Acute Kidney Injury Flashcards
what is hyperkalaemia and what are the symptoms?
muscle fatigue, weakness, paralysis, abnormal heart rhythm
what does an ECG show in a patient with hyperkalaemia, and why?
K+ affects action potentials
causes wide QRS and tall, tented t waves
= causes VF
how do you investigate and treat hyperkalaemia?
eGFR, ABG, ECG, blood glucose
stabilise myocardium using calcium gluconate 10%/10ml over 5 minutes
10 units of short acting insulin in 50 ml 50% dextrose solution and also 10ml nebulised salbutamol
= this shifts potassium back into cells
how do you treat hypokalaemia
consider other electrolyte abnormalities
administer potassium chloride in sodium chloride at max rate of 20mmol/hour
what is an AKI
clinical syndrome characterised by acute drop in kidney function
diagnosed by rise in creatinine of >25micromol in 48 hours or rise by >50% in 7 days
urine output of 0.5ml/kg > 6 hours
25% fall in eGFR in young people over 7 days
what are the risk factors of AKI
CKD heart failure diabetes liver disease older age oliguria nephrotoxic impairments such as NSAIDs and ACE-I
what are the pre-renal causes of AKI
inadequate blood supply to kidneys which reduces filtration
dehydration, hypotension, HF, sepsis, shock, hepatorenal failure
what are the renal causes of AKIs
intrinsic disease due to reduced filtration of blood
- glomerulonephritis, interstitial nephritis, acute tubular necrosis, NSAIDs, ACE-I
what are the post-renal causes of AKI
obstruction to outflow of urine from kidney
kidney stones, cancer mass, ureteral strictures, enlarged prostates
what are the clincial features of an AKI
fever, rash, joint pains, nausea, dehydration, confusion and drowsiness
uveitis, audible bruits
oliguria !!
how do you stage AKI?
stages 1-3, dependant on serum creatinine and urine output
look for table in notes
what are the investigations for an AKI?
- urinalysis (protein and blood = nephritis)
- glc for diabates
-US of KUB
ABGs = metabolic acidosis
how do you manage an AKI?
- underlying pathology
- support = treat sepsis, stop nephrotoxic meds (ACE-I, ARBs, NSAIDs)
pre renal: correct volume depletion and increase renal perfusion via circulatory or cardiac support
renal: biopsy and treat internal condition
post-renal: catheter and nephrostomy
also = FLUID for all
what are the complications of an AKI?
- hyperkalaemia
- fluid overload, heart faiure and pulmonary oedema
- metabolic acidosis
- uraemia
what is the SALFORD pneumonic for an AKI
S - sepsis A - ACE-I, NSAIDs drug review L - labs (creatinine) and leaflets F - fluid assessment and response (history and examination Obstructive cause? Renal care if specialist needed Dip urine and record
what is the SALFORD pneumonic for an AKI
S - sepsis A - ACE-I, NSAIDs drug review L - labs (creatinine) and leaflets F - fluid assessment and response (history and examination, fluid chart, measure daily weights, if hypovolemic give bolus IV 250mls and reasses) O - obstruction (USS) R - renal referral, non resolving AKI Dip urine
what are urea and creatinine?
urea = made from ammonia by liver, excreted into blood
creatinine = muscle breakdown product, equal concentrations released into blood each day
= creatinine is normally completely filtered out of blood into urine so hence used as marker of kidney damage bc none should be present in blood
what is the formula used in pre-renal failure for eGFR
GFR = 1/creatinine
what is acute tubular necrosis and what is shown on the histology?
combination of factors have caused renal ischaemia and toxicity = hypotension and dehydration
how do you treat ATN?
supportive
recovery is 2-3 weeks; high mortality
no meds unless septic
what are the 3 phases of ATN?
oligouric: high creatinine, low urine
maintenance: increased urinary output
polyuric recovery: large amounts of dilute urine, hypovolaemic, DCT and CD still recovering so do not allow water to be reabsorbed
what is sepsis
sepsis is defined as a life threatening organ dysfunction caused by dysegulated host response to infection
caused by body mounting a systemic inflammatory response to infection
what is the pathophysiology of sepsis
- release of IL and TNF
- nitrous oxide = vasodilation
- BV increase permeability
- space between blood and tissues - reduction in oxygen reaching tissues
- coag system activated = compromising organ perfusion
- thrombocytopenia
- haemorrhages
- DIC
why does blood lactate rise in sepsis?
hypoperfusion of tissues that starves the tissue of oxygen = anaerobic respiration = waste product
what is septic shock
defined when the arterial BP drops and you get hypoperfusion
systolic BP <90 despite fluid resuscitation
hyperlactaemia (>4)
what are the risk factors for sepsis
immunocompromised patients , eg very young or very old
chemotherapy, steroids or immunosuppressants
surgery, trauma, burns
pregnancy
indwelling medical devices eg catheters or centrals
what does sepsis present with?
NEWS score high
fever
high resp rate
confusion, drowsiness
may have: cellulitis, wound, cough, dysuria, non-blanching rash, mottled skin, reduced urine output
= kidneys often affected early in sepsis due to low blood flow in renal medulla
what is the investigations you would do for sepsis?
- FBCs U&Es LFTs CRP clotting for DIC blood cultures for bactaraemia blood gases for lactate, pH and glucose urine dipstick CXR CT
patients should be assessed and treated within ONE HOUR of suspected sepsis presentation
what is the sepsis six?
- blood lactate
- blood cultures
- urine output
- oxygen to maintain sats 94-98
- empirical broad spectrum AB
- IV fluids
