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Renal / Fluid Flashcards

1
Q

4 phases of fluid therapy

A
  • resuscitation
  • optimisation - organ rescue
  • stabilisation - organ support, conservative (-ve balance)
  • evacuation - removal

Fluid creep = difference between predicted and administered fluid (e.g. flushes, drug diluents)

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2
Q

balanced crystalloid vs saline evidence

A

possible harm from 0.9% saline - renal injury, hypercholraemic acidosis
SMART 2018- single centre, composite outcome of renal injuries lower in balanced group
PLUS 2022 - multi centre RCT 5000 patients nil difference

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3
Q

adverse effects of fluid

A

fluid overload
- pulmonary oedema / pleural effusions
- cerebral oedema
- renal congestion
- increase Vd some drugs
- immobility and weakness
- ileus
- compartment syndromes
electrolyte imbalance
- hyponatraemia
- hypercholaramic acidosis

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4
Q

Evidence for HAS

A

SAFE 2004 - nil excess mortality compared to saline in resuscitation, septic shock. significantly worse in TBI
lower mortality in SBP
British Gastroenteroly society advice HAS replacement during paracentesis
ALBIOS 2014 - HAS to maintain albumin > 30 in septic shock - no difference

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5
Q

Starches

A

research misconduct
CHEST - HES vs saline significant AKI
6S - HES vs CSL - death and dialysis significant

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6
Q

KDIGO AKI

A

Stage 1
- creatinine 1.5x baseline within last 7 days or > 26umol/L last 48hrs.
- UO < 0.5ml/kg/hr for 6-12hr
Stage 2
- creatine > 2 x baseline
- UO < 0.5ml/kg/hr for 12+ hrs
Stage 3
- creatinine > 3x baseline OR > 354umol/L with rise of 1.5x
- RRT started
- anuria > 12hr, UO < 0.3ml/kg/hr > 24hr

Limitations
- baseline creatinine may not be known
- differences due to muscle mass etc
- unreliable in sepsis, liver failure
- UO can be unreliable e.g. may be appropriate

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7
Q

When does AKI become CKD

A

Persistent AKI > 2 days
Acute kidney disease > 7 days
CKD > 90 days

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8
Q

AKI biomarkers

A
  • cystacin c - not dependent on muscle mass
  • TIMP-2 - tubular stress
  • NGAL, Kim-1 - tubular damage
  • urinary interleukins - inflammation
  • nephrocechk - TIMP-2 and IGFBP-7 - AKI risk
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9
Q

AKI screen

A

Bedside - urine dip
Bloods - FBC, film, U+E, bicarb. glucose, bone profile, VBG, LDH, CRP
Imaging - renal USS
Case dependent
- cultures
- viral screens
- immune - ANCA, ANA. antiGBM
- myeloma screen
- CK myoglobin - rhabdo

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10
Q

Commonest causes of AKI in critical care

A
  • septic shock
  • major surgery
  • cariogenic shock
  • hypovolaemia
  • drugs
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11
Q

STARRT-AKI

A

severe AKI critically ill
accelerated RRT < 12hrs of meeting criteria versus standard care
no mortality difference. higher RRT dependence at 90 days and adverse events in accelerated group

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12
Q

Renal recovery

A

KDIGO - absence of diagnostic criteria for AKI
cessation of RRT - UO > 400ml/24hr without diuretics, creatinine clearance > 20

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13
Q

Prognosis of AKI requiring RRT

A

40% survival to hospital discharge
survivors at 1 year
- 48% complete renal recovery
- 33% incomplete recovery
- 19% dialysis dependent

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14
Q

CKD diagnosis

A

eGFR < 60 for 3 months plus either
- ACR > 30mg/g
- urinary sediment abnormalities
- electrolyte disorder due to tubule dysfunction
- histological abnormality
- radiological abnormality

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15
Q

CKD stages

A

Stage 1 eGFR > 90 ml/min/1.73m2
Stage 2 eGFR 60-90
Stage 3a eGFR 45-60
Stage 3b eGFR 30-45
Stage 4 eGFR 15-30
Stage 5 eGFR < 15

Albuminuria categories
Albumin excretion rate mg/24h / AR mg/mmol
1 - < 30 / < 3
2 - 30-300 / 3-30
3 - > 300 / > 30

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16
Q

CKD management

A
  • BP / RAS treatment
  • Electrolyte management - low potassium, low salt, calcium supplements
  • glycemic control
  • anaemia management
  • lifestyle adaptation
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17
Q

