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In his Reith Lecture, medical author and surgeon Dr Atul Gawande says: “We always hope for the easy fix — the one simple change that will erase a problem in a stroke. But few things in life work this way. Instead, success requires making a hundred small steps go right — one after the other, no slip-ups, no goofs, everyone pitching in.”
Checklists have been routinely used in various occupations, mostly to impart efficiency and safety to a process. Over the years, medicine has embraced this practice, thereby leading to improved outcomes for patients and creating a culture of safety. It is surgeons and anaesthetists in the operating room that are predominantly utilising this tool currently.
However, nephrology and general medicine have increasingly been looking towards employing checklists for managing acute kidney injury (AKI).
A common and highly mismanaged condition
In the 2009 UK NHS National Confidential Enquiry into Patient Outcome and Death (NCEPOD) — in a review of the care of patients who succumbed with a primary diagnosis of AKI under the care of various specialties — the advisors concluded the following:
- Only 50 per cent of AKI care was considered ‘good’.
- There was poor assessment of risk factors for AKI; both in the assessment of patients in established AKI and those who subsequently developed it.
- An unacceptable delay in recognising post-admission AKI in 43 per cent of patients.
- Some 20 per cent of post-admission AKI was both predictable and avoidable.
- Complications of AKI were missed in 13 per cent of cases, avoidable in 17 per cent and managed badly in 22 per cent of cases.
Repeated studies of patients with AKI have demonstrated that mortality correlates with increased levels of creatinine. Moreover, survivors often have more protracted stays in ICU and hospital, greater declines in health-related quality of life and impairments in functional status.
Risk of death appears to extend well beyond hospital discharge, with significant declines in the survival curve not stabilising until after one year. This long-term risk of death was significantly higher for those with a higher burden of comorbid disease, surgical disease and, most importantly, those not achieving complete recovery of kidney function.
These findings are rather analogous to studies on the long-term survival of critically-ill septic patients, where an increased risk of death persists for several months to years beyond the index hospitalisation.
Ascertaining an exposure to a nephrotoxin is one of the most commonly-missed components of the history during an assessment
In consideration of the aforementioned, an inadvertent economic burden has resulted. It is estimated that, in England and Wales, costs associated with delivering care for AKIs are more than that involved in lung and skin cancer combined.
In the US, it was found that the multivariable-adjusted marginal costs of hospitalisation were increased by nearly $5,000 (€4,500) per case after an increase in serum creatinine of more than only 27umol/L. Extrapolating from estimates from a teaching hospital in Boston, the overall healthcare expenditures in the US attributable to hospital-acquired AKI may exceed $10 billion annually.
Although all of the aforementioned facts may appear grim, there is an immense opportunity here to transform care of AKI in our acute hospitals and improve the associated outcomes. It definitely does not require avant garde techniques to do so. ‘Simplicity is the ultimate form of sophistication,’ as Da Vinci emphasised.
As is advocated by the proponents of sepsis management, the initial assessment, if done in a timely manner, can bear a favourable outcome.
The following checklist can guide a physician in the management of AKI
- Volume status/blood pressure.
- Urine output.
- Ruling out obstruction.
- Electrolytes/acid base.
- Need for dialysis.
Eliciting a comprehensive history is indispensable, as it points to the most likely aetiology of the AKI, thereby classifying it into one of the classical triad — pre-renal, intrinsic and post renal. The exclusion of the latter should be one of the foremost measures employed in the evaluation.
Ascertaining an exposure to a nephrotoxin is one of the most commonly-missed components of the history during an assessment. Almost two-thirds of AKI cases encountered in hospitals are community-acquired and up to 30 per cent of AKI cases may be drug induced, with ACE inhibitors (ACEI)/angiotensin-II receptor blockers (ARBs), diuretics and non-steroidal anti-inflammatory drugs (NSAIDs) being the main culprits in the community.
The aforementioned agents can exponentiate the effects of volume depletion and cause a severe acute kidney injury, especially in the most vulnerable group, which include the following:
- Chronic kidney disease.
