Definitions, Tables, Facts - Renal And Endo Flashcards by Liverpool FFICM

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

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KDIGO 2

Creatinine 2-2.9x baseline

U/O 0.5ml/kg/hr 12 hours

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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

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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

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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

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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

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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

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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

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Components of an RRT circuit

Extracorporeal circuit including semi permeable membrane

Blood pumps

Pressure sensors and air detectors/traps

Vascular access device

Anit-coaguation

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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

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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

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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

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Types of RRT

Continuous or intermittant (usually IHD), or peritoneal

Continuous - HF, HD, HDF

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Flows needed for CVVHF

100-200ml/min

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Recommended dose

Effluent rate - 20-25mls/kg/hour

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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

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FWD in hypernatraemia

= 0.6 x weight x ((current Na/Target Na)-1)

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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

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ECG hypokalaemia

Prolonger PR
Flat T wave
Increased p wave amplitudfe
U waves
Apparent QT prolonged (QU)

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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