A 72 year old male was admitted with progressive shortness of breath on a Friday morning. A family member gave the majority of the initial history, as the patient was of Polish origin and did not speak much English. The patient had started to feel unwell the preceeding weekend, with some dysuria, frequency and lower abdominal pain, with increasing breathlessness 2 days prior to admission. The family member did also mention that they felt their father had not been producing as much urine as normal. He had a cough, worse at night time, but no expectoration, chest pain or palpitations. He felt he had increased swelling in his legs and the previous night had woken in the middle of the night gasping for breath.
Past Medical History
- Type 2 Diabetes
- Chronic Kidney Disease (secondary to diabetic + ischaemic nephropathy)
- Metformin 500mg tds
- Ramipril 2.5mg OD
- Humulin M3 22 Units am, 14 Units pm
- Aspirin 75mg OD
- Seretide 250 TT bd
- Salbutamol PRN
Initial observations were recorded:
- BP - 110/45
- Pulse - 90 (regular
- Temp - 35.9
- RR - 22
- Sats - 94% on 2L nasal cannulae
Blood tests, Chest X-ray and ECG were done:
• Na – 134, K – 4.5, Ur – 39.8, Cr – 312, eGFR – 9
• Hb – 8.9, WCC – 16.4, Plt – 241
• LFTs – NAD
• CRP – 34
(There were no previous blood results on the hospital system, as the patient had had all previous admissions and clinic appointments at a different hospital.)
ECG: normal sinus rhythm, normal voltage, normal axis. Rte 90/min
Chest X-ray showed small bilateral pleural effusions:
The admitting doctor felt that the patient had fluid overload secondary to heart failure and came up with the following plan:
- IV furosemide 80mg STAT and OM thereafter
- Record urine output
- Urine dip
- Repeat U&E 24 hours
On the post take ward round, results and X-rays were reviewed. The consultant stopped ramipril and metformin and asked for the patient to be catheterised to ensure accurated recording of urine output. He also asked for an ultrasound scan of the renal tract which was done that afternoon, and showed bilaterally slightly small kidneys, but no evidence of obstruction or dilatation.
The patient was moved overnight on Friday from the acute medical unit to a general medical ward. Overnight he became more breathless and saturations dropped despite oxygen therapy, the on-call nigh medical registrar was called to review, who felt the patient had respiratory and renal failure, and also decided that given his background he was not a candidate for ITU or escalation, but to carry on with diuretic therapy as part of 'maximal ward based care'. The patient was made not for resuscitation. The patient was taken off the hospital early warning score escalation policy, and was therefore not reviewed again all weekend.
On Monday morning the day team arrived (who had not seen the patient up until this point) and were asked by the nursing staff to see the patient with a view to starting end-of-life care. The team reviewed the case, and noted the patient was admitted with fluid overload and renal failure, but that he had background CKD. They noted that he had remained on IV diuretics over the weekend but had stayed oliguric (initially) and had been anuric for the previous 24 hours. Urine dip had been recorded and was negative. The patient had saturations of 87% on 10L oxygen and was sat up in bed, visibly struggling to breath. The SHO and FY1 were tasked with getting repeat bloods, blood gases, repeat CxR and trying to improve the patients saturations, while the medical registrar rang the family to ask for some extra background. She discovered that the patient had been seen in the pre-dialysis clinic at a neighbouring hospital 3 weeks prior to admission, and was otherwise fit and well, with a good pre-morbid functional status. The team then called the neighbouring hospital and spoke to the on-call renal registrar, asking specifically about the patients baseline renal function, and plans from the last clinic appointment. The registrar confirmed the patients baseline eGFR was around 18 and that at the last clinic appointment, dialysis had been discussed, the patient had opted for haemodialysis and plans were being made for fistula formation.
