AKI management: volume replacement—how much?
3 Treatment of dangerous hyperkalaemia
The following d serum K + acutely but DO NOT d overall elevated total body K + . Additional measures, described on b pp. 132–133, are 6 also required.
Calcium
• If K + ≥ 6.5mmol/L or ECG changes.
• 2 Ca 2+ is cardioprotective — it does not d K + .
• Antagonizes membrane K + effects by poorly understood mechanisms.
• 10mL 10% calcium gluconate (usually 1 ampoule — calcium gluconate contains 220 μ mol Ca 2+ /mL), or
• 5mL 10% calcium chloride (usually half an ampoule — CaCl 2 contains 680 μ mol Ca 2+ /mL).
• Give over 2 – 5min. Repeat if no ECG improvement after 5min (up to 40mL calcium gluconate).
• Acts within minutes, but protective effect lasts <1h .
• 1 Can induce digitalis toxicity ( l a pragmatic approach: halve the initial dose, and give more slowly if taking digoxin).
Insulin and glucose
• If K + ≥ 6.5mmol/L or ECG changes.
• Insulin binds to its cellular receptor and i Na-K-ATPase activity, moving K + into cells. Glucose alone will d K + through endogenous insulin release, but insulin/glucose is more effective.
• 10 – 15IU of soluble insulin (e.g. Actrapid ® ) in 50mL of 50% glucose IVI over 10min (alternative: 5IU of soluble insulin in 50mL 20% glucose over 15min by syringe pump and repeated).
• 50% glucose is extremely viscous and irritant. Find a large vein, and fl ush with saline afterwards.
• Effect within 15 – 30min (peak 7 60min), lasts for 2 – 4h. Expect a d of 0.5 – 1.5mmol/L. Can be repeated after 4h.
• Check BMs regularly for 6h, and infuse 10% glucose IVI if d glucose.
Sodium bicarbonate
• If i K + in the presence of acidosis (HCO 3 – <16) and volume depletion.
• i Na + /H + exchange l i intracellular Na + l i Na-K-ATPase activity (i.e.
K + in for Na + out). Additional pH-independent mechanisms operate.
• 1.26% or 1.4% solutions as 200 – 500mL over 15 – 60min IVI.
• In cardiac arrest: 50mL of 8.4% (1 ampoule) IVI.
• 1 CAUTION: do not infuse bicarbonate solutions into the same cannula as calcium gluconate/carbonate unless thoroughly fl ushed.
• Action within hours, not minutes.
• Involves an appreciable Na + load (150mmol Na + ). 1 Volume overload.
• Rapid correction of acidosis in a patient with d Ca 2+ may induce tetany and seizures, as ionized calcium drops rapidly as pH i .
B 2-agonists (salbutamol, etc.)
• 10 – 20mg (i.e. a large dose) of nebulized salbutamol will d K + by up to 1mmol/L but has limited additive benefi t beyond insulin/glucose (it acts via the same Na-K-ATPase and has a slower onset of action).
• 1 It may also precipitate angina or arrhythmias in those with underlying cardiac disease and can cause an increase in lactate acid ( l worsening acidosis).
Once (if) the immediate arrhythmic danger is past, the aim should be to reduce total body potassium to prevent further hyperkalaemic episodes.
Urinary K + wasting: diuretics
• Only useful in patients expected to pass urine and 6 urine into which K + can be excreted. Particularly useful if coexisting volume overload.
• Act on the renal tubule — K + loss as one of several effects.
• Furosemide 40 – 120mg IVI as a slow bolus or 10 – 40mg/h to a maximum of 1000mg/day. Bumetanide offers a better absorbed oral alternative.
• Effect depends on onset of diuresis. Can lose substantial amounts of K + over 24h, with a UO >2L/day.
• Much less effective, as GFR deteriorates.
Gut K + wasting: cation exchange resins Overused , particularly orally.
• Exchange Na + /Ca 2+ for K + in the gut so actually removes K + , rather than just redistributing it.
• Calcium polystyrene sulfonate (CPS) (Calcium Resonium ® ) or sodium polystyrene sulphonate (SPS) (Resonium A ® or Kayexalate ® ). Can give 15g orally (supplied as a powder to be suspended in water) up to qds or 15 – 30g suspended in 2% methylcellulose and 100mL water rectally up to qds, retained for at least 2 (preferably >4) hours. May require saline irrigation through a catheter to remove the resin from the colon.
• Rectal route is more effective, as there is more K + available for exchange:
colonic [K + ] = 60 – 90mmol/L, whereas upper GI tract = 5 – 10mmol/L.
• The constipating effect of these agents given orally may paradoxically prevent K + losses in the stool — equally, the laxatives (e.g. lactulose 10 – 20mL tds) given with these agents may be more effi cacious than the agent itself!
• Modest effect seen within 24 – 48h.
• May cause colonic ulceration and necrosis (recognized with SPS when given with sorbitol as a hyperosmotic laxative — previously a common practice in the USA. Post-op patients with an ileus are at highest risk).
AKI MANAGEMENT: HYPERKALAEMIA 133
Extracorporeal K + wasting: dialysis
• Consider if K + >6.0mmol/L, or rapidly rising, and renal function cannot be restored quickly.
• Lowers K + within minutes.
• Haemodialysis (HD) can process 20 – 60L of blood against a dialysate K + of 1 – 2mmol/L and is 6 a potent means of removing K + .
• Haemofi ltration ( b p. 174), with returned infusate free of K + , can achieve much the same thing although much slower.
