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Treatment of dangerous hyperkalaemia

Dalam dokumen Nephrology and Hypertension (Halaman 161-166)

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.

AKI management: electrolytes

Dalam dokumen Nephrology and Hypertension (Halaman 161-166)