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Last updated: Acute Kidney Injury…
on 10 Apr 2017

May 2012

Matthew Graham-Brown

Case Presentation

History

A 43 year old male was admitted to hospital with a 3 day history of fever and shortness of breath. He had not felt well for 2 weeks, with general lethargy and malaise, but presented to A&E on that day because of a small amount of haemoptysis. He had recently returned from the south of Spain, where he had on a business trip

He had no significant past medical history and took no regular medication and had no allergies. There was no family history of note and he was an ex-smoker of 15 pack years. He drank 15-20 units of alcohol per week, spaced out throughout the week and was happily married with 2 children at university

Examination

BP:  158/96
Pulse :  98
Sats: 93% on room air
Temp:  37.8˚C
Resp rate: 18

On examination, he was comfortable, with no peripheral/central cyanosis. His pulse was regular and 100 beats per minute. He had slightly pale conjunctivae, and was deemed to have dry mucous membranes, and his JVP was recorded as not being visible. His trachea was central

Examination of his chest revealed normal chest expansion bilaterally, with increased vocal fremitus in the right middle and upper zones, with coarse crackles throughout the right lung and occasional crackles in the left lung. Percussion note was normal throughout. Examination of his cardiovascular system was normal, including normal heart sounds; and abdominal examination did not reveal any tendernss, abdominal masses or organomegaly, with normal bowel sounds. The patient did have a strange rash over both his legs that he had noticed develop over the last 2 days, which was neither painful nor itchy

The admitting medical house officer made an initial diagnosis of right upper lobe pneumonia, with atypical features and advised the following management plan:

  1. Blood tests including: FBC, U&E, LFT’s and CRP
  2. Peripheral blood cultures
  3. Chest X-ray
  4. ECG
  5. Urine dip + urine legionella antibody testing
  6. IV access + IV antibiotics to be started after blood cultures sent
  7. IV fluid – 2l of 0.9% Saline were prescribed at 125ml / hour

Investigation

The patient was admitted to the medical admission unit (MAU) was reviewed on the post-take ward round. The chest X-ray was reviewed:  

The chest X-ray was felt to be consistent with right upper lobe consolidation. Blood tests were as follows:

FBC:  Hb 9.1, WC 12.2, Plt 323
U&E:  Na 143, K 5.3, Ur  22.6, Cr 258
LFT:  Bili 13, ALT 28, ALP 98
CRP:  104

It was noted that the patient had not had his urine dipped, or legionella antigen sent, as he had not passed urine since arrival in hospital

Diagnosis

The impression from the post-take ward round was that the patient had lobar pneumonia, with atypical features and a co-existent acute kidney injury (AKI) secondary to sepsis and dehydration (pre-renal AKI). The acute medical physician leading the round largely agreed with the management plan outlined by the house officer, but increased the speed of IV infusion, to help increase effective circulating volume and renal perfusion. He also suggested sending a ‘renal screen’ to make sure there was nothing else going on

The house-officer diligently went and looked up what was meant by a ‘renal screen’ and drew some more blood from the patient and sent it for:

  1. ANCA
  2. ANA + dsDNA
  3. AntiGBM
  4. Protein electrophoresis
  5. C3 and C4 levels

He was about to finish his shift, but before he went home he documented in the notes that he sent bloods for the above tests

What Happened Next?

The following day, the patient was reviewed by the day team (junior staff), who reviewed the diagnosis from the previous evening of pneumonia and consequent pre-renal AKI. They also noted that the patient had only passed a small amount of concentrated urine overnight, that had been dipped as requested and was positive for blood and protein. They decided to repeat blood tests, including U&E’s and continue IV fluid replacement, and also to continue his IV antibiotics. They also catheterised the patient (15ml residual urine) and started a fluid balance chart

Overnight the patient became increasingly short of breath, and had a further (larger) episode of haemoptysis, coughing up about 50ml of fresh blood. Alarmed by this, the nursing staff contacted the oncall medical SHO who promptly reviewed the patient. She found the patient to be in extremis, with Sats of 91% on 8L of oxygen. He was fluid overloaded with pulmonary oedema, a raised JVP and peripheral oedema. He had received 2L of IV fluid since commencement of fluid balance chart earlier the previous morning, and had passed only 38ml urine. She also noticed a widespread vasculitic rash, involving the thighs and abdomen. She reviewed his case history, and noted the initial blood results. She also noted the repeat U&E’s sent the previous day

U&E:  Na 143, K 5.4, Ur 30.2, Cr 337

She also noted the abnormal urine dip and the results of part of the immunological screen that was sent on admission:

c-ANCA – Strongly positive (with raised PR-3)
p-ANCA – Negative (with normal MPO)