Repeat blood tests and arterial blood gas showed:
• Na – 131, K – 5.3, Ur – 54.7, Cr – 345, eGFR – 8
• Hb – 8.6, WCC – 19.4, Plt – 225
• CRP – 62
• ABG on 10L Oxygen: pH- 7.16, pO2 - 7.5, pCO2 - 4.1, BE - -6.2, lactate - 1.6, Bicarb - 14
Repeat CxR showed the bilateral pleural effusions had worsened significantly:
The team immediately contacted the local renal unit and explained the case. The renal unit accepted the patient for transfer for urgent dialysis for fluid overload and metabolic acidosis secondary acute on chronic kidney injury with high urea (although no overt uraemic symptoms at that time).
The patient had 2 hours of dialysis the day of transfer, with 2.5L fluid removed. The renal team were careful not to try and lower the urea too quickly, to avoid causing dialysis dysequilibrium syndrome, and he had a further 2.5 hour session with 2.5L fluid removed the following day. He felt much better, and also received treatment for a likely UTI given his initial symptoms at presentation. Although he felt much better, his renal function never returned and he remained dialysis dependent.
There are many things wrong with the management in this case - some of them very wrong. The errors attributable to mis-diagnosis are in some way excusable in the hyper-acute setting, but some of the basic errors around proper history taking, to include complete past medical history, social history and background are not. Moreover, the decisions made by the night registrar were just wrong, and not based on any supporting evidence
- The initial diagnosis of fluid overload secondary to heart failure was incorrect. Although the clinical presentation may be similar, there was nothing in the past medical history to suggest heart disease, and the ECG was normal. Also the poor urine output and renal failure were largely ignored by the admitting medical Dr. It should also be remembered that 'heart failure' (like 'renal failure') is a syndrome, not a diagnosis and and underlying cause, or cause for decompenasation should always be sought.
- The consultant on the PTWR appropriately stopped nephrotoxic drugs, and stopped metformin due to the reduced eGFR. He also appropriately asked for the patient to be catheterised and for fluid balance to be recorded, and appropriately requested an USS. He should also have asked for baseline renal function to be found, and taken a more extensive social history, including pre-morbid status and asked for the team to find out what plans had been made from the patients recent renal appointment.
The night registrar did not get anything right. They made assumptions about the patients functional status that were proved wrong, they did not respond correctly to persistent oligo-anuria in the presence of renal failure, and
most crucially they did not discuss the DNAR order, or the limitations on the patient care with the patient or the family - presumably because this happened overnight and the patient did not speak much English.
- Never write 'patient does not speak English' in the notes - it is not at all helpful. A much better thing to do is to write down what language they do speak, and remember you can always get an interpretter.
- The incoming day team did very well to respond appropriately to the situation with fresh eyes (not just following what had gone before), and their management from that point was exemplary. They co-ordinated well with the renal unit at the patients normal hospital, acquiring all relevant information and the local renal unit were extremely helpful with arranging dialysis and taking over the patients care.
This patient had a lucky escape - another time the outcome may not have been as good. Heart failure syndrome can present with fluid overload and renal failure in what is termed cardio-renal syndrome. When this is the case renal failure is almsot certainly due to pump failure and an inability to maintain adequate renal perfusion. IV diuretics are appropraite in this setting in an attempt to offload fluid, improve cardiac output and renal perfusion, and has been shown to be equally (and possibly more effective) than ultrafiltration in these patients (Bradley et al. NEJM Dec 2012).
This patient, however, had fluid overload secondary to oliguric acute on chronic renal failure, and in this setting loop diuretics have no place in management (Bennett-Jones BMJ Aug 2006). This patient was probably going to need dialysis from the point he presented, regardless of how he was managed, and the initial dose of IV furosemide will probably not have done him any harm (although there is an increased risk of oto-toxicity in these patients). When he remained oliguric however, and as his fluid overload worsened, it should have triggered discussion with the local renal team much sooner, and the patient would have received the intervention he required (dialysis) much sooner.
Once again the keys to good patient care do not lie in fancy tests or expensive equipment, but in a good and thorough history, including thorough past medical and social histories, responding appropriately to abnormal test results, making accurate diagnoses and communication between teams and team members.