, sepsis, severe sepsis, and septic shock was 7, 16, 20, and 46 percent respectively. (UPTODATE)

The incidence of sepsis appears to be highest among African-American males and during the winter months (most usually secondary to a respiratory source). The site of infection in patients with sepsis may be an important determinant of outcome, with urosepsis generally being associated with the lowest mortality rates. One study found that mortality from sepsis was 50 to 55% when the source of infection was unknown, gastrointestinal, or pulmonary, compared to 30% when the source of infection was the urinary tract. (local health)

Blood cultures should be obtained in all septic patients. In cases where the source of infection is unknown and history and physical exam are not revealing, blood cultures can guide the selection and duration of an antimicrobial regimen and can be helpful in identifying the source of infection. Other cultures should be guided by the clinical presentation, including sputum culture and gram stain, urinalysis and urine culture, lumbar punctures. The focus of clinical evaluation is to identify a specific pathogen and/or localize the site of primary infection. Identifying the probable source can suggest likely pathogens, such as gram negative bacilli from a urinary source, and so guide selection of empiric antibiotic coverage and other interventions (relief of an obstruction or drainage of an abscess).

A urogenital tract origin is the focus in approximately 25% of all patients with sepsis. Gram-negative bacilli account for majority of the cases of urosepsis. These organisms include Escherichia coli (50%), Proteus spp. (15%), Enterobacter and Klebsiella spp. (15%), and Pseudomonas aeruginosa (5%) which dominate the bacterial spectrum in urosepsis, while Gram-positive organisms are involved less frequently (15%). (APPRAOCH TO A PATIENT WEBSITE). E.coli and other Enterobacteriaceae are the commonly isolated organisms in patients with community-acquired primary urosepsis. Enterobacter cloacae (the bacteria isolated in this patient case) is an anaerobic gram negative bacilli that is part of the normal flora of the human intestinal tract. Enterobacter species can cause a variety of infections including peritonitis, wound infections, nosocomial pneumonia, urinary tract infections (in the case of this patient), infected prosthesis devices/joints, post trauma or post-surgery meningitis. (Sanford) Any of the latter can lead to bacteremia, as seen in our patient (sanford guide)

Enterobacter cloacae is treated best with Pip-Tazo 3.375 grams intravenously every six hours or Ciprofloxacin 400 mg intravenously two times a day. There is a black box warning for ciprofloxacin and other fluroquinolones. These medications should be used with caution due to the association with increased tendinitis and/or tendon rupture risk. This risk is further increased in patients older than 60 years of age. (epocrates)

Early institution of adequate antibiotic therapy is associated with a 50% reduction in the mortality rate. In contrast, prior antibiotic therapy (antibiotics within the past 90 days) may be associated with increased mortality, at least amongst patients with gram negative sepsis. This is most likely due to a higher rate of antibiotic resistance.

Some evidence suggests that biomarkers unique to sepsis, like serum procalcitonin, may be useful in diagnosis and monitoring treatment or sepsis. The procalcitonin test is relatively new and can be used in conjunction with other laboratory findings and clinical assessments to assist in the risk assessment of critically ill people for progression to severe sepsis and septic shock. Low levels of procalcitonin represent a low risk of sepsis and progression to severe sepsis and/or septic shock but do not exclude it (as seen in our patient who had a negative procalcitonin and was blood culture positive). High procalcitonin levels indicate a high probability of sepsis. Procalcitonin has also been used to at intervals to monitor the effectiveness of antimicrobial treatment.

(LAB tests online)

Slimans paper: Complementary medicine not utilized in the treatment of this patient. Patient was fairly healthy and very independent elderly man who did not delay her care and followed the doctor’s recommendations, which allowed her to get proper diagnosis and treatment regimen.She did not come for a low socioeconomic status and had access to health care, did not face many of the burdens that many elderly people and minorities face when having health issues.

appropriate osteopathic components, minority health issues, patient safety issues, and complementary and alternative medicine issues.)

Osteopathic components (muscle energy or FPR, suboccipital release?? For bladder)

COMMENTS:

Put in picture of sepsis protocol from Washington manual p 269.

