Emergency Module Flashcards
(40 cards)
What is sepsis?
Sepsis is life threatening organ dysfunction caused by a dysregulated host response to an infection
How do you diagnose sepsis?
Sepsis is recognised by looking for signs of organ dysfunction in patients who are suspected of having an infection.
The SOFA and qSOFA scoring systems isn’t used for diagnosis, but is used to identify patients who are likely to have a poor outcome.
What is the utility of the qSOFA score? What are its components?
It is used to identify those patients with a suspected infection who are at a higher risk of a poor outcome.
Comprised of
- Mental status?
- RR
- Blood pressure
What is MODS?
Progressive organ dysfunction in an acutely ill patient, such that homeostasis cannot be maintained without intervention.
2 or more organ system dysfunction is required to be called MODS
What is shock?
- Shock is as state of organ hypoperfusion with resultant hypoxia, cellular death and organ dysfunction
- Includes hypovolemic, cardiogenic, distributive and obstructive
What are the stages of sepsis?
Non-progressive phase
○ Reflex compensatory mechanisms are activated;
○ Baroreceptor reflexes, catecholamine release, RAAAS, ADH release, and sympathetic stimulation
○ Net effect of tachycardia, peripheral vasoconstriction, and renal conservation of fluid
Progressive phase
○ With persistent tissue hypoxia you get anaerobic metabolism with lactic acid as its byproduct - this results in acidosis.
○ Acidaemia results and the vasomotor response is blunted leading to vasodilation, peripheral pooling, and worsening shock
Irreversible phase
○ In severe cases, widespread injury results in overwhelming lysozymal leakage and cell death. Bacterial superinfection catalyses this and multi-organ failure ensues
What is the pathophysiology of MODS?
MODs involves and exaggeration of normal responses to injury with systemic inflammation, immune dysfunction, and microcirculatory abnormalities.
- The key mechanisms driving MODS are:
○ SIRS response
- Triggering event initiates a SIRS response - release of TNFa, IL-1, IL-6, IL-8
○ Endothelial dysfunction
- Adhesion molecules are expressed which results in immune activation.
- Vasodilation and increased vascular permeability results in tissue oedema and hypoperfusion.
- Microthrombi occur - which leads to clotting factor and platelet consumption.
○ Immune dysfunction
- Immune suppression due to T cell exhaustion occurs resulting in relative immunosuppression.
○ Neuro-endocrine and hormonal dysfunction
- Release of cortisol, catecholamines and ADH further contributes to fluid and electrolyte abnormalities.
○ Hypoxic injury
- Due to peripheral vasodilatation, shunting, and oxygen demand-delivery mismatch
How is renal failure graded graded?
RIFLE
- Risk - 1.5x baseline creatinine or urine output < 0.5mls/6 hours.
- Injury - 2x baseline creatinine or urine output < 0.5mls/kg/12 hours.
- Failure - 3x baseline creatinine or urine output <0.5mls/kg/24 hours.
- Loss - persistent failure for 4 weeks.
- ESRD - renal failure for 3 months.
What is SIRS
Spiel for the exam
- SIRS is a dysregulated host inflammatory response to an injury or infection.
- Is a combination of humoral and cellular immune response, cytokine release and activation of the complement pathway.
- First there is an insult - infection or inflammation.
- Release of inflammatory cytokines including IL-1, IL-6, IL-8 and IFN -g, IFN-a - these amplify the inflammatory response and lead to recruitment of macrophages, lymphocytes and platelets to the area.
- PAMPS and DAMPS are released
- The complement pathway is activated with cleavage of C3a and C5a resulting in vasodilatation and capillary leak.
- Endothelial dysfunction results in activation of platelets as well as peripheral oedema.
If homeostasis is not restored - a widespread progressive systemic reaction occurs.
What is ARDS?
ARDS is an inflammatory injury to the lung which is acute in onset, and results in widespread alveolar injury It can occur from a primary lung pathology like pneumonia or as a secondary response to inflammation. It is defined by 3 stages, an exudative phase where damage to the alveolar-capillary membranes result in leakage or protein rich fluid along with neutrophile recruitment from inflammatory mediators. A proliferative phase occurs where macrophages replace neutrophils. Fibroblasts deposit collagen and fibrosis occurs. In some patients, a fibrotic phase will occur which is due to excessive collagen formation, resulting in a poorly compliant lung.
What are the three stages of ARDS?
- 3 well defined stages
○ Exudative phase: - Damage to the epithelial and endothelial layers of the alveolar-capillary barrier results in leakage of protein rich fluid into the alveolar space. - Inflammatory mediates (IL-1, IL-6, TNFa) result in neutrophil recruitment and release of toxic mediators exacerbating lung damage. - Oedema develops in the interstitial and alveolar spaces - impairing gas exchange and driving hypoxia. ○ Proliferative phase - Neutrophils decrease and macrophage increase. - Fibroblasts migrate into interstitial space leading to collagen deposition and fibrosis. - Type II pneumocytes undergo hyperplasia, in an attempt to restore the epithelial barrier. ○ Fibrotic phase - Occurs in some patients. - Excessive fibrosis occurs due to excessive collagen deposition Resulting in reduced lung compliance, persistent hypoxia and chronic restrictive lung disease.