Implications of CKD in critical care

A
  • post-op pulmonary complications
  • risk of CVS disease
  • autonomic and peripheral neuropathies
  • altered electrolyte and fluid status
  • anaemia
  • altered pharmacokinetics - increased Vd, increased free drug availability of protein bound drugs, reduced renal exrection
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18
Q

adaptation of critical care management for patients with CKD

A
  • meticulous fluid balance
  • limit nephrotoxins
  • adjust medication doses
  • preserve veins and arteries where possible
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19
Q

Potassium homeostasis

A

3.5-5. 1mmol/kg/day
absorption small intestine
Na/K ATPase regulares movement
exertion - 90% renal. influences by aldosterone, B receptors, insulin
Roles
- acid-base
- RMP excitable tissues
- cardiac, nerve conduction

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20
Q

Hypokalaemia

A

K < 3.5mmol/l
causes
- spurious
- reduced intake (malabsorption
- excess loss - diuretic, diarrhoea, vomiting
- altered homeostasis - insulin, metabolic alkalosis, B2 agonists, refeeding
Skeletal muscle weakness and arrhythmias. ileus
AF, T wave inversion, U waves
40mmol/hr KCl via CVC

21
Q

Hyperkalaemia

A

K > 5.5
Causes
- spurious - clotted blood
- increased intake - blood transfusion
- reduced loss - K sparing diuretics, ACEi
- altered homeostasis - metabolic acidosis, renal failure, rhabdo, TLS
arrhythmias if K > 7
emergency treatment, cardiac monitor if > 6m potassium binders - sodium zirconium

22
Q

Hypomagnesaemia

A

Mg < 0.7
causes
- reduced intake - dietary
- increased GI loss - diarrhoea, vomiting, laxatives
- increased renal loss - alcohol, diuretics, PPI
features - HTN, angina, arrhythmias (prolonged PR, QRD), neuromuscular hyper excitability (myoclonus, stridor, seizures)
5g (20mmol) IV
correct potassium and calcium

23
Q

hypermagnasaemia

A

> 2.5mmol/l (> 7mmol/l severe)
causes
- increased intake - IV infusions, PET treatment
neuromuscular depression - deep tendon reflexes, apnoea, respiratory depression
prolonged QRS, QT, complete hart block
IV calcium

24
Q

Hypocalcaemia

A

<2.1mmol/l
causes
- spurious - hypoalbuminaemia
- homeostasis - hypoparathyroidism, vit d deficiency, hyperphosphataemia, TLS, rhabdo
- loss - AKI, CKD, citrate chelation
features - tetany, seizures, altered mental state, arrhythmias, laryngospasm
prolonged QT

