Please enable JavaScript.

Coggle requires JavaScript to display documents.

Acute renal failure - Coggle Diagram

- - - - note: some CRF animals can have normal sized kidneys. Or cats can have enlarged kidneys e.g. renal lymphoma, polycystic kidney disease
- - - - e.g. dogs with leptospirosis or borreliosis
- - - - the severity of residual azotaemia will determine if can managed successful as a CKD patient
  - - - sensible losses (measured urine volume)
        
        indwelling urinary catheter to measure (also aids in facilitating fluid therapy in initial 24-48h)
      - insensible losses (GI and respiratory losses)
        
        approx 20 ml/kg/day
      - beware of over hydration with oliguria
        
        urine output of less than 2ml/kg/hr in an adequately hydrated animal receiving fluid therapy is considered relative oliguria
      - weight patient twice a day
      - normal urine output = 1-2ml/kg/hr
        
        2-5ml/kg/hr expected normal in dogs and cats receiving adequate fluid volume expansion
      - 0/9% NaCl initial choice due to Na content and lack of K
        
        once rehydrated can use hypotonic fluids (0.45% NaCl in 2.5% dextrose) for maintenance to prevent hypernatraemia
        
        monitor and potentially supplement K+
        
        varies depending on urine output, renal excretory function, severity of metabolic acidosis and oral intake
        
        ecg for physiologic effects of hyperk
        
        bradycardia
        
        prolongation of P-R interval
        
        widening of QRS complexes
        
        blunting/absence of P waves (atrial standstill)
        
        tenting of T waves
        
        serum K
        
        8-10mEq/L dangerous for cardiac function, above this are life-threatening.
        
        hyperK tx
        
        sodium bicarbonate IV
        
        usually infused first, esp. if metabolic acidosis present
        
        alternative: 20-30% hypertonic glucose can stimulate endogenous insulin release and translocation of potassium into cells
        
        may choose this over sodium bicarb if...
        
        3 more items...
        
        10% calcium gluconate solution can be infused to counteract effects of potassium on heart, but this approach does not lower serum K+ conc
      - to correct metabolic acidosis sodium bicarbonate can be added to maintenance fluids that do not contain calcium
      - attempt to correct hyperphosphataemia
        
        can contribute to worsening of renal lesions and excretory function
        
        renal mineralisation
        
        direct nephrotoxicity
        
        vasoconstriction
        
        also contributes to metabolic acidosis and hypocalcaemia
        
        intestinal phosphate binders
        
        alumininum hydroxide and alumininum carbonate
        
        excess can lead to aluminium toxicity which is manifested as dementia that may be difficult to distinguish from uraemia effects
    - - diuretics to attempt oliguria --> non-oliguria after rehydration
        
        poor prognosis if unsuccessful
        
        mannitol IV
        
        beware of hyperosmolarity and volume overload
        
        furosemide IV
        
        contraindicated in aminoglycoside toxicity
- - - - casts
      - cellular debris
      - tubular swelling
    - - interstitial oedema
      - cellular infiltrates
    - - e.g. afferent arteriolar vasoconstriction and efferent arteriolar vasodilation, decreased glomerular permeability
  - - - can result in renal ischaemia by blocking the renal production of vasodilatory prostaglandinsthat maintain renal blood flow during dehydration
      - renal ischaemia
    - - aminoglycosides
  - - - time after exposure to a nephrotoxin or renal ischaemia before onset of azotaemia
      - associated with increased severity and number of renal tubular lesions over time if renal insult not removed
      - not usually detected as clinical signs are absent/minimal
      - prompt removal of the inciting cause will result in rapid return to normal renal function
    - - critical amount of lethal injury has occurred in the renal tubules
      - 1-3 weeks of acute intrinic renal failure is expected before restoration of renal function
        
        removal of inciting cause will not result in immediate return of normal renal function
      - anuria, oliguria, normal urine production or polyuria may occur
        
        depends on the specific cause and severity of renal injury
        
        anuria or oliguria occurs with most severe renal injury e.g. ethylene glycol of lily toxicity in cats
        
        normal urine production or polyuria is more likely with amino glycoside nephrotoxicity
      - characteristics
        
        persistently increased serum creatinine concentration, despite correction of all prerenal factors (i.e. restoration of ECF and renal perfusion)
        
        may not survive this phase
        
        renal blood flow may be restored by volume expansion during the maintenance phase, but GFR remains low
    - - BUN and serum creatinine concentrations return to normal as the GRF and RBF recover and diuresis ensures in patients in patients that were previously oliguric/anuric
      - urine concentrating ability and acidification may not return to normal
        
        usually not of clinical consequence
      - BUN + serum creatinine concentrations may not completely normalise, depending on amount of renal injury sustained.
        
        this patients may show sufficient improvement to have reasonable QoL as CKD patient
- - - - acute tubulointerstitial nephritis