Acute Renal Failure and PreRenal Azotemia

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Acute Renal Failure and Pre-Renal Azotemia

• By
• Cathy Kitchen
• (senior lecturer,UCE)

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Fluid management in HDU
3
DEFINITIONS OF DEHYDRATION

• A reduction in the normal total body water
  (TBW) content, usually due to excessive fluid
  loss which is not balanced by appropriate
  increase in intake
• (Youngston, 1999)

4

• Distal Convoluted Tubule
• Secretion of H ions. Adjust the pH of the soon
  to be urine.
• Secretion is the process of taking waste
  substances from the body back to the filtrate.

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Reflex response to renal hypo-perfusion

•   1. Decreased GFR
• ? azotemia
• 2. Increased ADH (response to ? effective
  plasma volume)
• ? water retention
• 3. Na retention as follows
•  
• Increased renal renin release
• ?
• Angiotensin I production
• ?
• Angiotensin II production (there is ACE in the
  kidney)
• Local effect Systemic effect
• ? ?
• Efferent arteriole construction ? aldosterone
• ? ?
• ? Filtration fraction ? distal Na
  absorption
• ?
• ? proximal Na absorption

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Normal Fluid Distribution
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Fluid calculation

• Relationship between the volumes of major fluid
  compartments
• (The values shown are calculated for a 70 kg
  man).
• TBW 0.6 x Body weight

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Body Fluid Movement

• Fluid moves freely between compartments
• 4 basic pressures control this via the capillary
  membrane (CM)
• Capillary hydrostatic pressure (internal FP on
  CM)
• Interstitial fluid pressure (external FP on CM)
• Plasma osmotic pressure (fluid attracting
  pressure from protein concentration within
  capillary)
• Interstitial osmotic pressure (fluid attracting
  pressure from protein concentration outside
  capillary)

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Starlings Law of the Capillaries

• Whether fluids leave (filtration) or enter
  (re-absorption) capillaries depends on how the
  pressures in the capillary and interstitial
  spaces relates to one another.
• Volume re-absorbed is similar to volume filtered
  A net equilibrium
• Regulates relative volumes of blood
  interstitial fluid.

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DEFINITIONS OF ARF

• The syndrome is characterised by a sudden in
  parenchymal function which is usually but not
  always reversible
• This produces disturbance of water, electrolyte,
  acid base balance and nitrogenous waste products
  blood pressure.

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Acute Renal Failure

• Nephrologists Definition
• Plasma creatinine gt 120 mmols
• Creatinine clearance lt 70 mls/min

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Other Definitions

• Abrupt sustained decline in GFR
• Rising serum urea and creatinine
• Loss of water and salt homeostasis
• Life threatening metabolic sequelae
• Occurs over hours or days
• 5 of all surgical and medical admissions

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Cockcroft Gault equation
(140-age in years) x weight in kg serum
creatinine (µmol/L) (corrected for males x 1.23,
females x 1.04)
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Types of Dehydration (1)

• Isotonic (isonatraemic) dehydration
  proportional loss of Na and water (serum Na
  130-150 mmol/L)
• Body fluid solute concentration osmolality are
  maintained
• Fluid losses are largely confined to the
  extracellular compartment (ECC)

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Types of Dehydration (2)

• Hypotonic. (Hyponatraemic) dehydration
  disproportionate loss of Na over water (serum Na
  lt 130 mmol/L.)
• Net fluid loss is hypertonic.
• Water moves from the ECC to the ICC.
• This leads to an increase in brain volume
  increased risk of convulsions, marked ECC loss
  leads to greater shock per unit of water loss

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Deficit in ECC

• Decreased H2O intake
• Diarrhoea
• Vomiting
• Drain loss
• Diabetes insipidus
• Systemic infection
• Renal disease
• Adrenal insufficiency

• Intestinal obstruction
• Gastrointestinal suctioning
• Blood loss
• Diaphoresis
• Burns
• Diuretics
• Diet low in Na

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Clinical Manifestations

• Acute weight loss
• Oliguria or anuria
• Dry mucous membranes skin
• Hypotension
• Decrease in pulse
• Rapid deep respirations

• Change in consciousness
• confusion
• restlessness
• delirium
• unconsciousness
• convulsions

