Last updated: Lesson of the Month - January 2019…
on 01 Jan 2019

January 2013

James Yates and Matthew Graham-Brown

A 27 year old male was admitted to a district general hospital with severe pain in his right leg, which he noticed for the first time on waking. After assessment by the emergency department team, he was referred to the on-call surgical registrar who came to review the patient. He noted that the patient was in considerable pain; and noted the history and examination findings of the ED SHO. Initial observations showed:

  1. Pulse - 98
  2. BP - 106/64
  3. RR - 22
  4. Sats - 99% OA
  5. Temp - 37.3

The surgical registrar felt such severe pain was most likely to be caused by an acutely ischaemic leg and proceeded straight to examination. He noted the patients right leg was slightly swollen and tender to touch proximally. He felt good foot pulses in both feet, but thought the right leg was colder and 'duskier' than the left leg - confirming that the most likely explanation was an acutely ischaemic event. He decided to refer to the local tertiary referral centre for vascular cases, and reviewed the patients blood tests:

FBC:   Hb - 12.4, WCC - 12.3, Plt - 246
CRP:   56
U&E:   Na - 136, K - 5.8, Ur - 14.2, Cr - 146

After discussion with his surgical registrar colleague at the tertiary referral centre, a transfer was agreed (although the receiving registrar thought the story sounded a little strange, and not really consistent with acute ischaemia). After ambulance transfer, the patient was reviewed by the surgical registrar in the tertiary referral centre, and the history was taken again

The patient had woken that morning with extreme pain at the top of his right leg. He admitted that for the preceeding 24 hours he had drunk a very large amount of alcohol, and could not remember a great deal about the day before, or how or when he got home. He was able to move his leg, with great pain, but had normal sensation in the leg. The surgical registrar agreed that the distal leg appeared slightly swollen and cool to touch, but that all foot pulses were palpable. He the asked to examine the top of the patients leg and buttocks. On examining the patients right buttock, the registrar found the whole buttock to be swollen, dusky and extremely tender. The surrounding skin above and immeditely below were normal, and there were no signs of crepitus. The patient could not remember injuring the area, but did recall that he had woken up 'rather crushed up against the wall next to his bed'.

The surgical registrar immediately got a plain film X-ray of the area to ensure there was no bony injury or evidence of subcutaneous gas formation (X-ray was normal), and he also sent off an urgent repeat bloods, including (this time) a creatinine kinase and asked for a urine dipstick. It took a while for the patient to pass what turned out to be small volume dark, concentrated urine, and it was strongly positive for blood. CK came back very raised at 4,565.

The registrar recognised that this was likely to be rhabdomyolysis, caused by a gluteal compartment syndrome - either as a resut of an unknown injury, or because of a long-lie in the same position due to intoxication. The orthopaedic team came to review and agreed with the diagnosis made by the general surgical SpR. They also reviewed the repeat blood tests:

  1. FBC:  Hb - 12.2, WCC - 123.1, Plt - 221
  2. CRP:  54
  3. LFTs: NAD                                                                                                                                                                     
  4. U&E:  Na - 136, K - 5.9, Ur - 17.2, Cr -174                                                                                              
  5. INR:   1.3

They noted the deteriorating renal function and started IV fluids, and also asked for the patient to be catheterised, and strict fluid balance chart to be recorded. His observations remained stable, and it was agreed that he needed to go to theatre for emergency debridement of the necrotic tissue. The on-call anaesthetist reviewed the case, and noted the patient was oligo-anuric, with worsening renal function. He agreed to take the patient to theatre, but booked him a bed on HDU for afterwards.

Several large areas of necrotic gluteal muscle were debrided in theatre, and surgically the procedure went well. The patient, however remained oliguric throughout the operation, despite copious IV fluid. The following day repeat U&E's were sent, which showed a further deterioration in renal function:

Na - 131, K - 4.9, Ur - 24.0, Cr - 226

The HDU team were also concerned that the patient was becoming oedematous with some basal crackles, consistent with pulmonary oedema. Given these trends, the decision was made to commence renal replacement therapy with continuous veno-venous haemofiltration (CVVH). A temporary VasCath was inserted for filtration and CVVH commenced, initially aiming to take fluid off. After 48 hours, the patient started to pass urine again, requiring CVVH for a total of 3 days. His renal function improved, but never back to baseline completely, and he was left with a baseline Creatinine of 120. He was discharged from hospital after a short period of rehabilitation and was followed up in orthopaedics outpatients.


  1. The initial surgical registrar arrived with a pre-conceived idea of what the diagnosis was, and was not prepared to question his hypothesis, even in the face of evidence that he was probably wrong. This once again demonstrates the Semmelweis reflex (the rejection of new information that contradicts an established proposal or norm), which is something we will all have seen (or been guilty of) at one time or another. 
  2. Perhaps more concerning is the initial lack of thorough history or complete examination. The second surgical registrar demonstrated that the diagnosis was actually quite straightforward, it just required a proper chronological history of events and complete exposure on examination.
  3. The risk of AKI was spotted, and appropriate steps were taken with the timely administration of IV fluids. If the patient had been on any nephrotoxic medication, this should have been stopped.
  4. The anaesthetist ensured patient safety by admitting to HDU post-op, and this was proven to be an appropriate step with the patient requiring CVVH for a short period of time.
  5. The ITU/HDU staff noticed the trends in renal function and worsening fluid status, with prolonged oligo-anuria and although they did not formally score him, he had moved from stage 2 AKIN to stage 3 AKIN according to the recent KDIGO guideline.
  6. Basic investigations should form part of all patients admission to hospital, and should include a urine dipstick. In this case the urine being strongly positive for blood was not an indication of actual red blood cells in the urine, but one of the breakdown products of the necrotic muscle fibres myoglobin. Myoglobin will cause a urinary dipstick to be positive for 'blood', but in clinical context should alert the clinician to the likely diagnosis.


Rhabdomyolysis is an example of a haem nephropathy, and is a common cause of AKI. Rhabdomyolyis is most commonly caused by muscle trauma, but can be caused by strenuous exercise, seizures, alcohol abuse, limb ischaemia and pressure necrosis secondary to coma. In this case, it is possible the patient had a traumatic injury (he did not remember); or could have developed pressure necrosis from lying in the same position secondary to intoxication. The pathogenesis of haem pigment nephropathy is complex, and due to a combination of factors:

  1. Patients are invariably volume depleted due to fluid collecting in oedematous necrotic muscle. Volume depletion activates the renin-angiotensin system, causing vasoconstriction, which is worsened by depletion of nitrous oxide (normally a vasodilator) by increased circulating heme breakdown products.
  2. Myoglobin is filtered at the glomerulus and is toxic to tubuar epithelial cells. Also haem may cause direct renal injury, by lipid peroxidation and the formation of free radical oxygen species.
  3. Finally myoglobin is thought to precipitate with 'Tamm-Horsfall' proteins and tubular cells in the distal nephron, forming obstructive casts.

Treatment of rhabdomyolysis is to treat the underlying cause (remove the underlying insult), and supportive treatment for the renal tract as with any other cause of AKI. Compartment Syndrome is a recognised cause and complication of rhabdomyolysis, and the diagnosis shoud be actively excluded.

Back To Index