Acute Kidney Injury – Part 2

Acute Kidney Injury (AKI) is a disease process that carries a significant mortality impact (1). The complications that accompany AKI can be difficult to manage and may require specialist input if resistant to treatment. The management of AKI also changes when faced with some special situations.

Dr Aled Lewis is a Consultant Nephrologist at Glan Clwyd Hospital, North Wales. In this second part focussed on AKI, we discuss the complications of AKI, their management and some special situations that may alter the management of AKI. If you missed Part 1 which focussed on some general considerations AKI then check it out here. Or listen to part 2:

iTunes

Podbean (non-iphone)

 

Sepsis & AKI

Our case:

59 year old man with a background of Type 2 Diabetes, admitted with right lower lobe pneumonia

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Initially, the patient was seen in the Emergency Department and the lab have telephoned the following results through:

  • Urea: 42
  • Creatinine: 520
  • Potassium: 5.9
  • Bicarbonate: 16

Firstly, this patient is sick.

The combination of sepsis and AKI can result in an increased motality above that of the baseline conditions by themselves (1, 2). The worse the AKI, the higher the mortality (1, 2). A patient with sepsis and AKI is sick and needs treating with urgency.

This patient has diabetes and may well have an undetected reduction in glomerular function as a result. The “second hit” from a severe infection and the complex pathophysiology of sepsis may tip the balance to AKI.

 

Remember the most recent Sepsis 3.0 definition (3):

Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection

In this respect, you could consider the AKI as defining sepsis, being a potentially life threatening organ dysfunction. Worth remembering any time you see a clerking with the diagnosis as “AKI secondary to UTI”. Just as Aled points out, a simple UTI does not cause an AKI. Sepsis however, does.

Management

IV fluids right? Partly. Start with the basics. The AKI will not improve without treating the sepsis. If you want a more in depth recap of sepsis then check out our previous episode here. The Sepsis 6 bundle provides a good starting point and is simply a bit of give and take:

Sepsis-6

The main points here are about fluid management. Excess fluids is associated with increased mortality for these patients (4, 5). The dogma exists that those with an AKI and infection need fluids. What frequently occurs is a prescription of fluids with a quicker fluid bag, say over 1-2 hours, then 4-6 hours then maybe a third which would 8-12 hours, often “normal” saline. A patient in this situation who either has a low blood pressure, raised lactate or reduced urine output may benefit from fluid resuscitation.

Remember: resuscitation is an active and involved process.

If you give fluids: give a bolus and monitor the response. If the response is inadequate or transient, then patient may need more fluid or you may need to consider a higher level of care such as Intensive Care. There is no pre-specified amount if fluid that serves as a cut-off for the referral to ICU. Try and avoid a “fluid creep” that can occur, where background rates are increased to serve as a “pseudo-bolus”. A patient with a low blood pressure may require vasopressors. A patient with a low (<0.5ml/kg/hr or <50ml/hr), or no, urine output may require dialysis either from renal or ICU. A patient with a raised lactate may require all of the above and more. These patient need early escalation if simple measures have not had the desired effect.

 

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Nephrotoxics

Nephrotxic agents are plenty. The common ones to consider would include ACE-inhibitors and Angiotension 2 Receptor Blockers (ARBs). Diuretics will need careful attention as well. NSAIDs need to be stopped and avoided. Listing the various medications here would not be fruitful. Rather, any patient with an AKI needs a good medication review and your friendly ward pharmacist can help you with this.

Antibiotic dosing may need adjusting as well depending on the eGFR. Your local antibiotic guideline may suggest Gentamicin in a stat dose for a patient with sepsis and rightly so you would be concerned about the renal function. A single dose may be safe (6) but recurring doses will need close and careful monitoring.

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Nephrology Referral

Nephrology can’t see every patient with an AKI. The patient groups to refer include:

  • Stage III AKI
  • Patients with concern over poor recovery
  • Low urine output
  • Uncertain underlying diagnosis
  • Intrinsic renal disease such as vasculitis

 

 

Acute Kidney Injury with Chronic Kidney Disease

The next case:

68 year old male with known Polycystic Kidney Disease and eGFR 18 admitted with an NSTEMI whose creatinine has increased by 50 umol/L.

little engine

Patients with pre-existing renal disease have a limited amount of reserve to handle an acute insult. Their pre-existing reduced renal function is vulnerable to sometimes small acute physiologic changes affecting renal blood flow and perfusion and nephrotoxic agents. A pre-existing CKD confirs an increased mortality risk in patients who develop AKI, though this impact may lessen with a prolonged period of time (7). Patients with CKD are more likely to progress to needing dialysis in the presence of AKI (8).

