Definitions, Tables, Facts - Renal And Endo Flashcards
KDIGO stage 1
Increase in creatnine by 26.5mmol/L
Or 1.5x baseline in 7 days
AND
U/O <0.5ml/kg/hr for 6 hours
KDIGO 2
Creatinine 2-2.9x baseline
U/O 0.5ml/kg/hr 12 hours
KDIGO 3
Creatinine 3x baseline OR Rise by 353.6 umol/litre OR Needing RRT
Urine output 0.3mls/kg/hr for 24 hours
OR
12 hours of anuria
Complications of AKI
Metabolic - acidosis, hyperkalaemia, electrtolytes, uraemic enceph
Fluid - tissue overload, resp failure, postive balance
Long term - progress to CKD, need for long term RRT
Risk factors for AKI
Known CKD CCF, DM, Liver disease Previous AKI Any impairment limiting access to fluids (neuro, cognitive) Age 65 Sepsis and hypovolaemia
NEPHROTOXIC DRUGS - ACEi, ARBS, Gent, diuretics, NSAIDs
Obstructions
Other causes - ?contrast
Rhabdo, HUS, TLS, GN, nephritis
Surgery - emergency, intraperitoneal
Summary of management with AKI
Initial resus
Assess fluid status
Replace with isotonic crystalloids
Haemodynamic support
Hx and Exam D&V - hypovol Bloody diarrhoea - HUS No urine - obstruction Haematuria - GN, stones, Ca Haemoptyiss - Wegeners, vasculitis Joint pain/rask - SLE
Ix - Urinalysis, protein, blood, micropscopy FBC, U&E, LFT, CRP, CK, Glucose, Ca, PO3, Mg, ANtibodies - ANCA, GBM, ANA (SLE) Renal US
Stages of CKD
1 >90 mls/min/1.73m2BSA 2 60-89 3 30- 59 (A 45-59, B 30-44) 4 15-29 5 <15
Prognositcally worse if proteinuria
Problems with CKD in ITU
PK -
Altered Vd
Decreased clearence
Decreased protein binding
Fluid/Electro Hyperparathyroidism Hyperphosphate Acidosis Hyperkalaemia Overload
CVS
Hyptertension
Risk of CVD
Haem
Anaemia
Uraemic plt dysfunction
Impaired immuno
Neuro- polyneuropathy
May need dialysis OR conversion from intermittant to continuous
Components of an RRT circuit
Extracorporeal circuit including semi permeable membrane
Blood pumps
Pressure sensors and air detectors/traps
Vascular access device
Anit-coaguation
Basic principles of RRT
HF - Convection
HD - Diffusion (solutes down a gradient)
HF - hydrostatic pressure gradient across a semi permeable membrane
solvent drag carries low weigh solutes with water —> ultrafiltrate
fluid replaces ultrasfiltrate —> determines net fluid
HD - Blood and diasylate fluid run countercurrent to each other seperated by a membrane
Solutes diffuse across
Fluid removed by increasing pressure
What are membranes made of
Cellulose or Semi synth
Celluose - low permeability, good for HD
Activate inflammation, less useful in critical illness
Semi-synth - high permeabiliry to water, less inflammation, both HF and HD
Thinner large area membrances —> more diffusion/convection
Indications for RRT
Ureamia - enceph, pericarditis, bleeding
Absolute urea above 36??
Hyperkalaemia
Met acidosis
Oligo-anuria
Fluid overload
Extra:
Volume removal, prevent overlaoad
?sepsis
Drugs in overdose
Types of RRT
Continuous or intermittant (usually IHD), or peritoneal
Continuous - HF, HD, HDF
Flows needed for CVVHF
100-200ml/min
Recommended dose
Effluent rate - 20-25mls/kg/hour
Types of anticoag in RRT
None
Systemic —> UFH, LMWH
UFH - can monitor and reverse
Risk of HIT
LMWH - Xa monitoring, but partially reversed only
CItrate - chelates calcium pre filter, therefore hypocalcaemia
Prostaglandins - inhibits platelets —> hypotension
FWD in hypernatraemia
= 0.6 x weight x ((current Na/Target Na)-1)
Causes of hypokalaemia
Low intake - eating disorders, nutrition, malignancy
Increased loss - GI (D&V), Renal loss Dieuretics, Conn’s, Cushings, liquorice RTA releated to amphoetricin B Osmotic diuresis with hyperglycama
Movement into cells Alkalosis Sympathetics - salbut Insulin Refeeding
ECG hypokalaemia
Prolonger PR Flat T wave Increased p wave amplitudfe U waves Apparent QT prolonged (QU)
ECG in hyperkalaemia
Peaked T waves
Broad QRS
PR prolonged
Bundle branch, fasciculuar
Leads to vent arrhythmnia, sine wave, arrest
Causes of hyperkalaemia
AKI/CKD
Iatrogenic - potasssium supplement,
Nutritional - bananas
Cell lysis - TLS, rhabdo, haemolytic, blood transfusion
Addisons - hypo adrenal
Drugs - sprio, sux, b-blockers, ACEi
Treatment of hyperkalemia
Treat and remove cause
12 lead ECG
Monitored bed
If ECG changes or K>6
10mls 10% calcium gluconate 2 minutes
+/- nebs salbutatmol
10 units of actrapid in 50mls of 50% dex over 20 minutes
Calcium resonium
RRT
Causes of hypophosphataemia
Severe critical illness - sepsis, polytrauama, malabsorption, alkalosis, hyporthermia.