• Peritoneal dialysis is effective but rarely indicated acutely ( b p. 188).
• Requires dialysis access and transfer to a dialysing facility (which potentially introduces delays).
• 1 Never transfer a dangerously hyperkalaemic patient — if they are not responding to emergency measures, speak to your ITU ( b p. 123).
Further management
The aim is to prevent further dangerous rises.
• Restrict oral K + intake to <2g per day. 2 Speak to your dietetic staff ( b p. 258). 1 K + content of enteral and parenteral feeds may need modifi cation.
• 1 No K + in IV fl uids.
• Avoid K + -sparing diuretics, ACE-I, ARB, spironolactone, and NSAIDs.
• 2 Refractory i K + is an indication for dialysis.
• If i K + persists, despite dialysis, then:
• Review dietary intake and compliance.
• Triple-check the drug chart.
• Check for GI or occult bleeding (reabsorbed red cells are rich in K + ).
• Exclude concealed tissue or muscle damage (e.g. compartment syndrome).
• Review (and consider changing) dialysis access and dialysis adequacy ( b p. 181). Check dialysate K + concentration ( b p. 179).
Blood transfusion
1 Caution is needed when administering a blood transfusion to a patient with AKI, particularly if oligo-anuric. The volume and K + content of red cell transfusions can precipitate pulmonary oedema and hyperkalaemia, respectively. If the patient requires renal support, then transfusions are safest given during dialysis treatment ( 2 seek expert advice).
AKI management: pulmonary oedema
Introduction
Oliguric or anuric patients rapidly accumulate salt and water unless (and even if) tightly fl uid-restricted. Volume overload, often exacerbated iatro-genically, remains a relatively common presentation of AKI.
In AKI, the heart is often structurally normal, but salt and water over-load push it inexorably along the Starling curve. Many patients may also have poor underlying cardiac reserve ( l 1 mortality is high).
Findings
Cool, clammy, agitated patient. Tachycardia, tachypnoea, i JVP, i BP ( d BP in this context is worrying), gallop rhythm, respiratory crackles, and wheezes. Possibly: ascites, pleural effusions, and oedema.
Investigations
• Poor O 2 saturation.
• Hypoxaemia on ABGs (PaO 2 <8kPa).
• Widespread alveolar shadowing on CXR.
Management
• Sit the patient up, and stop all IV infusions.
• Oxygen . Maintain S a O 2 >95%. It should be possible to achieve an FiO 2
>60% using a well-positioned high-fl ow (e.g. Venturi) mask with an O 2 fl ow rate of 6L/min. Combine with nasal prongs, if necessary. Masks with reservoir bags may allow FiO 2 >80%. Consider ward CPAP if available (e.g. Boussignac system).
• Opiates . Give IV diamorphine (1.25 – 2.5mg) or morphine (2.5 – 5mg) as an anxiolytic and a venodilator (+ 5mg metoclopramide as antiemetic).
Can be repeated after 15min, but opiates will accumulate in AKI, so resist giving additional doses.
• Nitrates . If the systolic BP ≥ 90mmHg, start intravenous GTN 2 – 10mg/h. Start low, and titrate every 10min, as tolerated. Give 2 puffs of sublingual GTN while the pump is being set up. If systolic BP is <90mmHg ( 2 ? cardiogenic shock), call your ITU and consider inotropic support.
• Diuretics ( b p. 144). Administer 80 – 120mg furosemide bolus IV. If this initiates a diuresis, then repeat or start a continuous infusion (10 – 40mg/h). 2 If no increase in urine output, seek specialist help without delay.
• Renal replacement therapy . Oligo-anuric patients are likely to need renal support ( b p. 172). 1 If renal facilities are not on site, then ensure the patient is fi t for transfer — discuss with your ITU ( b p. 123).
AKI MANAGEMENT: PULMONARY OEDEMA 135
Consider respiratory support if:
• Continuing severe breathlessness.
• Falling respiratory rate (tiring patient).
• PaO 2 <8KPa, rising PaCO 2 . • Worsening acidosis (pH <7.2).
• Inform your ITU team about the patient before these occur.
Continuous positive airways pressure (CPAP)
Provides a constant positive pressure support throughout the respiratory cycle (typically 5 – 10cmH 2 O), allowing delivery of a higher FiO 2 (80 – 100%) and decreasing the work of breathing.
1 Patients must be conscious, able to protect their airway, and possess suffi cient respiratory muscle strength.
Endotracheal intubation and mechanical ventilation
Requires critical care transfer. PEEP — a preset pressure is added to the end of expiration to prevent airway/alveolar collapse and open up atelec-tatic and fl uid-fi lled lung.
How to give loop diuretics in AKI
• A bolus of 80 – 120mg IV furosemide can be administered initially.
• If no response, then call for expert help. Consider 250mg (25mL ampoule) furosemide IV, made up to 50mL (syringe driver) or 100mL (infusion pump) at a rate not exceeding 4mg/min to avoid ototoxicity. Bumetanide 5mg is an alternative.
• If this initiates a diuresis, give a further 250mg.
• If no response, further doses are likely to be futile. ( 2 Dialysis?) • If there is a reasonable, but transient, response, then a continuous
infusion 10 – 40mg/h over 24h may promote ongoing diuresis.
Venesection
• Exceptional circumstances and Hb ≥ 100g/L and SBP ≥ 120mmHg.
• 250mL blood removed from a large vein with venesection kit.
• Ideally, the blood should be saved to transfuse back when the patient is more stable.