A 74-year-old man with confusion and oliguria

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Problem 55 A 74-year-old man with confusion and oliguria

A 74-year-old man was brought into the emergency department confused and drowsy. According to his wife he had been unwell for approximately 1 week with a diarrhoeal illness, with nausea and anorexia. The changes to his mental state had appeared over the past 24 hours, and he had become bedridden. There was no history of chest pain.

Immediately prior to this acute illness he had been independent and well, although he had a past history of type II diabetes mellitus and ischaemic heart disease. He had been treated for hypertension for approximately 10 years. His current medications are combination perindopril/indapamide 5/1.25 mg one per day; gliclazide MR 30 mg twice daily; metformin 500 mg twice daily; aspirin 150 mg once daily; and celecoxib 200 mg once daily.

On examination, the man was drowsy but easily roused, and unable to give a clear history. His tongue was very obviously dry. Blood pressure was 100/55 mmHg lying, and he was unable to stand to check for a postural drop. Pulse rate was 90 and regular, although difficult to feel. Temperature was 36.5°C. There was no evidence of right or left heart failure, and his chest was clear to auscultation. Pedal pulses were not palpable, and he had a soft right carotid bruit. ECG is unchanged from previous.

An indwelling catheter was placed in his bladder, and it drained 50 mL of dark urine. Urinalysis showed protein + and blood +. A finger prick blood sugar level was 5.0 mmol/L.

Urgent blood results included the following:

Investigation 55.1 Summary of results

Sodium	143 mmol/L	(N: 137–145)
Potassium	7.8 mmol/L	(N: 3.5–4.9)
Chloride	105 mmol/L	(N: 100–109)
Bicarbonate	8 mmol/L	(N: 22–32)
Urea	65 mmol/L	(N: 2.7–8.0)
Creatinine	850 µmol/L	(N: 50–120)
Phosphate	3.5 mmol/L	(N: 0.65–1.45)
Calcium	1.64 mmol/L	(N: 2.10–2.55)
Albumin	30 g/L	(N: 34–48)
Haemoglobin	145 g/L	(N: 135–175)

You insert an intravenous catheter and commence a 5% dextrose infusion at an initial rate of 1 litre per hour.

Q.1

What are the most likely causes and contributing factors to his renal impairment?

Q.2

What are the priorities in his management in the emergency department?

Q.3

How do you treat the hyperkalaemia? How do you manage the renal impairment?

Q.4

How do you decide whether he needs to be acutely dialysed?

Q.5

How do you distinguish acute from chronic renal failure? Is it important?

Q.6

What (if any) changes would you make to his medications (short-term and long-term)?

Q.7

How do you manage his recovery from the acute renal impairment?

Answers

A.1 It is likely that he has developed acute renal failure secondary to dehydration and intravascular hypovolaemia, with consequent reduction in renal blood flow. A key question is whether he has acute or chronic renal failure (or both). The clinical picture, rapid deterioration and dramatically deranged biochemistry (particularly the severe hyperkalaemia and acidosis) is highly suggestive of marked acute deterioration in renal function.

An additional important possibility to consider is that the patient is septic associated with infectious diarrhoea, which would further predispose him to acute renal failure. This can occur in severe infectious diarrhoeal illnesses such as Salmonella. He was afebrile when seen in the emergency department, but this does not completely preclude an infectious illness, and a precipitating infection should be sought carefully.

A contributing factor to the acute deterioration in his renal function may be the use of celecoxib. While this non-steroidal anti-inflammatory drug (NSAID) may have less gastrointestinal toxicity, it has the same adverse effects as other NSAIDs on renal function.

Similarly, while the angiotensin converting enzyme inhibitor perindopril he is taking would not be a causative agent in his acute renal deterioration, in the setting of intravascular depletion and hypotension it would exacerbate deterioration of renal function by further lowering the blood pressure and also interfering with autoregulation of glomerular blood flow. It should be stopped for the time being.

A.2 The priorities of treatment in the emergency department are the most immediately life-threatening abnormalities:

• Severe hyperkalaemia is the most obvious priority, because of the high risk of refractory cardiac arrhythmias and death.

• He is hypotensive with evidence of poor peripheral perfusion, and so resuscitation with intravenous fluids is a high priority.

• There is also the possibility of contributory sepsis, and so intravenous broad-spectrum antibiotics should be considered.

The other biochemical abnormalities (low bicarbonate, high phosphate, low calcium), while impressive, are not immediately life threatening, and should correct with resolution of the severe renal impairment. The confusion and drowsiness are secondary to the acutely deranged biochemistry and should respond rapidly to appropriate treatment of the renal failure.

A.3 Severe hyperkalaemia is an emergency requiring rapid and aggressive treatment. While an electrocardiogram is a useful adjunct investigation and will show abnormalities such as peaked T waves and broadening of the QRS complex, at this potassium level it should not be used as a means of deciding whether to treat. Protocols for treatment of hyperkalaemia should be standard items in emergency departments, and consist of a combination of cardioprotective and potassium-lowering manoeuvres using calcium gluconate and dextrose-insulin. An example of such a protocol is shown in Box 55.1.