Refeeding
RRT
Drugs - diuretics, aluminium salts
Causes of hyperphosphatemia
Iatrongenic
Vit D toxicity
Acute - AKI, TLS, met acidosis, Rhabdo
Hypoparathyroid
Causes of hypercalcaemia
Malignancy Hyperparathyroidism CKD Immobility Pagets Granulamotous disease - Sarcoid, TB Immobility
Features of hypercalacemia
Lethargy, fatigue, abdo pain, constipation, pacnreatitis
> 3.5 coma, brady
Management of hypercalcaemia
Treat cause
Vit D and PTH levels
Remove precipitants
Fluid status - fluid resus
Pamidroniate
Furosemide if fkluid repletes
Steroids - sarcoid or Vitamin D
Anion Gap eqn
Normal range
(Na+K) - (Cl + HCO3)
4-12 (one book says 14-17)
What causes raised anion gap met acidosis
Strong acid accumulation Lactic acidosis Ketoacidosis - DM, starvation, alcohol AKI/CDK Methanol/ethylene glycol Glutathoine deficiency Salicylate Cyanide
What causes normal anion gap metabolic acidosis
Loss of bicarbonate, loss of renal excretion, ingestion of acids
Diarrhoea Ileostomy RTA Parenteral nutirtion Dilutional Colonic ureteric implant/diversionb
How to correct AG for albumin
= measured AG + (0.25 x (40-albumin)
Every 1g/L fall in albumin decreases Anion gap by 0.25 mmol
Causes of hyperglycaemia in crit care
Increased gluconeogenesis Insulin resistance Catecholamine administation Corticosteroid use Glucose in the drugs
In DKA what does the lipolysis lead to
Acetoacetic acid
Acetone
3-beta hydroxy butyrate
Precipitants of DKA
New undiagnosed DM
Poor treatment compliance
Out of date insulin
Lipohypertrophy of injection sites
Infection, gastroenterisits
Myocardial infaction
Surgery
Trauama
Goals of treatment in DKA
Glucose fall by 3mmol/l/hr
Ketones fall by 0.5mmol/L/hr
Bicarbonate rises by 3mmol/L/hr
Treatment principles
Fluid Bolus 500mls if hypotensive 1l NaCL over 1 hour Then 1NaCl with potassium over 2, 2, 4, 4 and 6 hours Add dextrose once BM <14
Insulin at FRII of 0.1units/Kg/hr
Maintain long acting insulin at night
Why admit DKA to crit care
Ketones >6 Bicarb <5 Ph<7.0 K <3.5 GCS <12 SaO2 <92% on air HR up or down Anion gap >16
When to restart sc insulin after DKA
Pt able to take diet and fluids
Ketones <0.6
pH >7.3
Stop insuline infusion 60 minues after first sc dose
Diagnostic criteria for DKA
Glucose > 11 (or known DM)
K - ketones >3
A - acid, pH <7.3 OR HCO < 15
Characteristics of HHS
Older patients
Type II DM
Marked hypovolaemia
BM>30 WITHOUT HYPERKETONAEMIA
PH>7.3M BICARB >15
Serum Osm>320 mosmol/kg
There is some insulin deficiency, but still some left to avoid lipolysis
Fluid defecit 100-220ml/kg fluid def
Treatment options of HHS
Fluid
1 litre over 1 hours
Aim 2-3 litres positive by 6 hours
6 litres postive by 12 hours
Aim 50% of fluid deficit in the first 12 hours
Allow BM to fall by 5mmol an hour
Insulin ONLY if - ketosis in which case treat as DKA OR BM not falling with fluid at FRII 0.05
Complications of HHS
Cerebral oedema
VTE
Feet problems
When should HHS go to crit care
Osm >350 Na >160 PH <7.1 GCS <12 SpO2 < 92% U/O less than 0.5mls/kg/hour Creatinine>200 Hypothermia Significant co-morbidites
What happens to the thyroid in critical illness
Total and free T3 falls
Reverse rT3 increases
Transient rise in T4, but may fall
TSH may rise transiently
THEN
Depression of HPT axis, decreased T4
Decreased TBG
These change are the LOW T3 SYNDROME, NONTHYROID ILLNESS or SICK EUTHYROID STATE
TSH falls
TFTs in a sick euthyroid
Low circuliating T3/4
BUT
Inappropriately low TSH (even normal is low)
Now evidence for supplementation
Drugs affecting thyroid
Glucocorticoids - TSH suppresion, reduced peripheral conversion
Contrast - inhibit synthesis/secretion
Propanolol - inhibit peripheral conversion
Amiodarone - same
Dopamine - TSH suppresion
Furomide - interferes with binding proteins
How is thyroid storm characterised
Triad of
Hypermetabolic state
Increased sympathetic activity and excess catecholaminwes
Increased oxygen consumption
Causes of a thyroid storm
Infection MI, CVA, PE Peri-op, thyroid surgery Burns, trauma Pregnancy
Contrast, amiodarone, excess T4
DKA
Thyroiditis