- Congestive heart failure.
- Chronic liver disease.
From a point of view of preventive medicine, it is imperative to advocate to patients on these therapies to exercise ‘sick day’ rules — to temporarily cease use of these medications in the event of a volume-depleting illness or infection. This simple measure in itself can ameliorate a significant number of incipient AKIs.
A caveat to the use of topical NSAIDs should be addressed. A number of case reports have highlighted the fact that its intradermal absorption, thereby eliminating first pass metabolism, can be hazardous to the previously-mentioned vulnerable population.
Turning the focus from the community to the hospital, it is a surprise that even in a well-monitored setting, the incidence of hospital-acquired AKI (HAA) is nearly 20 per cent, even accounting for it being an inadvertent consequence of the primary admitting illness. The same is associated with higher mortality and worse outcomes, compared with community-acquired AKI.
The following are the most common offending events associated with HAA
- Prolonged renal ischaemia (sepsis, surgery, progression of pre-renal insult).
- Cardio-renal syndrome (CRS).
- Primary drug nephrotoxicity.
- Contrast nephropathy.
Sepsis-induced AKI and CRS constitute a significant proportion of HAAs. AKI is a frequent and serious complication of sepsis in ICU patients, particularly in the elderly. Moreover, there is strong evidence that sepsis and septic shock are the most important causes of AKI in critically-ill patients, accounting for 50 per cent or more of cases of AKI in ICUs, and are associated with a very high mortality rate. Furthermore, there is evidence that even less severely-ill patients with infection (patients with non-severe pneumonia) have a significantly higher incidence of AKI and increased immune responses.
On a reciprocal note, AKI is an independent risk factor for severe sepsis. Even patients who recover from AKI have a high risk of long-term severe sepsis.
Data from the US Acute Decompensated Heart Failure National Registry (ADHERE) of over 100,000 patients (admitted with ADHF) revealed that almost one-third of patients have a history of renal dysfunction.
Another study found that, in a survey of outpatients with congestive cardiac failure, 39 per cent of patients in New York Heart Association (NYHA) class 4 and 31 per cent of patients in NYHA class 3 had severely-impaired renal function (creatinine clearance <30mls/minute).
Baseline renal function is as important an adverse prognostic marker as ejection fraction and NYHA functional class. Elevated serum creatinine on admission to hospital with ADHF and worsening renal function during admission for ADHF have both been shown to predict prolonged hospitalisation, increased need for intensive care facilities and increased mortality. The classification of CRS is elucidated in Table 1.
Table 1: CRS classification
As demonstrated by extensive evidence, the management of HAA lies primarily in prevention — identifying the susceptible patients and pre-empting the occurrence of AKI via fastidious monitoring of renal indices and early warning scores, along with enforcing measures to avert it.
Volume status and blood pressure
It is often an instinctive reaction for a physician to institute intravenous fluids in the setting of an AKI — a well-intentioned therapeutic intervention that may well be deleterious for a patient. Over-zealous fluid resuscitation has been associated with increased complications, increased length of ICU and hospital stay, and increased mortality.
An assessment of extracellular fluid volume status is crucial to guiding decisions around the dichotomy of fluid resuscitation versus renal replacement therapy.
Management of volume status in critically-ill patients with AKI is difficult, as it is often accompanied by oliguria or anuria, as well as total body fluid overload and tissue oedema. Guaranteeing adequate renal perfusion and intravascular volume is also important in the prevention and therapy of AKI.
Peripheral oedema is a useful sign, if present; however its absence does not exclude heart failure (sensitivity 10 per cent and specificity 93 per cent) and interestingly, only 25 per cent of patients with chronic cardiac failure under 70 years of age have oedema.