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Significant Lab Findings

• Haematocrit - elevated
• Haemoglobin - elevated
• RBC - elevated

• Serum Na
• Normal if deficit is due to loss of isotonic
  fluid (hypovolaemia)
• Increased if deficit is due to severe and greater
  loss of water than Na (hypernatraemia)
• Decreased if deficit is due to severe loss of Na
  (hyponatraemia)

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Types of Dehydration (3)

• Hypertonic (hypernatraemic) dehydration
  disproportionate loss of water over Na (serum Na
  gt 150 mmol/L.)
• Net fluid loss is hypotonic insensible
  losses
• Causes Fever or dry hot environment, excessive
  urinary loss (diabetes insipidus) or profuse, low
  Na diarrhoea

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Impact of Hypernatraemic Dehydration

• Extracellular fluid initially becomes hypertonic
  with respect to the intracellular fluid.
• This leads to a shift of water from the ICC to
  the ECC.
• Water is drawn out of the brain and cerebral
  shrinkage within a rigid skull may lead to small
  multiple haemorrhages and convulsions.

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Excess in ECC

• CHF
• Hyperaldosteronism
• Renal disease
• Steroid therapy
• Excessive intake of Na
• without adequate H20 intake
• Excessive intake of H20 without adequate Na intake

• Excessive administration of isotonic solution of
  sodium chloride
• Excess administration of sodium bicarbonate
• Excess tap water enemas!!!!!!!
• Excess H20 nasogastric irrigation!!

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Clinical Manifestations

• Acute weight gain
• Oedema
• Increase in pulse and BP
• Increase in urine output
• Rales (moist) in lungs
• headache

• Convulsions
• Rapid deep respirations
• Shortness of breath
• Change in consciousness
• confusion
• restlessness
• unconsciousness

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Laboratory Findings

• Haematocrit -decreased
• Haemoglobin - decreased
• RBC - decreased

• Serum Urinary Na
• Normal if excess due to Isotonic fluid overload
• Increased if excess due to hypernatraemia
• Decreased if excess due to hyponatraemia

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Aetiology

• Pre-renal ARF
• Intrinsic ARF
• Post-renal ARF

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Pre-renal ARF

• Reversible fall in GFR due to renal hypoperfusion
• Hypovolaemia
• Haemorrhage, burns, GI fluid loss, renal fluid
  loss
• Hypotension
• Cardiogenic shock, sepsis
• Renal hypoperfusion
• renal vasoconstriction, drugs, liver disease,
  renal vascular disease

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Differential diagnosis
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Acute renal failureUsing the urine

• U/A blood/ protein
• Urine Chemistry Na, K, urea,creatinine
• Na marker for volume depletion
• Creatinine Clearance UV/P can be estimated
  from spot sample 7 urine flow rate
• 24 hr urine urea x 0.033 x 6.25 Protein
  catabolic Rate

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PRE-RENAL AZOTEMIA

•  
• 1) ENHANCED FRACTIONAL TUBULAR NA REABSORPTION
•  
• 2) ENHANCED FRACTIONAL H20 REABSORPTION
•  
• 3) ENHANCED FRACTIONAL UREA REABSORPTION
•  

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ENHANCED Na REABSORPTION IN PRE-RENAL AZOTEMIA

•  
• A) STARLING FORCES
•  
• B) ANGIOTENSIN II
•  
• C) ALDOSTERONE
•  
• D) ADRENERGIC NERVOUS SYSTEM
•  

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BUN/ CREATININE RATIO IN PRE-PRENAL AZOTEMIA

• A) ENHANCED H20 REABSORPTION WITH AN INCREASE IN
  UREA CONCENTRATION IN THE COLLECTING DUCT.
•  
• B) INCREASED VASOPRESSIN
•  
• RISE IN BUN WILL EXCEED THAT OF PLASMA CREATININE

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Azotemia, Clinical Assessment

• Is there renal disease?
• Evaluate the following
• Patient hydration
• Serum creatinine
• Urine specific gravity
• Azotemia, dehydration, sp. gr. gt 1.030
  pre-renal
• Azotemia, dehydration, sp. gr. lt 1.020 renal
• Azotemia, normal hydration, sp. gr. lt 1.020
  renal
• Azotemia, hyponatremia/hypochloremia normal
  renal compensation (TGF)