The clinical presentation and diagnostic approach to sepsis and systemic inflammatory response syndrome varies among patients.

Surviving sepsis

http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001687/

Sanford guide

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2840933/

http://www.localhealth.com/article/urosepsis

current diagnosis and treatment book sarisha talked about.

http://www.sott.net/articles/show/218047-Vitamin-C-A-life-saving-treatment-for-sepsis alternatives

Homeopathy and Sepsis

alternative treatments

labtests online

Sepsis is a clinical syndrome defined by a systemic, dysregulated inflammatory response to infection. Clinical features include either a culture-proven or visually identified infection along with two or more abnormalities in temperature, heart rate, respiration, or white blood count in the response to an infection. This case study will discuss the clinical presentation, diagnosis, and medical management of a patient with urosepsis and subsequent bacteremia in a 78-year-old male.

KEY WORDS:

Sepsis, abdominal pain, urinary tract infection, bacteremia

INTRODUCTION:

Sepsis is the clinical syndrome that results from a dysregulated inflammatory response to an infection. The definition of sepsis involves either a culture-proven or visually identified infection, along with two or more of the following:

Temperature > 38.3°C or <36°C

Heart rate >90 beats/min

Respiratory Rate >20 breaths/min or PaCO2 <32 mmHg

WBC >12,000 cells/mm3, <4000 cells/mm3, or >10 percent immature (band) forms (UPTODATE ARTICLE)

Common sites of origin of sepsis include the following:

Central nervous system: meningitis

Lungs: pneumonia, empyema

Abdomen: peritonitis, intraabdominal abscess, appendicitis, pancreatitis

Genitourinary tract: indwelling catheters

Skin and soft tissue: cellulitis, trauma, catheters (AM Journal of medicine: sepsis)

Common bacteria causing sepsis are gram positive bacteria including staphylococci, streptococci, and enterococci, and gram negative bacteria including Escherichia coli, Proteus species, Pseudomonas, and Klebsiella species. (The American journal of medicine: SEPSIS)

Predisposing factors of sepsis include trauma, burns, surgery (especially abdominal procedures), diabetes mellitus type 1 or type 2, chronic renal failure, immunosuppression (as with patients with AIDS, chronic steroid use, chemotherapy, neutropenia, post organ transplant), indwelling intravascular and urinary catheters, old age, infancy, and malnutrition. (first consult)

To initiate appropriate supportive measures, it is important to identify the severity of the sepsis syndrome. The severity can be classified along a continuum of Systemic Inflammatory Response Syndrome (SIRS), sepsis, severe sepsis, or septic shock.

Systemic Inflammatory Response Syndrome (SIRS) criteria involve a dysregulated inflammatory response to a noninfectious etiology. Possible noninfectious insults include autoimmune disorders, pancreatitis, thromboembolisms, or surgeries. These noninfectious processes must be present along with two or more of the abnormalities in temperature, heart rate, respiratory rate, and white blood count listed above. UPTODATE

Sepsis, as mentioned above, is SIRS due to a suspected or confirmed infection (Sepsis The American journal of medicine). Two or more of the abnormalities mentioned above along with either a culture-proven or visually identified infection defines sepsis. UPTODATE

Severe sepsis is sepsis with atleast one of the following signs of hypoperfusion, hypotension, or end organ dysfunction. Signs of end organ dysfunction include areas of mottled skin, delayed capillary refill of greater than 3 seconds, urine output of <0.5 ml/kg for atleast one hour, lactate > 2 mmol, change in mental status, abnormal electroencephalographic findings, platelet count <100,000 platelets/mL, disseminated intravascular coagulation, acute respiratory distress syndrome, and cardiac dysfunction. (UPTODATE). With accurate blood pressure readings, the mean arterial pressure (MAP) can be calculated using the following formula:

MAP ~ 2/3 (Diastolic pressure) + 1/3 (SP).

The mean arterial pressure usually falls between 70 to 110 mmHg. If the mean arterial pressure falls below 70, this is a sign of hypoperfusion and thus results in end organ dysfunction.

