Electrolytes Case 1

Answer the questions at the bottom of the page when all data has been reviewed

History & Examination

On a hectic night in ED/ER, an elderly widower is seen in the West Hampton Hospital. He had been found by a visitor collapsed on the floor of his living room. Unable to get up, he had spent several hours lying on the floor before being discovered. He is a lifelong heavy smoker who rarely attends his doctor. A veteran of the North Africa campaign in WW2 he was accompanied by a member of the British Legion.

Chatty and instantly likeable, he was cheerful and although in some pain was clearly minimising his symptoms. CVS examination revealed an irregularly irregular pulse. Examination of his chest showed generalised poor air entry, a late expiratory wheeze and hyperexpansion. He had no evidence of CO2 retention.

As the ED/ER doctor removed his slippers and socks in order to carry out a neurological examination another problem became obvious. Three toes on Mr Smiths right foot were gangrenous. Removing his clothing, patchy mottling and discoloration of the skin was found to extend to the right  ankle. He told the doctor that it had been becoming increasingly discoloured over a period of weeks, well before his fall. He agreed that difficulty moving his foot may have contributed to the fall. Apart from being unsightly, it had not particularly bothered him, he had managed the discomfort with simple analgesics present in his home. He did not call the doctor as he had no phone and, anyway, he did not want to cause ‘any fuss’. On more detailed enquiry, he had suffered with symptoms suggestive of peripheral vascular disease for years. No dorsalis pedis, posterior tibial or politeal pulse is palpable on the right. Peripheral pulses were also difficult to palpate on the left. His lower limbs were covered in bruises.

ED/ER course

With multiple social problems, there is a dispute between the medics and the vascular surgeons as to who should admit the patient. Finally, after a further hour, the ED/ER consultant is contacted and insists that the medics review him.

Shortly before he is reviewed, he experiences a cardiac arrest. A printout from the monitor, recorded during the arrest, is shown below.

c1c1 rs

He is successfully electrically cardioverted with a single shock of 100J by the ED/ER nursing staff. An ABG is taken and a twelve lead ECG recorded.

c1c1 image 1

He arrests again, with the same rhythm on his monitor and again is successfully cardioverted.

The situation is reviewed by the ED/ER consultant. She immediately commences the patient on a set of therapies and there are no further episodes of arrest. The patient is placed on telemetry and transferred to CCU under the care of the medics.

Observations

Alfie 1

Alfie 2


Questions

Q1. Why did Mr Smith have a cardiac arrest?

Q2. What abnormalities are present on the ECG taken between arrests?

Q3. What has led to the problem identified in Q1?

Q4. What rhythm is present on the strip recorded during the arrest?

Q5. What treatment/s has the consultant initiated?

Q6. What are the possible aetiologies of his gangrenous foot?

Q7. What other issues will arise in this gentleman’s care?


Answers

Q1. Why did Mr Smith have a cardiac arrest?

c1c1 Q1 Ans

He has profound hyperkalemia, a major cause of cardiac arrhythmia. If you look at the values quoted for serum electrolytes on his ABG (taken between the episodes of cardiac arrest) the potassium level is grossly elevated at 7.9 mmol/l (normal range 3.5 – 5.0 mmol/l). We need to be careful interpreting the results of potassium levels on a departmental ABG (ie analysed on the ABG analyser in the ED/ER). Unlike laboratory analysed samples, departmental samples are not checked for hemolysis. Hemolysis of red cells, if present, will cause artefactual elevation of the measured ‘serum’ potassium. However, in this case the consultant in charge suspected that the value was real and this view was supported by the wise decision to obtain a 12 lead ECG/EKG.

Q2. What abnormalities are present on the ECG taken between arrests? 

The ECG is highly abnormal. The T waves are tall, symmetrical and rise rapidly to a narrow apex (so called tall ‘tented T waves’). Also note, that the qrs complexes are wide (>/= 0.12s). These are classic and predictable ECG manifestations of significant hyperkalemia. In the clinical context, this possibility must be considered. You will also appreciate that the qrs complexes are occurring in an irregularly irregular pattern. We cannot identify P waves. He is in atrial fibrillation. However, we cannot determine if this is chronic or of new onset.

c1c1 ECG Ans

Q3. What has led to the problem identified in Q1? 