Box 55.1

Example of a protocol for treatment of hyperkalaemia

Treatment of Serum K⁺ Greater Than 6.5 mmol/L OR ECG Changes Present

• Give 10 mL calcium chloride 10% IV over 5 minutes (OR if calcium chloride not available, give 10 mL calcium gluconate 10% IV), then

• Via a separate line, or only after careful flushing of the same line, give 100 mL sodium bicarbonate 8.4% IV over 30 minutes, then

• Give 10 units neutral insulin (Actrapid or Humulin R) IV and 50 mL 50% glucose IV over 5 minutes.

• Give Resonium 30 g by mouth or 30 g PR as enema.

• Repeat full biochemistry (including BGL if insulin given) in 1 hour.

• You may need to repeat the above steps and correct causative factors, e.g. dehydration, over replacement of K⁺, use of K⁺ sparing diuretics, etc.

• In severe, intractable hyperkalaemia, haemodialysis may be required.

Additional Interventions to be Considered

• β-agonist therapy (e.g. salbutamol 20 mg in 4 mL administered by nebulizer) is recommended in some protocols for treatment of hyperkalaemia.

• Consider holding NSAIDs, ACE inhibitors or any other potassium potentiating medications.

The approach to management of the renal impairment is to initially rapidly correct the underlying cause. In this case, infusion of intravenous fluids to correct the hypovolaemia/hypotension is necessary. Careful monitoring of the patient’s fluid status, preferably by a combination of clinical assessment and invasive monitoring as available in a high-dependency unit. Accurate urine output measurements must be charted, and fluid input re-assessed regularly. A risk of rapid correction of intravascular depletion is fluid overload, particularly if the patient remains oliguric.

Fluid resuscitation may be all that is required to re-establish a good urine output and recovery, although frequently if the condition has been present for any more than a few hours the patient will remain oliguric without improvement in biochemistry.

A.4 The absolute indications include;

• Severe pulmonary oedema in an oliguric/anuric patient.

• Severe intractable hyperkalaemia with imminent threat of life-threatening arrhythmias.

• Acute uraemic pericarditis manifested by typical pain and an audible pericardial rub. The latter is potentially life threatening because of the risk of intrapericardial haemorrhage and tamponade, and any acute dialysis must be conducted without anticoagulation.

Relative indications include lesser degrees of fluid overload and hyperkalaemia, severe acidosis and severe hyperphosphataemia, plus occasional situations where a dialyzable exogenous toxin complicates the clinical presentation.

The best treatment is rapid correction of the underlying cause of acute renal impairment, but dialysis is sometimes required as an interim measure.

In this patient, the most important indication for acute dialysis is the severe hyperkalaemia. While the acute treatment of hyperkalaemia is usually able to quite quickly (minutes to hours) lower potassium to relatively safe levels, it is not a sustainable option unless a good urine flow is established.

It is also reasonable to initiate acute dialysis for less ‘compelling’ reasons in patients with multiple acute medical problems, based on the assumptions that there is less acute reversibility to their underlying problems, and that correction of adverse biochemical abnormalities such as severe acidosis is likely to improve their short-term outcome. A simple example of this is a hypotensive septic patient in an intensive care setting with progressive acute renal failure.

A.5 Determining whether the patient is suffering from acute or chronic renal failure (or acute on chronic renal failure) will fundamentally alter your approach to their treatment. Acute renal failure in isolation is potentially completely reversible with timely therapy, whereas the management of established chronic renal failure is very different and much more dictated by medium and long-term goals and outcomes. The biochemical abnormalities seen in this case will respond to reversal of acute renal failure, whereas if the underlying problem is chronic renal failure the most appropriate intervention is chronic dialysis. Patients with underlying chronic renal failure of any severity are also very prone to acute deterioration, even with relatively minor insults such as dehydration or introduction of an NSAID. This is a plausible scenario for this patient.

The most simple and reliable way to determine whether the patient has underlying chronic renal failure is by careful history and review of previous investigations. The latter includes finding reports of previous biochemistry. For example, knowing that a patient such as this has a usual serum creatinine of 300 µmol/L fundamentally alters your expectations about response to treatment and overall treatment goals. Not uncommonly also the patient will be aware of a history of renal impairment, and may even know results of previous blood tests. The history of diabetes and vascular disease is also a clues, at a minimum to categorize him as at risk of renal impairment.

On the other hand, the normal haemoglobin level (albeit probably increased somewhat by intravascular hypovolaemia) argues against preceding underlying severe renal impairment, which would usually be accompanied by significant anaemia. A simple additional investigation is abdominal imaging (usually a renal tract ultrasound) to determine the size and appearance of the kidneys. Small, echogenic kidneys are diagnostic of underlying chronic renal failure, whereas acute renal failure alone usually has normal appearing kidneys.