Septic shock exists is defined as severe sepsis with hypotension despite adequate fluid resuscitation(American journal or medicine). Septic shock involves severe sepsis plus atleast one of the following: Systemic mean blood pressure is <60 mmHg (or <80 mmHg in a patient with baseline hypertension) despite adequate fluid resuscitation, and/or maintaining the systemic mean blood pressure >60 mmHg (or >80 mmHg in patients with baseline hypertension) requires vasopressors such as dopamine > 5mcg/kg per min, norepinephrine <0.25 mcg/kg per minutes, or epinephrine <0.25 mcg/kg per min despite adequate fluid resuscitation. (UP TODATE)

Empiric broad spectrum antibiotic coverage is indicated in cases of suspected sepsis. Early initiation of appropriate antibiotic therapy is the cornerstone of therapy.

CASE REPORT:

A 78-year-old Caucasian male presented to the emergency department with moderate and diffuse lower abdominal pain, fevers and chills that began earlier in the day. Two weeks prior to admission, he underwent lithotripsy and after lithotripsy he was given antibiotics (unknown which kind) that he just finished taking. Patient denies having abdominal pain like this before. Review of systems was remarkable for fevers and chills, dyspnea, and abdominal pain. Patient has chronic diarrhea for which he takes medication, and this is nothing new. Patient denied headache, chest pain, palpitations, nausea, and vomiting. Patient has an extensive past medical history of bladder cancer, hypertension, COPD for which he uses 2 L of oxygen at home as needed, hypercholesterolemia, pancreatitis, and cholelithiasis. Patient is unsure of family history. Surgical history includes a resection of bladder and placement of urinary diversion stoma in 1998. Patient had a 60 pack year history of smoking, he quit smoking 7 years ago, denied alcohol or drug use. He was a retired business man who lives at home with his wife. Home medications of patient include loperamide, hydrochlorothiazide 12.5 mg, and Tylenol arthritis. Patient was not on any medications for his COPD, just the home oxygen he used as needed. Patient had no known drug allergies.

On physical exam, his blood pressure was 158/81, heart rate was tachycardic at 126, respiratory rate was elevated at 26, temperature was 98.4 F, and oxygen saturation was 95% on 2L of oxygen via nasal canula. Patient was alert and oriented to person, place and time, and was in mild distress. Patient was tachycardic, regular rhythm with no clicks, rubs, murmurs or gallops noted. There was no peripheral edema. Patient had increased work of breathing with mild accessory muscle use, lungs were clear to auscultation bilaterally without wheezing, rhonchi, or crackles. Abdominal exam showed right lower quadrant diversion stoma in proper place with yellow urine output and without redness or drainage from the site. Abdomen was soft and nondistended without rebound, guarding, organomegaly or masses noted. A osteopathic structural exam was not performed, but it can be expected that the patient would have increased tissue texture in the paraspinal musculature of the lower thoracics and upper lumbar spine (specifically T12-L2), and sacral dysfunction (S2-S4). This somatic dysfunction can be explained by the viscerosomatic reflex- this occurs when continued visceral dysfunction will transmit abnormal sensory input to the spinal cord, resulting in exaggerated response to the somatic structures of the brain. (REWORD AND LOOK AT SAVARESE)The rest of the physical exam was unremarkable.

The following labs and imaging were ordered: complete blood count (CBC) with differential, renal function panel, urinalysis, lipase, lactate, pro-calcitonin, urine culture, chest x-ray. CBC showed a leukocytosis of 16.01 with absolute neutrophil count of 14.26. Renal function panel showed elevation of BUN and creatinine of 30 and 1.40 respectively and a low GFR of 49. Moderate blood, positive nitrites, large leukocyte esterases, and urine WBC elevation of 74 was noted on urinalysis. Lipase, lactate, and pro-calcitonin were all negative. Urine culture was read after 3 days and showed 3 colony types, none predominant. Chest x-ray impressions showed COPD and granulomatous and fibrotic-type appearance, and no other superimposed acute process seen. Patient was started on ceftriaxone due to the findings on the urinalysis showing a urinary tract infection and given intravenous fluid hydration for the acute renal failure (with creatinine elevated at 1.40) and/or sepsis.