Rhabdomyolysis. Rhabdomyolysis is a breakdown of muscle tissue resulting in the release of muscle fibre contents into the blood. Trauma to, or ischemia of, skeletal muscle are recognised causes. We frequently see this condition in elderly patients who have been found lying on the floor for prolonged periods after a fall. In our patient’s case, the syndrome will have been compounded by the presence of an ischemic foot.

When his venous blood results came back from the lab, they illustrated many of the problems associated with the syndrome of rhabdomyolysis:

CSi bloods Rhab 2

Note that the serum levels of enzymes and proteins normally present in skeletal muscle are markedly elevated reflecting their release from damaged muscle tissue in to the bloodstream (CK: creatinine kinase, AST, ALT). LDH will also be elevated.

Note also, the marked elevation of serum creatinine. Acute kidney injury (AKI) frequently complicates rhabdomyolysis as the oxygen binding protein, myoglobin, released from muscle is filtered at the glomerulus and is nephrotoxic. Myoglobin gives a false positive reaction on urine dipstick tests for hemoglobin, This phenomenon is seen in this gentleman’s case (see urinalysis on fluid chart). Microscopy of his urine showed no red cells present. The nephrotoxic effects of myoglobin will be compounded by dehydration, a prominent feature of rhabdomyolysis. We might reasonably expect that his AKI has been compounded by analgesic use at home, has he been taking NSAIDs for the pain? If so, they should be stopped.

Rhabdomyolysis is a recognised cause of hypocalcemia, possibly secondary to calcium deposition in damaged muscle. It can be severe and symptomatic but is usually self-limiting in this context.

Skeletal muscle is the major site of storage of potassium in the body and release of this cation from such intracellular stores into the bloodstream can result in life-threatening hyperkalemia. The hyperkalemia may be aggravated by an acute kidney injury. In our case, there probably was a degree of hemolysis in the ABG sample, the potassium level is somewhat higher on the ABG sample than the laboratory sample. However, the level on the laboratory sample (6.9 mmol/l) is life-threateningly high and the ECG changes necessitated prompt intervention.

Q4. What rhythm is present on the strip recorded during the arrest? 

c1c1 rs

Totally chaotic ventricular electrical activity i.e. ventricular fibrillation.

Q5. What treatment/s has the consultant initiated? 

Broadly speaking, there are three complimentary approaches to the management of dangerous hyperkalemia, each differing in their rapidity of onset.

1) Stabilise the myocardium. Intravenous calcium gluconate will stabilise the myocardium against the arrhythmogenic effects of hyperkalemia. This effect will occur virtually immediately on IV administration of calcium in the absence of any effect on serum potassium.

2) Reduce the serum potassium. This can be achieved by administration of an IV infusion of insulin in dextrose. Insulin will push potassium into skeletal muscle cells in conjunction with glucose. Equally, administration of an alkalising agent bicarbonate will shift K+into the cells, lowering extracellular fluid (ECF) levels. The same effect can be achieved by administration of nebulised beta-agonist.

Note that these approaches, effective in minutes, have no effect on total body potassium, they merely shift potassium from the ECF to the intracellular fluid compartment, thereby reducing the concentration of potassium at the myocardium.

3) Reduce total body potassium. Agents capable of chelating potassium in the bowel, such as calcium resonium, may be administered per rectum. This resin remains in the bowel and binds potassium reducing total body levels over a period of days.

Any drugs capable of elevating body potassium should be held (eg ACE inhibitors)

In the presence of significant acute kidney injury, immediate renal dialysis may be necessary to reduce potassium levels.

