Tuesday [23/11/2021] Flashcards
(104 cards)
Define AKI [3]
A rise in serum creatinine of 26 micromol/L or greater within 48 hours.
Be aware that in the absence of a baseline creatinine value, a high serum creatinine level may indicate AKI, even if the rise in creatinine over 48 hours is less than 26 micromol/L (particularly if the person has been unwell for a few days).
A 50% or greater rise in serum creatinine (more than 1.5 times baseline) known or presumed to have occurred within the past 7 days.
A fall in urine output to less than 0.5 mL/kg/hour for more than 6 hours (if it is possible to measure this, for example, if the person has a catheter).
Concern with using SGLT-2 inihibitors [1]
Euglycaemic DKA
What to assess in pt with AKI? []
Volume status:
- checking fluid intake/loss
- peripheral perfusion
- HR/BP
- JVP
- peripheral oedema, pulmonary crackles
Renal function and serum pot level [to excl/ hyperkalaemia]
Drug history, Sx underyling inflammatory disease
Urine dipstick
Stage 1 AKI
Creatinine rise of 26 micromol or more within 48 hours OR
Creatinine rise of 50–99% from baseline within 7 days* (1.50–1.99 x baseline) OR
Urine output** < 0.5 mL/kg/h for more than 6 hours
Stage 2 AKI
100–199% creatinine rise from baseline within 7 days* (2.00–2.99 x baseline) OR
Urine output** < 0.5 mL/kg/hour for more than 12 hours
Stage 3 AKI
200% or more creatinine rise from baseline within 7 days* (3.00 or more x baseline) OR
Creatinine rise to 354 micromol/L or more with acute rise of 26 micromol/L or more within 48 hours or 50% or more rise within 7 days OR
Urine output** < 0.3 mL/kg/hour for 24 hours or anuria for 12 hours
When to discuss Mx of AKI with a nephrologist [4]
Stage 4 or 5 chronic kidney disease. For more information, see the CKS topic on Chronic kidney disease.
A possible diagnosis that may need specialist treatment, for example, tubulointerstitial nephritis, glomerulonephritis (indicated by haematuria/proteinuria), systemic vasculitis that may also be affecting the kidney, or myeloma.
Inadequate response to treatment.
Other complications associated with acute kidney injury.
A renal transplant.
When to urgently admit people with AKI [4]
Likely stage 3 acute kidney injury.
An underlying cause that requires urgent secondary care management such as when an obstructed, infected kidney is suspected.
No identifiable cause for acute kidney injury.
A risk of urinary tract obstruction (for example known prostate or bladder disease; abdominal or pelvic cancer; known previous hydronephrosis; recurrent urinary tract infections; or other conditions consistent with possible obstruction, for example, anuria, single functioning kidney, neurogenic bladder).
Sepsis.
Evidence of hypovolaemia and a need for intravenous fluid replacement and monitoring.
A deterioration in clinical condition or a need for observation or monitoring of a frequency which is impractical in primary care.
A complication of acute kidney injury requiring urgent secondary care management such as pulmonary oedema, uraemic encephalopathy or pericarditis, or severe hyperkalaemia.
How ot Mx patient with stage AKI who don;t have any indication for admission? [4]
Manage the cause, if the expertise and resources are available in primary care.
Offer supportive measures such as advice on maintaining appropriate hydration.
Consider stopping potentially nephrotoxic medications (for example angiotensin-converting enzyme inhibitors, angiotensin II receptor antagonists, nonsteroidal anti-inflammatory drugs, and diuretics) or adjusting the doses of medication in relation to renal function. Seek specialist advice if unsure.
For more information, see the Think Kidneys documents Acute kidney injury - potentially problematic drugs and actions to take in primary care and Guidelines for medicines optimisation in patients with acute kidney injury.
Information on dose adjustment in renal impairment is available from the British National Formulary (BNF) or the manufacturers’ Summary of Product Characteristics (available at www.medicines.org.uk/emc).
Monitor creatinine regularly, using clinical judgement to determine frequency.
Be aware that even small increases in creatinine can be significant.
Reconsider the need to admit to hospital or discuss with a specialist if there is deterioration in the person’s condition, or an inadequate response to treatment.
First line Mx of AKI [10]
Find and treat the underlying cause.
Prevent fluid overload, and correct electrolyte imbalances—particularly hyperkalemia.
If patient is oliguric and not volume overloaded, a monitored fluid challenge may help.
Furosemide is ineffective in preventing and treating AKI but can (judiciously) be used to manage volume overload and/or hyperkalemia. Furosemide stress test may predict the likelihood of progressive AKI, need for RRT, and mortality (4)[B].
Dopamine, natriuretic peptides, insulin-like growth factor, and thyroxine have no benefit in the treatment of AKI.