A.6 Acutely all of his current medications should be stopped. He is hypotensive and so the combined ACE inhibitor/diuretic should not be given. The ACE inhibitor will also hinder recovery from the acute renal failure due to interference with glomerular blood flow autoregulation. The half life of the oral hypoglycaemic gliclazide will be prolonged in the setting of deteriorating renal function, increasing the risk of prolonged hypoglycaemia. Metformin serum levels also increase in renal impairment, which in turn increases the risk of lactic acidosis. His diabetes would probably be best managed in the short term with an intravenous insulin infusion and close monitoring of blood sugar levels. He will require a number of invasive investigations and treatments, and so it would be preferable to withhold the aspirin. Finally, the celocoxib is likely to have contributed to his acute renal deterioration, and should also be stopped.

Longer term medications will depend to a large extent on the level of renal function to which he recovers. He will need to resume antihypertensives, and an ACE inhibitor may be the best option again, particularly in view of his history of cardiac disease. In moderate to severe renal impairment hyperkalaemia can be a limiting side-effect of ACE inhibitors, so that will need to be monitored. Unless his underlying renal impairment is quite mild (e.g. GFR >45 mL/min), it will be best to avoid metformin use, and NSAIDs should be avoided if he has any significant degree of residual renal dysfunction.

A.7 It is likely that he will remain oliguric or anuric for a prolonged period (days to even weeks), failing to clear urea and creatinine and requiring regular dialysis. During this treatment phase his biochemistry must be monitored regularly, preferably at least daily, and the dialysis parameters adjusted to maintain safe levels of hydration and biochemical indices, in particular potassium. Fluid intake must be dictated by urine output, with account taken for insensible fluid losses. An accurate fluid balance chart, regular assessment of state of hydration, and daily accurate weighing of the patient, are all simple but vital tasks. At times there is an obligate excess fluid intake, for example for intravenous therapy or feeding (or nasogastric feeding). Attempts to increase the urine output with diuretics in this phase are unlikely to be fruitful, and additional fluid will need to be removed by regular dialysis.

The recovery phase from an episode of acute renal failure (acute tubular necrosis) is heralded by a steady increase in the urine output, followed some days later by stabilization and then fall in the serum creatinine.

Often urine output will dramatically increase to very large volumes; this is the dangerous ‘polyuric phase’ of recovery after acute renal failure, which requires even more careful monitoring of fluid status. Fluid intake must not be reduced, as a patient who is producing 500–1000 mL of urine per hour will quickly become profoundly hypovolaemic. Intravenous fluid, where volume is still dictated by the urine output (input = output + insensible losses, i.e. ‘chase the urine’!) is essential. Ongoing daily weighing, assessment of state of hydration and an accurate fluid balance chart continue to be fundamental tasks.

Patients in the polyuric recovery phase waste salts, and supplementation of potassium is frequently necessary (whereas before you were trying to get rid of it). Sodium and chloride can be adjusted in the intravenous fluids. The severe acidosis recovers as renal function improves, as do the derangements in phosphate and calcium levels. Occasionally supplemental calcium is needed, particularly if tetany is present. Oral phosphate binders may be useful during the established phase of acute renal failure, although only if the patient is taking adequate amounts of food.

Revision Points

Acute Renal Failure

Pre-renal – due to inadequate perfusion, with structurally intact nephrons:

• Hypotension.

• Hypovolaemia (dehydration, blood loss, burns).

• Heart failure (low cardiac output).

• Shock (septic, toxic, cardiogenic, other).

• Drugs (ACEI, NSAIDs, ARBs).

Intrinsic renal – structural and functional damage to nephrons:

– macrovascular: renal artery or vein obstruction

– microvascular angiopathy: TTP/HUS, pre-eclampsia.

• Glomerular:

– glomerulonephritis (immune complex (e.g. post-infectious), anti-basement membrane antibodies (Goodpasture’s), ANCA (Wegener’s)).

– acute tubular necrosis (ischaemia or toxins)

– drugs and crystals.

• Interstitial:

– infections (pyelonephritis)

– interstitial nephritis (drug or allergen)

– amyloidosis (deposit in the tubules).

Post-renal – obstruction to passage of urine:

• Ureteric obstruction (kidney stones, retroperitoneal fibrosis).

• Bladder outlet obstruction (prostate cancer, neurogenic bladder).

• Renal injury/trauma.

Issues to Consider

• What are the most common causes of renal failure leading to dialysis?

• What forms of dialysis are available, and how are they chosen for individual patients?

• What are the indications for renal transplantation?

• What are the other complications of NSAID therapy?

Further Information

www http://emedicine.medscape.com/article/243492-overview. eMedicine acute renal failure

Pannu N., Klarenbach S., Wiebe N., et al. Renal replacement therapy in patients with acute renal failure: a systematic review. Journal of the American Medical Association, 299;7. 2008:793-805. Free full text at http://jama.ama-assn.org/cgi/content/full/299/7/793.

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