Although patient met sepsis criteria, with most likely source of infection being from urinary tract, he appeared stable and was admitted to ICU step down. That same night, a rapid response was called to the patient’s room and he was noted to be more tachypneic (respiratory rate of 34 from previous 26) and febrile (100.3 °F from 98.4 °F previously) requiring 5 L of oxygen from his previous 2 L to keep oxygen saturation at 95%, and with a drop of blood pressure to 116/69 from previous 158/81 and was transferred to ICU for closer observation. Blood cultures and blood gases were obtained. Blood cultures grew gram negative bacilli Enterbacter cloacae. Arterial blood gases showed an acidotic pH of 7.32, pCO2 of 36, and HCO3 of 18.3 representing a metabolic acidosis, there was no anion gap looking at CMP so this was a non anion gap metabolic acidosis that can most likely be contributed to patient’s chronic diarrhea. Patient was switched from third generation ceftriaxone to a fourth generation cephalosporin cefepime for broader coverage. The patient never required pressors or intubation and was transferred to ICU step down the following day.

The differential diagnosis included: Sepsis secondary to urinary tract infection, pneumonia, cellulitis, appendicitis, inflammatory bowel disease, urinary calculi, intestinal ischemia or intestinal obstruction, diverticulosis, or diverticulitis.

After 3 days in the hospital on intravenous cefepime, the patient began to feel much better without subjective fevers, chills or abdominal pain, his vitals stabilized and his white blood count trended down to 12.2. Patient was discharged from the hospital with a diagnosis of a lower urinary tract infection and was placed on Bactrim BID for 14 days. His serum creatinine was stable at 1.2 on discharge and the patient’s hydrochlorothiazide was changed to Norvasc 5 mg. Patient is to follow up with primary care physician regarding urinary tract infection progress, hypertensive medication switch, and to obtain pulmonary function tests as the patient has never had these tests done and is a COPD patient without any medications.

As the patient met 4 out of 4 sepsis criteria upon admission to the hospital, urine culture showed 3 colony types- none predominant, and a blood culture that grew gram negative bacilli Enterobacter cloacae, it can be said that the patient has a diagnosis of urosepsis with subsequent bacteremia. Enterobacteriaceae is a commonly isolated organism in patients with community-acquired primary urosepsis. In such cases a third generation cephalosporin, piperacillin in combination with a beta-lactamase inhibitor or a fluoroquinolone with propensity to achieve high urinary concentration (e.g. ciprofloxacin, levofloxacin) should be used for empirical therapy. (approach to a patient website)

Alternative treatments- vitamin A study?

DISCUSSION:

This patient’s clinical presentation, laboratory data, urine and blood cultures were consistent with urosepsis with subsequent bacteremia. Urosepsis is defined as a clinically proven infection of the urinary tract (evidenced as positive urinalysis and/or urine culture) and/or the male genital tract (prostate) with features consistent with a dysregulated inflammatory response. (DEFINITION in that article of approach to a patient). In this case, the urosepsis led to subsequent bacteremia as evidenced by the patient’s positive blood culture growing Enterbacter cloacae.

In the late 1970s, it was estimated that 164,000 cases of sepsis occurred in the United States each year. Due to the advancing age (60% of severe sepsis episodes have been reported amongst patients older than 65 years old), immunosuppression, and multi-drug resistant infections, this trend has increased with a recent estimate of 750,000 cases of sepsis cases diagnosed annually. (American journal of medicines). Sepsis has a high mortality rate, with estimates ranging from 20-50%, depending on the severity of sepsis. In one study, the mortality rate of SIRS, sepsis, severe sepsis, and septic shock was 7, 16, 20, and 46 percent respectively. (UPTODATE)

The incidence of sepsis appears to be highest among African-American males and during the winter months (most usually secondary to a respiratory source). The site of infection in patients with sepsis may be an important determinant of outcome, with urosepsis generally being associated with the lowest mortality rates. One study found that mortality from sepsis was 50 to 55% when the source of infection was unknown, gastrointestinal, or pulmonary, compared to 30% when the source of infection was the urinary tract. (local health)