Our case

In this case, the consultant has a few problems to deal with as a full drug history has not been taken as of yet. Is there a possibility that the atrial fibrillation is chronic and if so has the patient been on digoxin therapy? If so, what about the possibility of digoxin toxicity? In this scenario, calcium administration will aggravate digoxin toxicity. What are the alternatives? Rhabdomyolysis is frequently associated with hypomagnesemia and hyperkalemia associated arrhythmias have been reported to respond to magnesium administration. However, magnesium therapy can cardiovert a case of atrial fibrillation to sinus rhythm. If this arrhythmia is chronic, such a chemical cardioversion may carry a risk of thromboembolic stroke. However, repeated episodes of ventricular fibrillation carries a very real risk of death!

The consultant decided to go with immediate calcium gluconate injection, insulin dextrose infusion and subsequent resonium administration. Also note, clinically, the patient has some evidence of underlying COPD. Nebulised salbutamol will also help reduce serum potassium levels. Thankfully, the approach worked. Telemetry on CCU, showed no further episodes of ventricular fibrillation.

Q6. What are the possible aetiologies of his gangrenous foot? 

A lifelong smoker, he is clearly an arteriopath. We find it difficult to palpate his peripheral pulses in both lower limbs. We have no idea if his atrial fibrillation is chronic or acute perhaps related to the electrolyte disturbances associated with his rhabdomyolysis. Therefore, his ischaemic limb may be thrombotic secondary to clot formation on a local plaque or embolic secondary to an embolism from his atrial fibrillation.

Q7. What other issues will arise in this gentleman’s care? 

He is a lifelong smoker and has evidence of COPD on examination. Note the low SpO2 on his observation chart pre-arrest and clinical evidence of hyperexpansion and wheeze on examination. This should be addressed and a target SpO2 set on the ward of 90%. His ABG post arrest is taken while he was on oxygen but we are not told how much oxygen was being administered and so cannot calculate his A-a gradient. Usefully, there is no evidence of CO2 retention of his post arrest ABG.

He is elderly and living alone. We must pay attention to his nutritional status and request a review by the dieticians. Is there any suggestion of alcohol use? If there is, we may administer appropriate supplements and consider the possibility of alcohol withdrawal should he become agitated on the ward.

He is immobile. He was commenced on low molecular weight heparin.

He has atrial fibrillation on his ECG/EKG. This puts us in the tyrannical land of preventative medicine. He will need an echocardiogram. If the rhythm persists after his current illness we will have to at least consider long-term anticoagulation.


Subsequent Course

g

He recovered well following the cardiac arrest. His renal function and serum potassium returned to normal in the days post-admission. On vascular review, it was felt that it was not possible to salvage the leg and a below-knee amputation was recommended.

The House Officer (Intern) was sent to consent him for the operation. The House officer was Irish and although he had lived in England for a number of years, still had a hint of a Dublin accent. He had long-since given up trying to persuade Mr Smith that he was a doctor and not a priest. The House Officer told the patient that he was sorry to have to say that the leg could not be saved and would have to be amputated. Mr Smith looked at his leg and after a momentary pause, and without an ounce of self-pity, told the doctor. ‘Don’t you worry about me, Father. I’ve nothing to complain about, I’m one of the lucky ones. A lot of my mates lost arms, legs when they were still young men.’ He looked away and his mood changed. ‘Bloody awful it was, the Germans could hit us from five hundred yards further out than we could hit them! We were close to mutiny more than once I can tell you, nothing like the rubbish you have to listen to about it today, anyway, we stuck at it.’ After a pause he looked scornfully at his leg and said. ‘That leg is what you call a bad job, Father, get rid of it-cut it off! Then concerned that his forthrightness had caused offence, qualified what he had said with ‘If it’s not too much trouble to you and the medical team?’

These were very civilised times in the NHS, when we are able to prescribe nightcaps for elderly patients. It is the only aspect of being a Junior doctor that the Intern involved in this case would truly miss in later years. Mr Smith enjoyed his stout that evening and slept well.  Following the amputation, he stuck at it again, working hard with the physiotherapists. He made a brilliant recovery, eventually walking with a stick.