My Acute medicine

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Author:
Mike2556
ID:
127593
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My Acute medicine
Updated:
2012-01-17 17:04:50
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AKI ARDS ICU Sepsis
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AKI, ARDS, ICU, Sepsis
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  1. What are the functions of an intensive care unit?
    • Specialised monitoring
    • High degree of expertise
    • High nurse:patient ratio
    • Organ support
    • All used for patients with a critically ill or unstable condition
  2. What does the APACHE II scoring system predict?
    The likelihood of mortality or morbidy of ICU patients
  3. What observations are used in the APACHE II scoring?
    • Obs: Temp, MAP, HR, RR, PaO2
    • Bio: pH, Sodium, Potasisum Creatinine
    • Bloods: Haematocrit, WBC
    • GCS
  4. What is the signifance of the following in a clinical setting:
    - Heart rate
    - RR
    - SBP
    - GCS
    - O2
    - Temp
    • Tachycardia is related to a poor outcome
    • Tachypnoea occurs in sepsis/PE and other acute disease
    • Lowers in sepsis and blood loss
    • Disease affects cellular function
    • Lung/airway/CV pathology
    • Disease affects metabolism or sepsis/drug
  5. Describe some other important investigations used in ICU, apart from general observations
    • Urine output: Normal suggests adequate perfusion. Hypovolaemia, renal disease.
    • Bioch: Lactate, glucose, [acid/base] = metabolism/perfusion
    • Pain: Actual/potential tissue damage
  6. What does the SOFA score predict?
    Determines the rate and extent of a patient's organ function and failure
  7. What factors are used in the SOFA score?
    • Pa02: <400 = 1, <100 = 4
    • GCS: <14, <12, <9, <6
    • Bilirubin: >1.9, >12
    • Platelets: <150, <20
    • Creatinine: >145 (2), >382 (5)
  8. Outline the pathogenesis of sepsis
    • Microorganism invades blood stream
    • Endo/exotoxins cause mediator release, including NO
    • Profound vasodilation = renal failure+ albumin enters ECM
    • Pulmonary oedema + tissue hypoxia
    • Multiple organ dysfunction syndrome
  9. What are the adverse effects of mechanical ventilation?
    • Infection
    • Barotrauma
    • O2 toxicity
    • Together may cause ARDS
  10. - Define sepsis
    - Define severe sepsis
    - Define septic shock
    • SIRS criteria + confirmed or presumed infection
    • Sepsis with 1 or more organ dysfunctions
    • Severe sepsis and hypotension unaffected by IV fluids
  11. How are septic patients managed?
    • 1. High flow O2
    • 2. Take 2 blood cultures
    • 3. Investigations; CSF, urine culture, CXR etc
    • 4. Antibiotics, within 1st hour. 1+ active against likely pathogen
    • 5. 250 ml IV crystalloids + consider fluid challenge
    • 6. Vasopressors if severe hypotension
    • 7. Lactate and Hb measured; hypoperfusion/hypovolaemia
    • - Check urine output constantly
  12. What is the significance of AKI in ICU?
    • ~10% of patients in hospital are at risk of AKI
    • Directly related to mortality, even at risk stage
    • Increases likelihood of organ failure
    • 20% of patients in ICU require RRT
  13. What are the classical reasons for renal failure?
    • Pre-renal: Hypovolaemia, stenosis
    • Renal: Vasculitis, glomerulonephritis, drugs
    • Post-renal: Obstruction, e.g prostate, stone
  14. What are the multi-factorial reasons for AKI?
    • Theory that many factors cause AKI at once
    • Many sepsis related: poor CO + PR = renal ischaemia
    • Toxin mediated (including rhabdomylysis/drugs)
    • Obstruction
  15. What are the RIFLE criteria used for?
    • Assessing measurements (RIF) and outcomes (LE) of AKI (after resuscitation + IV fluids)
    • R: Risk; Creatinine x 1.5, urine <5ml/kg/hr for 6 hrs
    • I: Injury; Creatinine x 2, urine <5ml/kg/hr for 12 hrs
    • F: Failure; Creatinine x 3, urine <3ml/kg/h x 24 hr
    • L: Loss; Persistent ARF= complete function loss >4 weeks
    • E: End stage renal disease
  16. What are the indications for dialysis?
    • When urine production lowers and urea/creat rises
    • Renal function related disease; hyperkalaemia, acidosis, uraemia
    • Survivable injury/decent prognosis (age, ESRD etc.)
