Renal/Endo Flashcards by Peter latham

KDIGO stage 1

Increase in creatnine by 26.5mmol/LOr 1.5x baseline in 7 daysAND U/O <0.5ml/kg/hr for 6 hours

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KDIGO 2

Creatinine 2-2.9x baselineU/O 0.5ml/kg/hr 12 hours

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KDIGO 3

Creatinine 3x baselineORRise by 353.6 umol/litreOR Needing RRT

Urine output 0.3mls/kg/hr for 24 hoursOR12 hours of anuria

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Complications of AKI

Metabolic - acidosis, hyperkalaemia, electrtolytes, uraemic encephFluid - tissue overload, resp failure, postive balanceLong term - progress to CKD, need for long term RRT

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Risk factors for AKI

Known CKDCCF, DM, Liver diseasePrevious AKIAny impairment limiting access to fluids (neuro, cognitive)Age 65Sepsis and hypovolaemia

NEPHROTOXIC DRUGS - ACEi, ARBS, Gent, diuretics, NSAIDsObstructionsOther causes - ?contrastRhabdo, HUS, TLS, GN, nephritisSurgery - 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/1.73m2BSA2  60-893  30- 59 (A 45-59, B 30-44)4  15-295 <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 CVDHaem Anaemia Uraemic plt dysfunctionImpaired immunoNeuro- polyneuropathyMay need dialysis OR conversion from intermittant to continuous

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Components of an RRT circuit

Extracorporeal circuit including semi permeable membraneBlood pumpsPressure sensors and air detectors/trapsVascular access deviceAnit-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 filter 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, bleedingAbsolute urea above 36??HyperkalaemiaMet acidosisOligo-anuriaFluid overloadExtra: Volume removal, prevent overlaoad ?sepsis Drugs in overdose

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Types of RRT

Continuous or intermittant (usually IHD), or peritonealContinuous - 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

NoneSystemic —> UFH, LMWHUFH - can monitor and reverse           Risk of HITLMWH - Xa monitoring, but partially reversed only

CItrate - chelates calcium pre filter, therefore hypocalcaemiaProstaglandins - 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 wavesBroad QRSPR prolongedBundle branch, fasciculuarLeads to vent arrhythmnia, sine wave, arrest

Causes of hyperkalaemia

AKI/CKDIatrogenic - potasssium supplement, Nutritional - bananasCell lysis - TLS, rhabdo, haemolytic, blood transfusionAddisons - hypo adrenalDrugs - sprio, sux, b-blockers, ACEi

Treatment of hyperkalemia

Treat and remove cause12 lead ECGMonitored bedIf ECG changes or K>610mls 10% calcium gluconate 2 minutes+/- nebs salbutatmol10 units of actrapid in 50mls of 50% dex over 20 minutesCalcium resoniumRRT

Causes of hypophosphataemia

Severe critical illness - sepsis, polytrauama, malabsorption, alkalosis, hyporthermia.RefeedingRRTDrugs - diuretics, aluminium salts

Causes of hyperphosphatemia

IatrongenicVit D toxicityAcute - AKI, TLS, met acidosis, RhabdoHypoparathyroid

Causes of hypercalcaemia

```MalignancyHyperparathyroidismCKDImmobilityPagetsGranulamotous disease - Sarcoid, TBImmobility```

Features of hypercalacemia

Lethargy, fatigue, abdo pain, constipation, pacnreatitis>3.5 coma, brady

Management of hypercalcaemia

Treat causeVit D and PTH levelsRemove precipitantsFluid status - fluid resusPamidroniateFurosemide if fkluid repletesSteroids - sarcoid or Vitamin D

Anion Gap eqnNormal 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```DiarrhoeaIleostomyRTAParenteral nutirtionDilutionalColonic 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 acidAcetone3-beta hydroxy butyrate

Precipitants of DKA

New undiagnosed DMPoor treatment complianceOut of date insulinLipohypertrophy of injection sitesInfection, gastroenterisitsMyocardial infactionSurgeryTrauama

Goals of treatment in DKA

Glucose fall by 3mmol/l/hrKetones fall by 0.5mmol/L/hrBicarbonate rises by 3mmol/L/hr

Treatment principles in DKA

```FluidBolus 500mls if hypotensive1l NaCL over 1 hourThen 1NaCl with potassium over 2, 2, 4, 4 and 6 hoursAdd dextrose once BM <14```Insulin at FRII of 0.1units/Kg/hrMaintain long acting insulin at night

Why admit DKA to crit care

```Ketones >6Bicarb <5Ph<7.0K <3.5GCS <12SaO2 <92% on airHR up or downAnion gap >16```

When to restart sc insulin after DKA

Pt able to take diet and fluidsKetones <0.6pH >7.3Stop insuline infusion 60 minues after first sc dose

Diagnostic criteria for DKA

Glucose > 11 (or known DM)K - ketones >3A - acid, pH <7.3 OR HCO < 15

Characteristics of HHS

Older patientsType II DMMarked hypovolaemiaBM>30 WITHOUT HYPERKETONAEMIAPH>7.3M BICARB >15Serum Osm>320 mosmol/kgThere is some insulin deficiency, but still some left to avoid lipolysisFluid defecit 100-220ml/kg fluid def

Treatment options of HHS

Fluid1 litre over 1 hoursAim 2-3 litres positive by 6 hours6 litres postive by 12 hours Aim 50% of fluid deficit in the first 12 hoursAllow BM to fall by 5mmol an hourInsulin ONLY if - ketosis in which case treat as DKA OR BM not falling with fluid at FRII 0.05

Complications of HHS

Cerebral oedemaVTEFeet 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 BUTInappropriately 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

```InfectionMI, CVA, PEPeri-op, thyroid surgeryBurns, traumaPregnancy```Contrast, amiodarone, excess T4DKAThyroiditis