What is the management or ARDS?
○ Low tidal volume mechanical ventilation
○ PEEP to prevent atelectasis
○ Avoiding prolonged high Fi02
○ Prone positioning
○ Conservative fluid management
Treatment of underlying cause.
What is the diagnostic criteria for ARDS?
- Insult must have occurred within a week of a clinical insult.
- Must have bilateral opacities on CXR or CT
- Respiratory failure cannot be explained by cardiac failure of fluid overload.
Must have hypoxemia
What is DIC and what causes it?
- DIC is a systemic condition characterized by widespread activation of coagulation pathways, leading to thrombosis and bleeding.
Causes:
- sepsis, malignancy, trauma or obstetric complications.
What is the pathophysiology of DIC?
DIC a systemic condition characterized by widespread activation of coagulation pathway leading to both thrombosis and bleeding. It typically occurs due to an underlying insult - such as sepsis, malignancy, trauma or obstetric complications. Factors which drive DIC are endothelial injury from cytokines resulting in Tissue factor exposure and activation of the extrinsic pathway. This results in microthrombi formation result in coagulation and platelet consumption. Fibrin is broken down resulting in the formation of fibrin degradation products which further impairs clot formation.
How is DIC diagnosed?
Prolongation of the APTT and PT
Low fibrinogen
Declining platelets
High D-Dimer (as it is a fibrin degradation product)
Peripheral smear may show fragmented cells - due to shear stress
What is brain death?
Brain death is the permanent, irreversible, and complete loss of brain function, including the capacity for the brainstem to regulate respiratory and vegetative activities.
It is different from persistent vegetative state, in which the person is alive and some autonomic function remains.
What are the pre-requisites needed before you can begin an assessment of brain death?
- Clinical or neuroimaging of an acute central nervous system catastrophe that is compatible with brain death.
- Exclusion of complicating medical condition which may confound clinical assessment (i.e. electrolyte, acid-base, endocrine disturbance)
- No drug intoxication or poisoning.
- Temp > 36 degrees
- Systolic blood pressure > 100mmHg - vasopressors can be used.
How is the neurological examination performed when assessing someone for brain death?
- Absence of cranial nerve reflexes
- pupillary
- corneal
- gag and cough
- oculovestibular (caloric reflex). - Absent motor responce.
- absence of motor response to painful stimul to head/face (CN V distribution)
- NB: presense of spinal reflexes does not preclude braindeath - Absence of spontaneous respiration
- patient is pre-ventilated with 100% oxygen - disconnected from ventilator for 10 minutes - pc02 needs to be above 60mmHg to ensure adequate respiratory stimulation.
- oxygen is delivered during the apnoeic period
What is the pathophysiology of a rectus sheath haematoma?
Rectus sheath haematoma
- Arise from disruption of a branch of the inferior epigastric artery at its insertion into the rectus muscle combined with an inability to tamponade bleeding.
- The inferior epigastric artery is relatively fixed within the muscle, making its branches vulnerable to shearing forces
The arcuate line, which is a horizontal line occurring 1/3 of the distance from the umbilicus to the pubic symphysis, demarcates the lower limit of the posterior rectus sheath.
What are the risk factors for a rectus sheath haematoma?
- Arise from disruption of a branch of the inferior epigastric artery at its insertion into the rectus muscle combined with an inability to tamponade bleeding.
- The inferior epigastric artery is relatively fixed within the muscle, making its branches vulnerable to shearing forces
The arcuate line, which is a horizontal line occurring 1/3 of the distance from the umbilicus to the pubic symphysis, demarcates the lower limit of the posterior rectus sheath.
- The inferior epigastric artery is relatively fixed within the muscle, making its branches vulnerable to shearing forces
What are the signs of a rectus sheath haematoma
Carnett’s sign - site of pain is the same with patient supine as it is when sitting up.
Fothergills sign - abdominal mass does not cross midline and does not change with movement of the lower extremities.
How is rectus sheath haematoma graded?
- 1 - small and confined to within rectus, does not cross midline or dissect fascial planes.
- 2 - confined within rectus muscle, but can dissect along fascial planes or cross the midline
3 - large, below arcuate line, associated with haemoperitoneum.
What is the pathophysiology of frostbite?
- Freezing
○ Exposure to temperatures below freezing results in ice crystals in the extracellular space which leads to cell dehydration.- Vasoconstriction
○ Cold exposure causes intense vasoconstriction, reducing blood flow and oxygen levels to tissues.
○ Stasis of blood flow and thrombosis can result in ischaemia. - Reperfusion injury
Upon re-warming - can get release of ROS.
- Vasoconstriction