    • Opportunity to stop RRT in future
  17. What is the difference between haemofiltration and dialysis?
    • Dialysis: Withdrawal of desirable ions using concentration gradients across a semi-permeable membrane.
    • Haemofiltration: Similar, but positive hydrostatic pressure also used to remove larger solutes. More expensive
  18. If urine output decreases, and urea increaes, how should the patient be managed?
    • ABCDE to check for hypoxia/hypotension/sepsis
    • Ensure perfusion (peripheral temp or capillary refill)
    • Exclude obstruction, e.g. flush catheter/bladder with saline
    • Next give IV fluids to ensure perfusion/BP
    • Renal replacement therapy if no difference
    • NOTE: Diuretics should NOT be used
  19. What are the clinical findings of ALI?
    • Hypoxaemia
    • Pulmonary oedema: bilateral infiltrates
    • Decreased compliance
    • No evidence of left atrial hypertension
  20. What are the main causes of ALI?
    • Pulmonary: Pneumonia, aspiration, injalation, fatty emboli
    • Extra-pulmonary: Sepsis, trauma
  21. What are the acute pathological mechanisms of ALI?
    • Early phase: Exudative
    • Type 1 pneumocytes swell and detach from BM after damage
    • Thrombi in capillaries = V/Q mismatch
    • Respiratory membrane dysfunction = proteinacious leak
    • Type 2 pneumocyte damage = reduced surfactant = alveolar collapse
    • Neutrophil infiltration and cytokine release = damage/thrombi
  22. How does ALI resolve?
    • Late phase: Fibroproliferative
    • Myofibroblast infiltration + exudate = granulation
    • Type 2 pneumocytes become type 1
    • Neutrophil apoptosis
    • Either recovery or 'honeycombing' (end stage fibrotic lung disease)
  23. What co-morbidities are common in ALI?
    • Chronic liver disease
    • Sepsis
    • Chronic alcoholism
    • Chronic respiratory disease
    • Low serum pH
  24. Define ARDS
    • Acute respiratory distress syndrome
    • A more severe result of ALI
    • A Pa/Fi ratio less than 26kPa and persistence, with an associated cause
  25. What does the Murray score measure and estimate?
    • Measures alveolar consolidation, Pa02/Fi02 ratio and lung volume
    • Used to estimate the severity of ARDS
  26. Outline the clinical presentation of ARDS
    • Within 1-2 days of insult
    • Progressive, severe dyspnoea and dry cough
  27. What are the clinical findings of ARDS?
    • Diminished air entry into lung base
    • Coarse crackles
    • May be unexpectedly normal
  28. What are the systemic effects associated with ARDS?
    • Pulmonary manifestation of systemic response
    • Hypotension/vasodilation
    • AKI
    • Pulmonary hypertension/Right heart failure (thrombi)
  29. What investigations are appropriate in ARDS?
    • General Obs: Patient's well being
    • Bronchoalveolar lavage: Neutrophils/macrophages
    • Transbronchial/open lung biopsy
    • Radiology
  30. Outline the treatment of ARDS
    • High 02 to maintain tissue xygenation
    • Fluids used to prevent shock, but may cause late damage via oedema
    • Support other failing organs
  31. What are the clinical features of respiratory failure?
    • RR <8 or >30 (slow = exhaustion)