Blood cultures should be obtained in all septic patients. In cases where the source of infection is unknown and history and physical exam are not revealing, blood cultures can guide the selection and duration of an antimicrobial regimen and can be helpful in identifying the source of infection. Other cultures should be guided by the clinical presentation, including sputum culture and gram stain, urinalysis and urine culture, lumbar punctures. The focus of clinical evaluation is to identify a specific pathogen and/or localize the site of primary infection. Identifying the probable source can suggest likely pathogens, such as gram negative bacilli from a urinary source, and so guide selection of empiric antibiotic coverage and other interventions (relief of an obstruction or drainage of an abscess).

A urogenital tract origin is the focus in approximately 25% of all patients with sepsis. Gram-negative bacilli account for majority of the cases of urosepsis. These organisms include Escherichia coli (50%), Proteus spp. (15%), Enterobacter and Klebsiella spp. (15%), and Pseudomonas aeruginosa (5%) which dominate the bacterial spectrum in urosepsis, while Gram-positive organisms are involved less frequently (15%). (APPRAOCH TO A PATIENT WEBSITE). E.coli and other Enterobacteriaceae are the commonly isolated organisms in patients with community-acquired primary urosepsis. Enterobacter cloacae (the bacteria isolated in this patient case) is an anaerobic gram negative bacilli that is part of the normal flora of the human intestinal tract. Enterobacter species can cause a variety of infections including peritonitis, wound infections, nosocomial pneumonia, urinary tract infections (in the case of this patient), infected prosthesis devices/joints, post trauma or post-surgery meningitis. (Sanford) Any of the latter can lead to bacteremia, as seen in our patient (sanford guide)

Enterobacter cloacae is treated best with Pip-Tazo 3.375 grams intravenously every six hours or Ciprofloxacin 400 mg intravenously two times a day. There is a black box warning for ciprofloxacin and other fluroquinolones. These medications should be used with caution due to the association with increased tendinitis and/or tendon rupture risk. This risk is further increased in patients older than 60 years of age. (epocrates)

Early institution of adequate antibiotic therapy is associated with a 50% reduction in the mortality rate. In contrast, prior antibiotic therapy (antibiotics within the past 90 days) may be associated with increased mortality, at least amongst patients with gram negative sepsis. This is most likely due to a higher rate of antibiotic resistance.

Some evidence suggests that biomarkers unique to sepsis, like serum procalcitonin, may be useful in diagnosis and monitoring treatment or sepsis. The procalcitonin test is relatively new and can be used in conjunction with other laboratory findings and clinical assessments to assist in the risk assessment of critically ill people for progression to severe sepsis and septic shock. Low levels of procalcitonin represent a low risk of sepsis and progression to severe sepsis and/or septic shock but do not exclude it (as seen in our patient who had a negative procalcitonin and was blood culture positive). High procalcitonin levels indicate a high probability of sepsis. Procalcitonin has also been used to at intervals to monitor the effectiveness of antimicrobial treatment.

(LAB tests online)

Slimans paper: Complementary medicine not utilized in the treatment of this patient. Patient was fairly healthy and very independent elderly man who did not delay her care and followed the doctor’s recommendations, which allowed her to get proper diagnosis and treatment regimen.She did not come for a low socioeconomic status and had access to health care, did not face many of the burdens that many elderly people and minorities face when having health issues.

appropriate osteopathic components, minority health issues, patient safety issues, and complementary and alternative medicine issues.)

Osteopathic components (muscle energy or FPR, suboccipital release?? For bladder)

COMMENTS:

Put in picture of sepsis protocol from Washington manual p 269.

The clinical presentation and diagnostic approach to sepsis and systemic inflammatory response syndrome varies among patients.

Surviving sepsis

http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001687/

Sanford guide

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2840933/

http://www.localhealth.com/article/urosepsis

current diagnosis and treatment book sarisha talked about.

http://www.sott.net/articles/show/218047-Vitamin-C-A-life-saving-treatment-for-sepsis alternatives

Homeopathy and Sepsis

alternative treatments

labtests online

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