She immediately contacted the oncall renal registrar and requested an urgent review of the patient, as she believed he had a rapidly progressive glomerulonephritis (RPGN), likely secondary to Wegener’s Granulomatosis. She also obtained an arterial blood gas, which showed the patient was hypoxic (pO2  8.2; pCO2 normal), and acidotic with pH of 7.29 and Base Excess of -2.1

With this additional information, she also contacted the ITU team and requested urgent review, with a view to management on an ITU/HDU setting. The renal registrar and ITU registrar reviewed the patient and agreed with the diagnosis of RPGN. The patient was moved to ITU and central venous access obtained, as well as a temporary dialysis line. The patient was started on IV methylpred immediately and commenced on continuous veno-venous haemofiltration (CVVH)

The following day, after review by the renal consultant, pulsed IV methylpred was continued, and Cyclophosphamide started (as per hospital protocol). Renal biopsy was deferred as the patient was deemed too unwell

Fortunately the patient quickly improved and was moved to the renal ward. A renal biopsy confirmed an ANCA+ve RPGN. He required several sessions of intermittent haemodialysis. His rash faded, his urine output returned and his renal function returned to near normal over the following 2 weeks. He was discharged home on Cyclophosphamide and oral steroid, with follow-up in the renal vasculitis clinic 

Discussion

The first thing to say is that the diagnosis of RPGN is not always obvious immediately, and the original diagnosis of lobar pneumonia, with atypical features and associated pre-renal AKI is probably a reasonable initial thought. A high index of suspicion is often required in the early stages to diagnose RPGN, and the plan from the post-take ward round highlighted this issue, as the acute physician specifically requested a renal screen to ensure there was no intrinsic cause for the patient's AKI. Up to this point the team did quite well, but in retrospect it is easy to see that care from then on was sub-optimal. Outlined below, are the failings in the patient care from that point onwards and how they could have been averted:

  1. Although the house-officer went back and took bloods as instructed for the 'renal screen', and wrote what he had done in the notes, he should have handed over to the person taking over his shift to chase up the blood tests
  2. The day team only reviewed the diagnosis from the post-take ward round, and carried on treating the patient as if they had pneumonia and pre-renal AKI. They did not react to the changing clinical picture and question the original diagnosis and management plan. The Simmelweis reflex
  3. The day team did not notice or chase up the immunological screen sent the night before. Perhaps this is partially excusable, as it was not verbally handed over that it needed chasing (although it was written in the notes). What is not excusable is then repeating the U&E’s and not chasing up the results.
  4. Nobody responded appropriately to abnormal urine dipstick. Blood and protein in the urine is NOT normal, and in the context of AKI and hypertension should have triggered thoughts of intrinsic renal failure and RPGN much sooner
  5. The team did not respond appropriately to the prolonged period of oliguria, and they did not appear to reassess the fluid status of the patient, and pulmonary oedema could have been predicted. Even if this had been pre-renal AKI, the prolonged oliguric period despite IV fluid replacement should have triggered a call to the renal team for review much sooner, as the patient may have been developing ATN
  6. It is surprising that nobody did a blood gas until it was done with the patient in extremis. A lot of information can gleaned from a venous or arterial blood gas, and with hindsight, oxygen saturations of 93% on air and AKI in a previously healthy individual should have triggered an ABG on admission. A simple pneumonia in a fit young man with normal lungs will not usually make the patient hypoxic
  7. The 'Sepsis Six' requires an ABG (to check O2 and lactate) and urinary catheter. Even at admission, the patient fulfilled the criteria for a Sepsis Six approach, which was not fully carried out - specifically these two procedures. Both could have benefited the patient. In retrospect, this patient was not septic, but the approach is still useful in sick patients admitted on a medical take

So. The diagnosis was clear in retrospect. Everything is easy in retrospect. And it would be easy to criticise the admitting team for not making the diagnosis straight away. However, the initial diagnosis and management (apart from not obtaining an ABG and inserting a urinary catheter) were probably appropriate, and requesting the renal screen (in case something more unusual was going on) shows vision, and an ability to challenge the initial diagnosis. This is good. The systemic failings in this case were to do with communication between team members and following up tests that had been organised. The team also did not respond to the changing clinical picture, or make adequate reassessment of the patient after starting treatment

Lesson

In conclusion, the night SHO showed that the diagnosis was just waiting to be made, it only took a proper reassessment of the patients and review of tests that had already been requested - but not reviewed

RenalMed will eventually publish an article on renal vasculitis, but for more information follow the links below:

References

Anthony D Booth, Charles D Pusey, David RJayne. Renal vasculitis—an update in 2004. Nephrol Dial Transplant 2004; 19 (8): 1964-1968

Rachel B Jones et al. Rituximab versus Cyclophosphamide in ANCA-Associated Renal Vasculitis. N Engl J Med 2010; 363: 211-220 



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