25
Hypercalcaemia
> 2.6mmol/l causes - increased intake - hyperparathyroidism - malignancy - hyperthyroidism Features - calculi, psychosis, constipation, bone pain, fatigue, confusion, nausea, vomiting, pancreatitis fluids, diuretics, bisphosphonates, RRT
26
Phosphate homeostasis
0.8 - 1.4mmol/l absorbed in small intestine 85% in bone (with calcium) 90% filtered phosphate reasborpted in the PCT. exertion increased by PTH, magnesium exertion decreased by Na, D3 Roles - bone mineralisation - energy production - membrane function - buffer
27
hypophosphataemia
< 0.8mmol/l causes 1. renal loss - high PTH - alcoholism - acetazolamide 2. altered balance - stimulation of glycolysis, intracellular phosphoryllation - referring - sepsis - insulin - adrenaline 3. GI loss - chronic diarrhoea - malbaspriton - reduced intake features (< 0.3) - respiratory weakness, reduced cardiac contractility, delirium, muscle weakness, dysphagia treatment - sando-phos, polyfusor
28
hyperphosphataemia
> 1.46mmol/l causes 1. reduced exretion - renal failure - low PTH - low magnesium 2. exogenous load - enemas - iatrogenic 3. increase release - rhabdo, TLS - haemolysis chelates calcium --> Hypocalcaemia, tetany Mx - stop phosphate administration - give calcium, magensium - diuretics, RRT
29
Rhabdomyolysis
rupture of skeletal muscle cells, leading to intracellular contents moving into circulation, including CK, myoglobin, potassium, phosphate clinical diagnosis, myoglobinuria, CK weakness, myalgia, dark urine causes - crush injury - trauma, long lie - compartment syndrome - electrical injury - non traumatic - statins, exertion, seizures, NMS, MH, infections e.g. strep pyogenes
30
Complications of rhabdo
- AKI - pre-renal - 3rd space losses - renal tubule blockage by myoglobin and urate crystals - ROS and haem direct tubular damage - sympathetic renal vasoconstriction - Compartment syndrome - acidosis - multi organ dysfunction
31
management of rhabdomylosis
- stop precipitant - limit further muscle injury e.g. fasciotomy, adequate perfusion, dantrolene (NMS, MH) - treat electrolyte disorders - bicarb, insulin, RRT - prevent AKI - volume replacement - aim for 200ml/hr UO. debatable forced alkalisation
32
Severe hyponatraemia
Clinical features - seizures, reduced GCS, encephalopathy < 135 mild < 130 moderate < 125 severe - acute < 48h chronic > 48h
33
Approach to patient with hyponatraemia
History - moderatley severe - nausea, confusion, headache - severe - vomiting, somnolescence, seizures, coma - neurological arise from brain swelling - known pathology - drugs Examination - fluid status - clinical assessment, in/out charting investigations - bloods - paired osmolalities - urinary sodium - underlying cause - CXR, Echo, TFTs, CT head
34
Causes of hyponatramia based on serum osmolality
< 285 - hypotonic hyponatraemia --> volume status, urinary sodium 285-295 - isotonic hyponatraemia (pseudo) - hyperproteinaemia, hyperlipidaemia > 295 - non-hypotonic hyponatraemia - hyperglycaemia, glycine, mannitol
35
Pseuohyponatraramia
lab artefact abnormally high protein or lipids interfere with accurate measurement osmolality will b ein normal range
36
Causes of hypotonic hyponatraemia
Hypovolaemic - urine na > 20 - CSWS, diuretics, addisons - urine na < 20 - GI loss, burns, sweating Euvolaemia - urine na > 20 - SIADH, diuretics - urine na < 20 - hypothyroidism , polydipsia Hypervolaemia - urine na > 20 - renal failure - urine na < 20 - CCF, liver failure
37
Diagnosis of SIADH
essential - serum osmolality < 275 - urine osmolality > 100 - euvolaemia - urinary Na > 30 - absence of adrenal, thyroid, pituitary, renal insufficiency - no recent diuretics
38
Causes of SIADH
Cranial - SAH, trauma, tumours, meningoencephalitis Pulmonary - pneumonia (bacterrial / viral), TB Malignancy - SCLC, lymphoma, mesothelioma Drugs - PPI, SSRIs, TCA, carbamazepine, MDMA, oxytocin Miscellaneosu - exercise, anaesthesia, pain, stress
39
Management of hyponatramia
- cause, severity, chronicity, volume status - acute < 24 chronic > 48 if in doubt manage as chronic Acute severe - 3% NaCl 150ml over 20 mins - repeat until risen by 5mmol/l then switch to 0.9% Acute non-severe - stop precipitating casue - hypovolaemia - 0.9% saline Chronic - 4-8mmol/24hr - high risk ODS 4-6mmol/24hr (alcoholism, Na < 105, malnutrition, liver disease) - hypovolaemic - restore volume 0.9% saline - euvolaemic - TFTs cortisol, Short synacthen if normal fluid restriction for SIADH. if fails Demeclocycline (nephrogenic DI), vaptans (VP antagonist) - hypervolaemic - fluid restriction
40
SIADH specific management
electrolyte free water clearance (urine Na + urine K / serum Na) - < 0.5 - 1L fluid restriction - 0.5 - 1 - 0.5L fluid restriction - > 1 - no restriction 24/48 hr response Demeclocycline / Tolvaptan (lift restriction)
41
Hypernatraemia causes
water loss - DI - Burns - GI loss - renal disease - diuresis Reduced intake - inappropriate thirst Increased solute intake - salt poisoning - sodium bicarbonate - hypersonic saline
42
Hypernatraemia management
underlying cause water deficit - rehydrate nephrogenic DI - thiazide, DDAVP (acetazolamide if lithium induced) Craniogenic DI - DDAVP, 5% dextrose
43
Prescribing RRT
- Mode - CVVHD / HDF / F - 'dose' - 25-35ml/kg per KDIGO - replacement fluid - prismasol - anticogulation - fluid removal dose = effluent rate - determines amount of solute and electrolyte exchange
44
KDIGO vascular access for RRT
1. RIJ 15cm 2. femoral vein 25cm 3. LIJ 20cm 4. dominant SCV R 15-20cm L 20cm 5. non-dominant SCV
45
Reducing anticoagulation in RRT
General - minimise duration of RRT - Haemodialysis requires less than filtration Optimise circuit lifespan - access with good flow - citrate longer lifespan - equipment - prompt response to alarms, minimise interruptions, built in safety devices - viscosity - maintain filtration fraction < 25%
46
Problems with filter clotting
- slower correction of metabolic and fluid disturbances - potential life threatening e.g. hypoerclaemia - anaemia - thrombocytopenia - increased LOS
47
Suspicion of citrate toxicity
post-filter calcium substitution rising total:ionised calcium > 2.5 HAGMA
48

FFICM (14 decks)

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