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Acute Renal Failure features 1

• Azotemia(Uraemia)
• Non excretory morbidity renal effects
• fluid balance
• Na / K disturbance
• acidosis
• hypertension
• anaemia
• renal bone disorders

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Acute Renal Failure features 2

• (Uraemia)
• Non excretory morbidity non-renal effects
• Malnutrition
• Bleeding tendency
• Predisposition to Sepsis
• Pericarditis
• accelerated vascular disease cardiac,
• stroke
• endocrine dysfunction thyroid, gonadal,
• Peptic ulceration

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Fluid and Electrolyte Replacement

• Getting the diagnosis right
• Getting the Balance Right

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Estimating fluid/electrical requirements

• Separate consideration for
• Maintenance requirements
• Vary according to calorie expenditure (hence age,
  mass, body temp, level of activity, environmental
  temp humidity)
• As opposed to deficit replacement
• Directly related to function of body mass

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Fluid resuscitation

• Met-analysis of fluid resuscitation in Critical
  Care patients (Choi et al 1999 Alderson et al
  2002)
• Insufficient evidence for fluid resuscitation in
  ARF patients (Ragaller et al 2001)
• Volume versus type of replacement- no evidence to
  support improved survival according to type
  (Nolan 2001 Pulimood Park 2000))

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Aim of fluid therapy

• Tissue perfusion and organ function
• Targeted to a specific pre-load, stroke volume
  rather than MAP
• CVP, PCWP- popular surrogate markers of pre-load
• RCT Study- fluid challenge use of CVP monitor
  influenced the peri-operative
• morbidity of patients with hip fractures
• (Venn
  et al 2001)

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Pathophysiology of ATN

• NB. This is not completely understood
• 60 of ARF cases
• related events include-
• induction by hypoxia of nitric oxide synthases
  with increased production of nitric oxide
• vasoconstriction
• liberation of toxic endothelial factors
• tubular obstruction by desquamated cells and
  casts..

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Chemical mediators of inflammation

• Plasma-derived
• Circulating precursors
• Have to be activated
• Cell-derived
• sequestered intracellularly
• synthesized de novo

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Figure 2-9 Kumar p 34
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Oxygen-derived free radicals

• Oxygen-derived free radicals responsible for
  tissue injury
• Direct injury to endothelial cells
• Injury to extracellular matrix via activation of
  proteases
• Injury to other cell types (e.g., RBCs, tumor
  cells)

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Global Tissue Perfusion

• Parameters
• Lactate, PH, Base excess, SvO2
• Can vary in sepsis
• Gut mucosa- Gastric Tanometry can detect occult
  hypovolaemia (PCO2 is independent of cell
  metabolism PH )

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Water Balance in Third spacing

• Capillary Permeability -Third -Spacing period
• Alteration of normal homeostasis, intravascular
  volume and cardiac output
• 12 - 36 hours post burn fluid shifts from
  intravascular to interstitial space
• Due to increased capillary permeability
• Third spacing is most significant during first 12
  hours post burn injury

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Fluid Shifts / Third Spacing (1)

• Leakage of intravascular protein rich fluids,
  electrolytes and plasma
• Degree of shift dependent upon severity of burn
• lt15 burns only produce minor shifts
• Vicious circle more proteins lost increases
  colloid osmotic pressure thus increasing the
  intravascular to interstitial fluid shift

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Fluid Shifts / Third Spacing (2)

• Fluid in the interstitial space and
  connective tissues between the cells
• Leads to oedema
• Then hypovolaemia SHOCK
• Occult hypovolaemia- needs high index of
  suspicion subtle invasive monitoring

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Acute Renal Failure

• potentially reversible
• delay may be critical treatment of the renal
  failure
• management of the cause
• often coexists with disease of other organs
• renal vascular disease - vascular disease
  elsewhere
• diabetes
• nephritis - SLE/ drug allergy/ vasculitis
• amyloid - myeloma

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Renal Failure

• Acute or chronic?
• Acute rise in creatinine by gt30 may be ARF
• potentially reversible
• delay may be critical
• eg Creat 129, 10 days later 176, rise 47 (36)
• ARF until proven otherwise

