Sepsis and critically ill Flashcards
Define SIRS
Systemic Inflammatory Response Syndrome is an exaggerated widespread inflammatory reaction to a noxious stimulus e.g. infection, trauma etc
Characterised by 2 or more of the following:
fever >38/<36
tachycardia >90bpm tachypnoea >20 and abnormal WCC (>12, <4, >10% bands)
It is driven by cytokine cascade where excessive release of pro-inflammatory cytokines like TNF-a, IL-1 and IL-6 leads to widespread endothelial damage, vasodilation and increased vascular permeability. This uncontrolled inflammation can result in tissue damage, organ dysfunction and shock.
Define Sepsis
Life-threatening organ dysfunction caused by a dysregulated host response to infection.
Carries >10% risk of mortality
qSOFA criteria 2 of:
RR>22
SBP<100
GCS <14
What is ERAS
Enhanced Recovery After Surgery is a multidisciplinary evidence-based approach aimed at improving surgical outcomes through optimisation of preoperative, intraoperative and postoperative care. It focuses on reducing surgical stress, promoting early recovery and mobilisation and minimising complications.
How does SIRs resolve?
- restoration of normal structure
- cellular death and necrosis scarrring
- transition into chronic inflammation
What are the different forms of necrosis?
Liquifactive - most commonly in CNS or in most bacterial infections > pus. Dying cells ingested by hydrolytic enzymes hence lose their structural integrity and turn into viscous mass
Coagulative - most common with ischaemic insult. Retains cell structure but cells look anucleate, eosinophillic. Eventually dead cells are ingested by phagocytosis and leukocytes.
Caseous e.g. in TB infection. Creates cheese-like appearance. Necrotic area is referred to as a granuloma.
Fat - occurs in pancreatitis. Release of pancreatic enzymes leads to liquifaction of the fat which then combines with calcium in process called saponification.
Fibrinoid - Occurs in blood vessels due to deposition of immune complexes in vessel walls leading to leakage of fibrin.
Gangrenous - not a morpholigical pattern but rather clinical terms for ischaemic necrosis of limbs. Can have ‘wet’ (liquifactive) or ‘dry’ (coagulative).
all involve irreversible cell injury and uncontrolled cell death through swelling of organelles, plasma membrane rupture and cell lysis leading to spillage of cell contents to surrounding tissue causing further damage.
What is abdominal compartment syndrome?
Increased abdominal pressure >/= 20mmHg with associated end-organ dysfunction
What is the surgical sieve you use?
VITAMINS CDEF
Vascular
Infectious
Trauma
Autoimmune
Metabolic
Idiopathic or iatrogenic
Neoplastic
Social factors incl occupation
Congenital
Drugs or degenerative
Endocrine
Functional
What is haemolytic uraemic syndrome?
Triad of:
- microangiopathic haemolytic anaemia
- thrombocytopaenia
- acute kidney injury
Secondary to Shiga toxin producing E.Coli (STEC), no other causative organisms in NZ.
What are general non-surgical considerations for patients with surgical diseases?
Analgesia, antibiotics
Breathing optimisation, bowel prep
Catheter, consent
DVT prophylaxis, drain insertion (NGT)
Electrolyte correction, emesis prevention
Fluid resuscitation, ferrous (iron)
Gastric protection, glucose (nutritional provision)
What is the pathophysiology of Spontaneous bacterial peritonitis?
Spontaneous bacterial peritonitis (SBP) is an acute infection of the abnormal accumulation of fluid in the abdomen (ascites) without an identifiable source of infection.
majority of isolated organisms being gram-negative enteric organisms (e.g., Escherichia coli or Klebsiella pneumonia), pointing to the gastrointestinal (GI) tract as the main source of infection.
Decompensated cirrhotic patients are those at the highest risk of developing SBP. Infecting organisms typically originate from the intestinal lumen, from where they pass via translocation to mesenteric lymph nodes.
Additional risk factors for SBP include a previous history of SBP, low complement levels, and reduced hepatic synthesis of proteins with (1) an associated prolonged PT time and reduced protein levels in ascitic fluid (less than 1 g/dL), and (2) long-term proton pump inhibitor (PPI) therapy such as increased gastric pH with PPI use, which promotes gut bacterial growth and translocation.
https://www.ncbi.nlm.nih.gov/books/NBK448208/
Define and classify shock.
A global state of cellular and tissue hypoxia and hypoperfusion due to circulatory failure and reduced oxygen delivery, increased oxygen consumption or inadequate oxygen utilisation resulting in multisystem organ failure.
The cell is unable to maintain homeostasis of ionic transfer, pH and osmosis.
4 classifications (CHOD)
Cardiogenic - cardiac eitiology causing reduced cardiac output
Hypovolaemic - reduced intravascular volume. (haemorrhagic vs non-haemorrhagic)
Obstructive - cardiac pumo failure e.g. tamponade or extra-cardiac e.g. tension pneumo/haemo
Distributive
- septic
- SIRS
- anaphylactic
- neurogenic
- endocrine (e.g. addisonian/adrenal crisis)
- drug/toxin induced
At what spinal level do severe injuries put people at risk of neurogenic shock?
T6 and above.
Cervical injuries - 19%
Thoracic spinal injuries 7%
What is the pathogenesis of neurogenic shock in spinal cord injuries?
In injuries above T6, results in loss of sympathetic tone and widespread vasodilation.
As such leads to flushing in skin, hypotension, bradycardia and may induce priapism due to vasodilation.
Treat with IVF and vasopressors (norepinephrine preferred).
Describe the hormones involved in the bodies response to hypovolaemic shock.
Early:
- adrenaline and noradrenaline > vasocontriction, increased HR and contractility.
Late:
Renin (kidney) - RAAS vasoconstriction and water retention
ACTH (pituitary) - increases cortisol
ADH (pituitary) - water resorption
What is TNF-α?
Tumor Necrosis Factor Alpha (TNF-α)
Produced by Macrophages
Increases Adhesion & Coagulation
Activates Neutrophils & Macrophages
Causes Cachexia in Cancer Patients
What are the peritoneal spaces in which abscess’ track.
The intraperitoneal space can be divided into areas based on peritoneal ligaments.
Supramesocolic & Inframesocolic are divided by the transverse mesocolon.
Inframesocolic spaces and paracolic gutters communicate freely with pelvis.
The left paracolic gutter is seperated from the supramesocolic space by the phrenicocolic ligament.
The Supramesocolic space is divided into left and right by falciform ligament
Note the peritoneal cavity is completely closed in males but open in females due to fallopian tubes communication with the abdominal cavity. Relevance is genital tract infections in females can lead to intraabdominal fluid tracking and peritonitis.