    • Pale/sweaty/clammy
    • Exhaustion/accessory muscle use
    • Confusion/convulsion 2nd to hypoxia
    • Prolonged expiratory phase, maybe with wheeze
    • Low GCS 2nd to hypercapnia
    • Tachycardia or late bradycardia
  32. How does O2 therapy administration differ in COPD
    • T1RF: High flow 02 used and steadily decreased
    • T2RF: Low flow 02 used and steadily increased, with GCS, RR and ABGs monitored
  33. Define Fi02
    • The percentage of O2 inspired that participates in gas exchange in the alveoli
    • Differs from Pa02 as it is unaffected by V/Q
  34. When are fixed performance masks used?
    • When Fi02 must be a known, acceptable amount
    • E.g. in COPD where 02 delivery is essential but must be monitored
  35. What are the indications for respiratory support?
    • Unresponsive hypoxaemia
    • Exhaustion
    • Severe hypercapnia
    • Time needed to investigate/treat underlying condition
  36. How can CPAP reduce gas exchange?
    • In unilateral or lobar diseases, CPAP forces blood out from the ventilated to the 'dead space'
    • In fully compliant lungs, CPAP can increase pulmonary vascular resistance
    • Flattening diaphragm may increase expiratory muscle use
    • In pneumothorax, GI bleeds etc. positive pressure a bad thing
  37. Define and outline some 'rescue therapies'
    • A procedure which aids the treatment of respiratory failure but doesn't rely on gas exchange
    • NO: Vasodilation improves oxygenation (no effect on outcome)
    • Extra-corporeal: Blood removed from body and CO2 removed.
  38. What are the causes of unilateral effusions found on a CXR?
    • Pneumonia
    • Empyema
    • Trauma
    • Malignancy
  39. What are the causes of bilateral effusions found on a CXR?
    Heart or renal failure
  40. What are the findings of ARDS on a CXR?
    • Diffuse alveolar shaddowing/patchy opacity
    • Progressive changes
    • Effusions are not a major feature
  41. What are the findings of heart failure or fluid overload in a CXR?
    • Interstitial thickening occurs across the lung, highlighting the lobules
    • Underlying lung is normal, with effusions
    • Cardiomegaly
  42. What are the problems with diagnostic imaging in ICU?
    • Suboptimal positioning and exposure, which varies between images
    • Magnification of mediastinal contours
    • Reduced kilovoltage of portable units = underexposure and motion blur
  43. Describe some commonly used IV fluids
    • Crystalloids: Different ionic concentrations in solute. Associated with oedema
    • Colloids: Larger molecules e.g. albumin; preserve osmotic pressure (helpful in oedema)
  44. Outline the process and purpose of a fluid challenge
    • An end point is selected (e.g. normal HR, GCS, perfusion)
    • 250ml given rapidly; response monitored
    • Patient reassessed, especially SV
    • No response = further challenge and continued treatment
  45. What is the mechanism of action of catecholamines?
    • B1 effect: Inotropy via calcium release, chronotropy via calcium channel opening = Increase CO and ischaemia
    • B2 effect: Vasodilation via calcium uptake into sarco. ret. = smooth muscle relaxation and greater muscle 02
    • A1 effect: Vasoconstriction via G proteins = increase PR
  46. What are the effects of Dobutamine?
    • B1 and B2 receptor effect (3:1 ratio of strength)
    • Strong inotrope, weak chronotrope
  47. What are the effects of noradrenaline?
    • Alpha agonist, slight B activity
    • Vasoconstriction, weak inotropy/chronotropy
    • Reliable increase in BP and cardiac blood flow
  48. What are the effects of adrenaline?
    • Mainly Beta agonist in lower doses
    • Increase pulmonary pressure and peripheral ischaemia
  49. What are the effects of PDE inhibitors?
    • Used if catecholamines ineffective/resistant
    • Increase cAMP = calcium entry = inotropy (not via beta receptors)
  50. What are the effects of vasopressin?
    • Used in refractory septic shock
    • V1a receptor = inotropy and noradrenaline sensitivity
    • V2 receptor = increased ion/water uptake in kidneys
  51. Describe the CV monitoring of a septic patient
    • Goal to monitor BP and CO
    • Tissue oxygenation measured (not ABG)
    • If low value despite normal ABG, CO insufficient
  52. What does MEWS predict?
    • "Modified Early Warning Score"
    • Guide used to quickly determine the degree of illness
    • Four readings: SBP, HR, RR, temp and GCS
    • The more the patient's diverse from the norm, the greater the score
  53. Apart from OBs, what other investigations are important in acute medicine? What do they indicate?
    • Urine output: Hypovolaemia, renal disease, overhydration, drugs. Normal = adequate perfusion
    • Biochem: lactate, glucose, acid/base. Metabolic function and perfusion
    • Pain: Associated with actual or potential tissue damage
  54. What are the problems with the measurements used in the RIFLE criteria?
    • Several conditions can cause a drop in urine production unrelated to renal failure
    • Creatinine can also be affected by other conditions (e.g. diabetes, muscle mass)

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