Such patients may already be known to nephrology services. Even if they aren’t, given the potential for worse outcomes, an early referral is appropriate. The patient may not return to their baseline even once the acute insult has been treated and you may see a step-wise and progressive decrease in renal function with each insult.

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Risk Factors

Which came first: CKD or ischaemic heart disease? Both share common risk factors (9):

  • Smoking
  • Hypertension
  • Obesity
  • Diabetes

CKD and cardiovascular disease are frequently associated with each other with cardiovascular disease often not fully appreciated (10). Treating the cardiovascular disease is therefore treating the CKD.

As with every AKI, treating the underlying cause will treat the AKI rather than just prescribing fluids.

Statins in CKD have been shown to reduce mortality and morbidity. This may be a simple interventionto undertake if you encounter these patients in clinical practice (11, 12)

 

AKI and Fluid Overload

You are the F2 on call for medicine. The bleep goes off and its for the call that is often dreaded: a patient with worsening renal function who is known to be fluid overloaded. You already know treatment options are limited and answers are not always forthcoming.

78 year old lady with known congestive cardiac failure on oral furosemide, ramipril and bisoprolol. Hb recently dropped andbecause these patients may have a higher transfusion threshold, 2 units of blood was transfused.

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Heart failure is a low output state which may already have existing chronic kidney disease. Before prescribing liveral IV fluids we must ask ourselves if the heart can take it. Granted, there will be the occasional patient with CCF where they may need IV fluids, but often they don’t but what is needed is very careful attention to fluid status and adjustment of current treatments.

Whilst we use an example of a blood transfusion, it could be that slow fluid creep seen in a patient with AKI that occurs. Fluid overload has been exacerbated by liberal and ill-considered IV fluid use. The treatment for this is diuretics.

If you wish to read about the various definitions of cardio-renal syndrome, I suggest you read this consensus statement (13). Discussion of these would be outside the scope of this article though as they are complex and require good quality, joined up specialty care between cardiology and nephrology.

The points to consider are:

  • Diuresis: can the blood pressure handle it? The options are either bolus dose higher dose furosemide (typically 40-80mg IV) twice daily or infusion (anywhere up to 500mg daily)
  • Beta-bocker: continue unless a good reason for reducing/stopping exists which is essentially toxicity (which does happen in AKI)
  • ACE-inhibitor/Angiotension Receptor Blocker: consider a lower dose or stopping. The temptation is often to stop but adopting a lower dose may be more appropriate
  • Referral: both Nephrology and Cardiology will need to be involved with these patients and they are often encountered on the cardiology ward

Be cautious at just stopping every medication as the knee jerk as abrupt stopping of ACE-i/ARB and diuretics can cause deterioration of heart failure which could paradoxically worsen the AKI.

 

The question sent to me by email that sparked this whole discussion was:

What do you do when faced with a patient on a furosemide infusion with decreasing urine output and worsening renal function?

comic-1296117_1280

Do you stop the infusion and give fluids? Maybe. Do you increase the rate of the infusion? Maybe. Albumin?!?! Erm…… There is no right answer that can be given to this. It will always depend upon the patient you are faced with. Often these situations occur overnight when you can’t just call a friendly cardiologist or nephrologist.

Escalate these patients to your senior for help. They are difficult to manage and have limited treatment options. You need to take into account the severity and chronicity; is this crushing fluid overload that is going to kill the patient or a rapid escalation in renal deterioration that poses a threat to life? Also consider the patients existing quality of life and any ceilings of care already established.

An acute deterioration that is not being adequately managed in a ward situation may need escalation for a higher level of care with CCU/ITU. If the situation is one of progressive cardiac and renal decline and failing function, this may require difficult conversations to happen which are best saved for daylight hours with the patient’s parent team where possible.

Cardiac failure is a low output state and may not tolerate dialysis whether on the dialysis unit or as continuous renal replacment therapy in ITU.

Cardiorenal syndrome is something that carries a high mortality greater than the sum of the constituent parts (14). Patients in these situations are sick and difficult to treat and will need a joined up approach and as a junior doctr, you should not feel obliged to manage these patients alone.

 

Hyperkalaemia

Lets recap our first case and the blood results except with a higher potassium

  • Urea: 42
  • Creatinine: 520
  • Potassium: 6.3
  • Bicarbonate: 16

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Hyperkalaemia is a medical emergency

In general it can be diveded into gradients of severity:

  • Mild 5.5-6.0 mmol/L
  • Moderate 6.0-6.5 mmol/L
  • Severe >6.5 mmol/L OR any level with ECG changes

Whilst these values are frequently used in guidelines as treatment thresholds the individual patient must be considered in line with acute rises in serum potassium and deterioration in renal function. This is one of the guidelines you should familiarise yourself with wherever you work.