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Prevention

• Identify at risk patients
• pre-existing CRF, diabetes, jaundice, myeloma,
  elderly
• Optimise renal perfusion
• IV fluids, inotropes, central line
• Maintain adequate diuresis
• Mannitol, frusemide, NOT dopamine
• Avoid nephrotoxic agents
• ACE inhibitors, NSAIDS, radiological contrast,
  aminoglycosides

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Acute Renal Failure What to do when youve got
it

• Treat the uraemia
• Treat the complications
• Treat the underlying disease
• Watch drug usage dosage
• Anything to reduce the mortality

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Acute Renal Failure Treat the uraemia

• Conservative measures
• Inform Renal unit now,
• not when these measures have failed
• Dialysis

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Resuscitation

• Recovery from ARF is first dependent upon
  restoration of RBF. Early RBF normalization
  predicts better prognosis for recovery of renal
  function. In prerenal failure, restoration of
  circulating blood volume is usually sufficient.
  Rapid relief of urinary obstruction in postrenal
  failure results in a prompt decrease of
  vasoconstriction. With intrinsic renal failure,
  removal of tubular toxins and initiation of
  therapy for glomerular diseases decreases renal
  afferent vasoconstriction

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Calculation of Maintenance Fluids

• Calculate for 24 hours
• Multiply weight in kg. By appropriate number of
  mls for age
• Add or subtract a volume according to any
  modifying factors present, including any abnormal
  continuing losses

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Treatment Targets (1)

• Hypovolaemia should be corrected promptly using
  plasma or blood to replace the circulating blood
  volume (2-4 hrs)
• Measure CVP core peripheral temp
  differential.
• Vasodilator drugs may be required to improve
  perfusion

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Treatment Targets (2)

• Restoration of urine flow should follow
  restoration of circulating blood volume
• Delay may lead to further kidney damage with
  accompanying hyperkalaemia and metabolic
  acidosis.
• Care is required to prevent fluid overload.

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Treatment Targets (3)

• Restoration of ECC fluid deficit and acid base
  status replacement of normal and/or ongoing
  loses (2-4 to 24 hrs)
• Potassium replacement/maintenance
• Complete correction of Na water deficits and
  restoration of potassium stores (24hrs to 2-4
  days) Additional caution with KCL replacement if
  renal function is impaired

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Maintenance Requirements
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Modifying Factors
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Nursing Care

• Hourly intake / output record
• output lt1-2 ml/kg/hr
• ? Catheterise for accuracy
• ? Repeat samples for osmolality / SG
• Monitor colour of urine
• Assess systemic perfusion...

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Fluids debate

• A meta-analysis -looked at mortality in eight
  human trials in patients receiving 1) crystalloid
  or 2) colloid for resuscitation. It showed an
  overall 5.7 decrease in mortality rate in
  patients resuscitated with crystalloid rather
  than colloid solutions.
• Subgroup analysis showed that trauma/sepsis
  patients had a 12.3 decrease in mortality when
  crystalloids were used. 
• However, when crystalloids were used in patients
  undergoing elective surgery, there was a 7.8
  increase in mortality. The proposed explanation
  was that patients with trauma and sepsis have an
  increase in capillary permeability that allows
  the administered colloid to leak out of the
  vasculature, to be less effective as an
  intravascular volume expander and to slow
  resolution of oedema from the affected tissues.
• (Valanovich, 1988)

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Fluids debate

• In patients undergoing elective procedures, the
  amount of capillary leak compared to major
  trauma, is more limited to the surgical site
  thus, the use of colloids may be more efficacious
  in increasing intravascular volume.
• Most colloid advocates do not recommend these
  substances as the sole resuscitative fluid. The
  usual protocol involves initial infusion of
  crystalloids, followed by the administration of
  colloids when large volumes are necessary to
  reduce the amount of crystalloids.
• In general, crystalloids need to be administered
  in volumes that are approximately 2-3 times that
  of iso-oncotic colloid to obtain the same
  haemodynamic effect.
• Exception 25 albumin, this ratio is no longer
  valid.