Fenoldopam, a dopamine agonist, has been equivocal in decreasing risk of RRT and mortality in AKI; not currently recommended (1)[C]
Hyperkalemia with ECG changes: Give IV calcium gluconate, isotonic sodium bicarbonate (only if acidemic, and avoid use of hypertonic “amps” of NaHCO3), glucose with insulin, and/or high-dose nebulized albuterol (to drive K+ into cells); sodium polystyrene (Kayexalate) and/or furosemide (to increase K+ excretion); hemodialysis if severe/refractory
Fluid restriction may be required for oliguric patients to prevent worsening hyponatremia.
Metabolic acidosis (particularly pH <7.2): Sodium bicarbonate can be given (judiciously); be aware of volume overload, hypocalcemia, and hypokalemia.
Effective strategies for AKI prevention: isotonic IVF, once-daily dosing of aminoglycosides; use of lipid formulations of amphotericin B, use of iso-osmolar nonionic contrast media
Risk of contrast-induced AKI is reduced by avoidance of hypovolemia: isotonic saline 1 mL/kg/hr morning of procedure and continued until next morning or isotonic NaHCO3 3 mL/kg/hr × 1 hour before and 1 mL/kg/hr × 6 hours after contrast administration; N-acetylcysteine not of benefit
WHy is furosemide not very good to treat AKI [2]
Furosemide is ineffective in preventing and treating AKI but can (judiciously) be used to manage volume overload and/or hyperkalemia. Furosemide stress test may predict the likelihood of progressive AKI, need for RRT, and mortality
2nd line for AKI [2]
Tamsulosin or other selective α-blockers for bladder outlet obstruction secondary to BPH
Dihydropyridine calcium channel blockers may have a protective effect in posttransplant ATN.
Dietary changes for patients with AKI [4]
Total caloric intake of 20 to 30 kcal/kg/day (1)
Restrict Na+ to 2 g/day (unless hypovolemic).
Consider K+ restriction (2 to 3 g/day) if hyperkalemic.
If hyperphosphatemic, consider use of phosphate binders, although no evidence of benefit in AKI.
Avoid magnesium- and aluminum-containing compounds.
Indications for emergent haemodialysis [3]
Indications for emergent hemodialysis: severe hyperkalemia, metabolic acidosis, or volume overload refractory to conservative therapy; uremic pericarditis, encephalopathy, or neuropathy; and selected alcohol and drug intoxications
Causes of prerenal kidney disease
Decreased renal perfusion (often due to hypovolemia) leads to a decrease in glomerular filtration rate (GFR).
Caused by hypotension, volume depletion (GI losses, excessive sweating, diuretics, hemorrhage); renal artery stenosis/embolism; burns; heart/liver failure. Also hypercalcaemia, sepsis
If decreased perfusion is prolonged or severe, can progress to ischemic acute tubular necrosis (ATN)
Causes of intrarenal kideny disease
ATN (from prolonged prerenal azotemia, radiographic contrast material, aminoglycosides, nonsteroidal anti-inflammatory drugs [NSAIDs], or other nephrotoxic substances), glomerulonephritis (GN), acute interstitial nephritis (AIN; drug induced), arteriolar insults, vasculitis, accelerated hypertension, cholesterol embolization (following an intra-arterial procedure), intrarenal deposition/sludging (uric acid nephropathy and multiple myeloma [Bence Jones proteins])
Causes of postrenal kidney disease
Extrinsic compression (e.g., benign prostatic hypertrophy [BPH], carcinoma, pregnancy); intrinsic obstruction (e.g., calculus, tumor, clot, stricture, sloughed papillae); decreased function (e.g., neurogenic bladder), leading to obstruction of the urinary collection system
ABCDE approach to managing unwell patient [5]
A – airway patent [can they respond verbally]
B – sats, RR [>94 aimed for, >92 in hypoxic drive COPD, some COPD pts 88-92], respiratory effort [accessory muscle]
C – ECG, pulses, listen to chest
D – pupils, AVPU, GCS, glucose
E – exposure/everything else
What are airway adjunts? [2]
Adjuntcs: guedel, O2 mask, nasopharyngeal airway
When would you not use an nasopharyngeal airway adjunct? [1]
Not use nasopharyngeal airway in skull base fractures
Features of airway collapse [4]
Reduced movement affected side, trachea moved toward affected side, dull percussion, bronchial/reduced breath sounds
Features of consolidation [4]
Reduced movement affected side, trachea central, dull percussion, bronchial breath sounds
Features of pneuothorax [4]
Reduced movement affected side, trachea moved away affected side or central, hyper-resonant percussion, /absent reduced breath sounds
Plueral fluid features [4]
Reduced movement affected side, trachea moved away from affected side or central, stony dull percussion, reduced breath sounds
