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FFICM > Renal / Fluid > Flashcards

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
Q

Hypercalcaemia

A

> 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
Q

Phosphate homeostasis

A

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
Q

hypophosphataemia

A

< 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
Q

hyperphosphataemia

A

> 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
Q

Rhabdomyolysis

A

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
Q

Complications of rhabdo

A
  • 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
Q

management of rhabdomylosis

A
  • 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
Q

Severe hyponatraemia

A

Clinical features - seizures, reduced GCS, encephalopathy
< 135 mild
< 130 moderate
< 125 severe
- acute < 48h chronic > 48h

33
Q

Approach to patient with hyponatraemia

A

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
Q

Causes of hyponatramia based on serum osmolality

A

< 285 - hypotonic hyponatraemia –> volume status, urinary sodium
285-295 - isotonic hyponatraemia (pseudo) - hyperproteinaemia, hyperlipidaemia
> 295 - non-hypotonic hyponatraemia - hyperglycaemia, glycine, mannitol

35
Q

Pseuohyponatraramia

A

lab artefact
abnormally high protein or lipids interfere with accurate measurement
osmolality will b ein normal range

36
Q

Causes of hypotonic hyponatraemia

A

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
Q

Diagnosis of SIADH

A

essential
- serum osmolality < 275
- urine osmolality > 100
- euvolaemia
- urinary Na > 30
- absence of adrenal, thyroid, pituitary, renal insufficiency
- no recent diuretics

38
Q

Causes of SIADH

A

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
Q

Management of hyponatramia

A
  • 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
Q

SIADH specific management

A

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
Q

Hypernatraemia causes

A

water loss
- DI
- Burns
- GI loss
- renal disease
- diuresis
Reduced intake
- inappropriate thirst
Increased solute intake
- salt poisoning
- sodium bicarbonate
- hypersonic saline

42
Q

Hypernatraemia management

A

underlying cause
water deficit - rehydrate
nephrogenic DI - thiazide, DDAVP (acetazolamide if lithium induced)
Craniogenic DI - DDAVP, 5% dextrose

43
Q

Prescribing RRT

A
  • 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
Q

KDIGO vascular access for RRT

A
  1. RIJ 15cm
  2. femoral vein 25cm
  3. LIJ 20cm
  4. dominant SCV R 15-20cm L 20cm
  5. non-dominant SCV
45
Q

Reducing anticoagulation in RRT

A

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
Q

Problems with filter clotting

A
  • slower correction of metabolic and fluid disturbances
  • potential life threatening e.g. hypoerclaemia
  • anaemia
  • thrombocytopenia
  • increased LOS
47
Q

Suspicion of citrate toxicity

A

post-filter calcium substitution rising
total:ionised calcium > 2.5
HAGMA

48
Q
A

FFICM (14 decks)

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