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Controversy of Albumin

• Human albumin solution has been used in the
  treatment of critically ill patients for over 50
  years. Currently, the licensed indications for
  use of albumin are emergency treatment of shock,
  acute management of burns and clinical situations
  associated with hypo-proteinaemia.
•  Our systematic review of randomised controlled
  trials showed that, for each of these patient
  categories, the risk of death in the
  albumin-treated group was higher than in the
  comparison group.
• The pooled relative risk of death with albumin
  was 1.68 and the pooled difference in the risk of
  death was 6 or six additional deaths for every
  100 patients treated. We consider that use of
  human albumin solution in critically ill patients
  should be urgently reviewed.

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Crystalloids

• Slow restoration of circulatory vol.
• Most common administration
• 5 Dexlost rapidly from IVC( 660mls IC 130mls
  EC)
• N/Sal 250mls intravasc. 750mls interstitial

• Usually need larger vol.than colloids
• Large vol. may initiate metabolic acidosis

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Nursing Care (b)

• Watch for hyponatraemia
• change in consciousness
• muscle cramps
• anorexia
• abnormal reflexes
• Cheyne-stokes respiration
• or seizures

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Hyponatraemia

• Clinical manifestations Change in consciousness
  seizures.
• Usually only when plasma Na lt120 mmol/l, and the
  fall has been rapid
• Causes Dilutional
• Na wasting

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Hyponatraemia Treatment

• Hypertonic saline 3 NaCl (0.5 mmol/ml) Iv to
  increase plasma Na by 10 mmol/l
• Dialysis or haemofiltration
• Rate of correction rapid. Central pontine
  myelinosis rare / unheard of in children.

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Nursing Considerations (3)

• Potential metabolic acidosis related to-
• Poor systemic perfusion associated with pre-renal
  failure
• Decreased renal ability to excrete hydrogen ions

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Acute Renal Failure K handling

• Normal intake 80 150 mmol/day
• Bleeding/? catabolism ? K release from
  tissues
• Excretion renal 80
• faeces 5-15
• Handling adrenaline K ?muscle insulin K
  ?muscle
• acidosis causes ? K
• Filtration
• if K 5 1 litre/hr removes 120 mmols K/
  day

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Hyperkalaemia Emergent Care

• Elimination of K
• Calcium Resonium 0.5-1g/kg daily in divided doses
• Diuretics e.g. Frusemide 2-10 mg/kg
• Dialysis

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Hyperkalaemia

• Immediate action redistribution of K
  stabilization of membranes
• Salbutamol 2.5-5mg by nebulizer
• Ca gluconate 10 0.5 ml/kg over 2-4 mins
• Bicarbonate 2 mmol/kg over 30 mins
• Glucose insulin 0.5-1 g glucose/kg IV over
  15-30 mins, may add 0.5-1 u soluble insulin / 5g
  glucose

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Hyperkalaemia Non-emergent Care

• Dietary restriction of potassium
• IV Fluids !!
• Oral ion exchange resins (Ca resonium)

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Distribution of body calcium
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Nursing Care (c)

• Watch for hypocalcaemia
• muscle tingling or changes in muscle tone
• Seizures
• Tetany
• ve Chvostek sign ( twitching of side of face
  when the facial nerve is tapped in front of the
  ear)
• Drugs antacid phosphate binders Vit D

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Hypocalcaemia Hyperphosphataemia

• Hypocalcaemia usuually secondary to
  hyperphosphataemia
• If symptomatic (tetany, muscle spasm of face,
  hands feet, hypotension, cardiac insufficiency)
  give IV Ca gluconate infusion
• Oral phosphate binders e.g. aluminium hydroxide,
  Ca carbonate

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Metabolic Acidosis

• Bicarbonate therapy when pH lt 7.25 and
  bicarbonate lt 12 mmol/l
• Dialysis

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Is the patient?

• Non-catabolic
• Single system failure
• Intermittent dialysis / no dialysis
• Nutritional requirements not increased
• Catabolic
• Multi-organ failure
• Continuous renal replacement therapy
• Increased nitrogen requirements

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Acute Renal failureRenal replacement Dialysis
or filtration

• Haemodialysis simple (on renal unit)
• rapid correction (eg K?, fluid)
• disequilibrium, fluid ??
• Haemofiltration (CVVH(/-D), CAVH(/-D)
• smooth, good control of fluid
• slowish, cant mobilise patient
• Peritoneal Dialysis avoids heparin,
• less haemodynamic disruption slow,
  may impair breathing, peritonitis,
  politically incorrect

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