ECG changes are unlikely below 6.0 mmol/L The earliest change seen is a tall tented T-wave due to repolarisation abnormalities.

ECG_Hyperkalaemia_7.1_s

Image credit Life In The Fast Lane: https://lifeinthefastlane.com/hyperkalemia/

The next changes seen relate to atrial dysfunction which include prolongation of the PR interval with widening and flattening of the P wave

ECG_Potassium_9.2_s

Image credit Life In The Fast Lane: https://lifeinthefastlane.com/hyperkalemia/

Following this, the QRS becomes broad, the ST segment “slurs” and becomes sloped as the rhythm approaches a sinusoidal pattern with bradycardia and junctional rhythms.

ECG_Hyperkaemia_s

Image credit Life In The Fast Lane: https://lifeinthefastlane.com/hyperkalemia/

In an unwell patient, the blood gas may be what highlights hyperkalaemia to you before the laboratory sample result is available and with good agreement with the laboratory values (15).

Hyperkalaemia Treatment

Any severe (K+ 6.5 or above OR ECG changes OR acute rises of 0.5 mmol/L OR associated acute reductions of renal function) should receive immediate treatment:

  • 10ml 10% Calcium Gluconate or Chloride as an IV push over 2-3 minutes. Sometimes nursing staff may not be comfortable giving this and you may have to yourself. Don’t begrudge them this, 2 minutes to give it may be what stabilises the patient.
  • 10-20 mg nebulised sambutamol. This is likely easier to access than a ready made insulin/dextrose infusion and can be given whilst the other treatments are being prepared
  • Rapid acting insulin with dextrose. Traditional teaching has always been 10 units Actrapid in 50ml 50% glucose over 30 minutes. More frequently, 250ml 10% glucose is being used instead. This still requires a pump, but is less viscous and irritant than 50% glucose so may be better tolerated. If there is concern for fluid overload, then the restricted volume of 50ml 50% glucose would be appropriate.
  • IV fluids can also be used. Often these patients will need acute resusitation alongside their treatment. In the setting of hypovolaemia and AKI, IV fluid may even treat the underlying cause too.

These are temporising measures only. They do not alter total body potassium levels and a rebound hyperkalaemia is possible if the underlying cause is not treated. Further treatment options include diuretics, sodium bicarbonate and calcium resonium but these will be guided by local policies and specialty opinion rather than the initial therapy.

Potassium needs rechecking following treatment, approximately 4 hours afterwards.

Any ECG changes need cardiac monitoring to watch for deterioration.

electrocardiogram-16948_1280

A potassium that is not responding to treatment is an indication for emergency dialysis or renal replacement therapy on ITU

 

Indications for Renal Replacement Therapy

RRT encompasses both intermittent haemodialysis under nephrology and continuous venous haemofiltration under ITU. Broadly speaking, the acute reasons for consideration and referral include:

Hyperkalaemia refractory to medical management

Acidosis refractory to medical management

Uraemia, often very high with symptoms such as encephalopathy or pericarditis

Fluid overload refractory to diuretics

Pulmonary oedema with anuria

Toxin or medicaton removal

Obviously, this is not exhaustive and other reasons exist. If you have any doubt then escalate to your seniors/specialties. If the patient fits the criteria then they need referring to the appropriate service, whether ITU or nephrology, immediately.

 

Take home points

When faced with a patient with AKI remember that these patients are sick first and foremost. Identify the ill patient with correctable abnormal physiology and aim to correct this as quickly as possible, escalating when necessary.

Avoid a fluid creep in patients with AKI. IV fluids are not always the answer and liberal fluids can worsen outcomes. These patients need active management.

Familiarise yourself with local policies for AKI. IF you are struggling then look at the London AKI Network documents. Accessible via: http://www.londonaki.net/

Refer patients early to nephrology or critical care as needed so further management is not delayed.

Remember to STOP and think about the causes:

Sepsis

Toxins

Obstruction

Parenchymal

 

Speak soon

Gareth

@garEMlyn

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References

  1. Lopes JA et al, Acute kidney injury in patients with sepsis: a contemporary analysis. Int J Infect Dis. 2009 Mar;13(2):176-81
  2. Seymour CW et al, Assessment of Clinical Criteria for Sepsis For the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016;315(8):762-774. 
  3. de Olieira et al, Positive fluid balance as a prognostic factor for mortality and acute kidney injury in severe sepsis and septic shock. J Crit Care. 2015 Feb;30(1):97-101
  4. Cobussen M et al, No increased risk of acute kidney injury after a single dose of gentamicin in patients with sepsis. Infect Dis (Lond). 2016 Apr;48(4):274-280. Epub 2015 Nov 15.

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