Clinical Case 1 PDF

Clinical Presentation: A 65-year-old male with a history of diabetes and chronic obstructive pulmonary disease (COPD) presents to the emergency department with fever, chills, hypotension, and altered mental status. Laboratory tests reveal leukocytosis, elevated C-reactive protein, and positive blood...

Clinical Presentation: A 65-year-old male with a history of diabetes and chronic obstructive pulmonary disease (COPD) presents to the emergency department with fever, chills, hypotension, and altered mental status. Laboratory tests reveal leukocytosis, elevated C-reactive protein, and positive blood cultures for Escherichia coli. Vitals: BP: 80/45 mmHg, PPM: 118 ppm, RR: 25 rpm, Temp: 40 C Medical Therapy: The patient is initiated on intravenous (IV) broad-spectrum antibiotics, including a cephalosporin and an aminoglycoside. However, despite aggressive treatment, the patient's condition continues to deteriorate, and they are transferred to the intensive care unit (ICU). Clinical disease #1 Systemic inflammatory response syndrome (SIRS) (score should 2-4) fever is >38 C (>100.4 F) or 90 beats/min Leukocytes with white blood cell count >12,000/micro litre; leukopenia (10% bands = low number of white blood cell. Sepsis life-threatening condition characterized by the organ dysfunction resulting from a dysregulated host response to infection ◦ Criteria 1. A suspected infection 2. Acute organ dysfunction Septic Shock a severe subset of sepsis where circulatory and cellular/metabolic dysfunction significantly increases the risk of mortality. ◦ Criteria administration nor of therapy 1. Sepsis + need for vasopressin epinephrine + a serum lactate concentration >2.0 mmol/L after adequate fluid resuscitation. needtoincreasebloodpressure we=, Give vasopressin and fluids if it doesn’t work that’s when we say that they have a septic shock. Sevehypotension we decreasethelumen vasopressor add more blood water concentration give more fluids 199 Source of infection sepsis can result from both community-acquired and hospital-acquired infections, with pneumonia being the most common cause. We know that we have bacterimia and we have COPD (have bacteria in the lungs) the patient had a difficulty peeing. ◦ We have to find the criteria for UTI ◦ Can e.coli cause UTI? E.coli ffffduae.ua Lowerurinary part of the microbiota from the GI tract (normal conditions) Tractdisorder Women is more suceptible to UTI because anus is closer to vagina Innoculated E.coli is gram negative via acatheter urethra Bacteria has a flagellum = moves CCW and CW (moves two ways) ◦ CCW they move when they are being attracted by nutrients ◦ Movement is random until they get another signal and they start moving CCW until they get to that signal again. ◦ Attached to the end of the bacteria. Bacteria have adhesive to help them attach to the epithelium  UTI is not common for male, they are innoculated via a catheter. Increases the chances of the e.coli to reach the bladder. The e.coli will use virulence factors. The patients will have symptoms. When not treated, it will go up. They might have kidney stones that will help them climb up to the kidneys, ◦ This is worst that the Lower UTI. ◦ Kidney has more blood vessels. = main function is to filter the blood. ◦ If not treated can lead to bacterimia ◦ 2nd most common cause of sepsis is SEPSIS and GI tract infections. ◦ 2ndary from UTI infection Not killing the e.coli : wrong antibiotics, resistant, strain, or really strong endotoxins. ◦ Endotoxin ‣ Gram negative bacteria = Lipid A present in the outer membrane. LPS. It’s inside the structure of the outer membrane. When they are lyses they are released. ◦ Exotoxin ‣ Gram positive bacteria SOFA = evaluate the organs of the patients via a score creative - Kidney Bilirubin - liver No time because you need labs. Quick SOFA - 3 characteristic (high risk of mortality) altered mental status = Brain Respiratory rate > or equal to 22 = Lungs Systolic BP < or equal to 100. = Heart we are evaluating how bad the organ failure is. CRITERIA IN 2016 Sepsis suspected (or documented) infection and an acute increase in greater than or equal to 2 sepsis related organ failure assessment (SOFA) points. Septic shock suspected (or documented) infection Plus vasopressin therapy neede to maintain mean arterial pressure ate greater than or equal to 65 mmHg and serum lactate greater than 2.0 mmol/L despite adequate fluid resuscitation. Pathogenesis introduction host response to infection occurs when pathogens are recognized and bound by innate immune cells (ex. Macrophages) Pathogen recognition receptors (PRRs) present on the surface of immune cells bind pathogen-associated molecular patterns (PAMPs) -> upregulation of inflammatory gene transcription and activation of innate immunity. ◦ Different molecules from the microbe that is specific to the microbe trigger the response. (PAMP) PAMP Lipid A from lipopolysaccharude (LPS) Triggers endotoxic syndrome LPS binds to LPS binding protein on monocytes, macrophages, and neutrophils, then signals via TLR4 to release pro inflammatory cytokines like TNF and IL-1, amplifying the immune response.  bloodvesse endothelial O o 1 Interactingwithourtissue infectioncoming theoutside from DAMPS and PAMPS will interact with the receptors (PRR) will detect the pathogen and tissue damage. We are are gonna start inflammatory mediators they (TLR/NLR/CLR) are attaches to receptors and start the proteins and molecules to start the communication with the immune system We will attract leukocyte and trigger inflammation. ◦ We will start having symptoms (signs of inflammation) ‣ Redness ‣ Swelling ‣ Pain ‣ Inflammatory mediator is histamine Histamine = we will find vasodilation ◦ We will increase the separation of endothelial cells, allows these immune cells to go out if the infection is out, or go in if the infection is in the inside. ◦ By causing vasodilation = we are leaking fluid to the interspacial space. ‣ Increase site of infection because of the increase of space by fluid. ‣ This will increase oxygen diffsion distance. ‣ O2 comes from the blood to the cells. ‣ Because the cells are not getting enough oxygen, because we are increasing the space. Decrease atp production, some cells will die, no gas exchange (O2 goes down). We increase lactate when we dont have oxygen = depending on how much we have is how severe the patient is. ◦ Throbs/platelets = increase due to inflammation ‣ Micro clots will lead to less oxygen to go to the cell. ◦ The blood pressure is decreasing ◦ The blood volume is decreasing because it is going to the enterspatial space. ◦ Hypotension ◦ Hypovolemia ◦ Vasodilation. We see all these manifestation through the SOFA test. Treatment fluids Corticosteroids = reduce inflammation Addressing the clots Approaching a patient with sepsis and septic shock 1. Initial question: is the patients septic? A. Consider consensus criteria: suspected/documented infection + life-threatening organ dysfunction 2. Infection presence: is there a documented infection? A. If yes, determine the cause and assess severity of organ dysfunction 3. Assess severity A. Use clinical judgement; infection-specific bio markers/molecula diagnostic are under study but not commonly used. B. Clinical’s acumen is crucial for diagnosis 4. Assess organ dysfunction A. Apply six organ framework to quickly assess organ function at the bedside B. Use SOFA score for evaluation 5. Shock presence: focus on identifying shock A. Shock is an emergency: look for arterial hypotension, tissue hypoperfusion. B. Lactate and if patient is not responding to norepinephrine. SepsisTreatment 1 Obtain appropriatesamples for microbiologiccultures before starting antibiotics 2 Start IV antibiotics as soon aspossible Usebroad spectrumto cover allpathogens 3 Oncespecific pathogen is identified or patientstarts improving narrow the antibiotic treatment 4 Provide respiratory support if needed 5 Useprotocal to mange blood glucose for ICUpts 6 pts w sepsisand kidney injury do dialysis 7 Use bloodclotprevention