Renal / Fluid Flashcards
4 phases of fluid therapy
- 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)
balanced crystalloid vs saline evidence
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
adverse effects of fluid
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
Evidence for HAS
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
Starches
research misconduct
CHEST - HES vs saline significant AKI
6S - HES vs CSL - death and dialysis significant
KDIGO AKI
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
When does AKI become CKD
Persistent AKI > 2 days
Acute kidney disease > 7 days
CKD > 90 days
AKI biomarkers
- 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
AKI screen
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
Commonest causes of AKI in critical care
- septic shock
- major surgery
- cariogenic shock
- hypovolaemia
- drugs
STARRT-AKI
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
Renal recovery
KDIGO - absence of diagnostic criteria for AKI
cessation of RRT - UO > 400ml/24hr without diuretics, creatinine clearance > 20
Prognosis of AKI requiring RRT
40% survival to hospital discharge
survivors at 1 year
- 48% complete renal recovery
- 33% incomplete recovery
- 19% dialysis dependent
CKD diagnosis
eGFR < 60 for 3 months plus either
- ACR > 30mg/g
- urinary sediment abnormalities
- electrolyte disorder due to tubule dysfunction
- histological abnormality
- radiological abnormality
CKD stages
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
CKD management
- BP / RAS treatment
- Electrolyte management - low potassium, low salt, calcium supplements
- glycemic control
- anaemia management
- lifestyle adaptation
Implications of CKD in critical care
- 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
adaptation of critical care management for patients with CKD
- meticulous fluid balance
- limit nephrotoxins
- adjust medication doses
- preserve veins and arteries where possible
Potassium homeostasis
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
Hypokalaemia
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
Hyperkalaemia
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
Hypomagnesaemia
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
hypermagnasaemia
> 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
Hypocalcaemia
<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
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
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
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
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
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
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
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
Severe hyponatraemia
Clinical features - seizures, reduced GCS, encephalopathy
< 135 mild
< 130 moderate
< 125 severe
- acute < 48h chronic > 48h
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
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
Pseuohyponatraramia
lab artefact
abnormally high protein or lipids interfere with accurate measurement
osmolality will b ein normal range
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
Diagnosis of SIADH
essential
- serum osmolality < 275
- urine osmolality > 100
- euvolaemia
- urinary Na > 30
- absence of adrenal, thyroid, pituitary, renal insufficiency
- no recent diuretics
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
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
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)
Hypernatraemia causes
water loss
- DI
- Burns
- GI loss
- renal disease
- diuresis
Reduced intake
- inappropriate thirst
Increased solute intake
- salt poisoning
- sodium bicarbonate
- hypersonic saline
Hypernatraemia management
underlying cause
water deficit - rehydrate
nephrogenic DI - thiazide, DDAVP (acetazolamide if lithium induced)
Craniogenic DI - DDAVP, 5% dextrose
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
KDIGO vascular access for RRT
- RIJ 15cm
- femoral vein 25cm
- LIJ 20cm
- dominant SCV R 15-20cm L 20cm
- non-dominant SCV
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%
Problems with filter clotting
- slower correction of metabolic and fluid disturbances
- potential life threatening e.g. hypoerclaemia
- anaemia
- thrombocytopenia
- increased LOS
Suspicion of citrate toxicity
post-filter calcium substitution rising
total:ionised calcium > 2.5
HAGMA