A raised jugular venous pressure (JVP) can help predict raised venous pressure and volume status; predicting central venous pressure more than 12cm H20: sensitivity 78-to-95, specificity 89-to-93 per cent, likelihood ratio (LR) if present, 10.4 and if absent, 0.1. It also has a negative prognostic value predicting death from heart failure with relative risk (RR) of 1.37. Crepitations are the most common sign in volume overload, seen in 66-to-87 per cent.
Patients with volume overload are often tachypneic, but this may also be a result of respiratory compensation secondary to AKI-induced metabolic acidosis, which is a very valuable sign and is unfortunately often neglected as a vital sign. Over half of the patients suffering a serious adverse event on the general wards had a respiratory rate greater than 24 breaths/minute. In unstable patients, the change in respiratory rate is better at predicting an at-risk patient than heart rate or blood pressure.
An accurate assessment of fluid balance and fluid responsiveness is central to the optimisation of volume management in patients with AKI.
Ruling out obstruction
Renal ultrasound scans are now widely available and rapidly provide information about renal and urinary tract appearances, without exposure to ionising radiation. The early identification of urinary tract obstruction as a cause of AKI allows urinary tract decompression by catheterisation, nephrostomy or antegrade stenting, with subsequent rapid reversal of AKI.
However, although urinary tract obstruction accounts for only about 10 per cent of adult AKI, the ultrasound appearances can be helpful for the healthcare professional managing a patient with AKI. Enlarged, echo-bright kidneys may indicate parenchymal renal disease (ischaemic injury, pyelonephritis, glomerulonephritis or interstitial nephritis), while scarred, small kidneys indicate prior renal damage, suggesting CKD complicated by AKI. Anatomical variations might be detected, such as a single kidney, which might be of relevance to management of the AKI, even if not the direct cause of it.
Another simple but frequently-neglected investigation is a urinalysis by reagent strips. In patients with no readily apparent cause for AKI, a urine dipstick positive for microscopic haematuria and proteinuria can point towards a diagnosis of glomerulonephritis. Prompt specialist input should be sought, since early diagnosis and treatment is the main prerogative for arresting the disease process.
We cannot manage what we do not measure. The urine output is a useful tool to alert the physician of an impending kidney pathology. Both urine output and serum creatinine (SCr) are used as measures of an acute change in glomerular filtration rate.
The theoretical advantage of urine output over SCr is the speed of the response. For example, if GFR were to suddenly fall to zero, a rise in SCr would not be detectable for several hours. On the other hand, urine output would be affected immediately.
The Acute Kidney Injury Network (AKIN) (www.akinet.org) has established stages to ascertain severity of the AKI based on the serum creatinine and urine output (Table 2).
Table 2: Classification/Staging system for acute kidney injury
Electrolytes/acid base and dialysis
The incidence proportion of dialysis-requiring AKI cases among critically-ill patients increased by almost four-fold between 1996 and 2010. This was accompanied by a significant decline in mortality, but the risk of long-term dialysis dependence continues to affect a substantial minority of surviving patients, with no clear evidence of improvement over time.
Initiating dialysis is a clinical decision influenced by several factors, including assessment of electrolytes and metabolic acidosis. It is widely accepted that hyperkalaemia, metabolic acidosis and volume overload (most importantly, refractory to medical management) or overt uraemic signs and symptoms constitute traditional indications.
Thresholds for starting dialysis appear to be lower when AKI is accompanied by multiple organ failure, the rational being the earlier institution will facilitate other aspects of management while maintaining fluid, solute and metabolic control.
Early commencement of dialysis (oliguria less than six hours with creatinine clearance less than 20ml/min) compared to conventional criteria has been shown not to confer a mortality benefit, although only shown in a small randomised control trial.
Back to basics
In this medical epoch, we are enthused by bench medicine, which is unravelling various novel molecules and therapies, which have given us an immense sense of control. But in this pursuit, we sometimes forget to focus on efforts to monitor, improve and transform clinical performance using know-how already in existence.
As demonstrated in this article, we have an opportunity to employ simple measures to immensely improve outcomes for a common medical ailment, and for a cause that is central to all of us — the patient.
References available on request