Hong Kong Journal of Emergency Medicine A case of nonfatal non-collapsed patient with extreme hyperkalaemia YH Lim and J Hendricks This is a report of a non-collapsed patient with nonfatal, extreme hyperkalaemia of 10.7 mmol/l. The patient's hyperkalaemia was initially treated in the Emergency Department and then transferred to the Department of Renal Medicine of another hospital for further stabilisation. There have only been a few reported cases of successful management of extreme hyperkalaemia in excess of 10.0 mmol/l. (Hong Kong j. emerg.med. 2007;14:228-232) 10.7 mmol/l 10.0 mmol/l Keywords: Chronic kidney failure, potassium Introduction Hyperkalaemia is defined as a serum potassium level of more than 5.5 mmol/l. 1 The most concerning and serious dangers associated with hyperkalaemia are mainly secondary to cardiac arrhythmia and even cardiac arrest. 1-2 It is commonly accepted that a serum potassium level of more than 10.0 mmol/l is fatal unless urgent treatment is instituted. 1-2 There have only been a few reported cases of successful management of extreme hyperkalaemia in excess of 10.0 mmol/l. 1-2 Potentially fatal hyperkalaemia can develop rapidly and patients may be asymptomatic. However, hyperkalaemia Correspondence to: Lim Yong Hwa, MBBS(S pore), FRCSEd(A&E), DIMC RCSEd Western General Hospital, Grange Road, Uphill, Weston-Super- Mare, North Somerset BS23 4TQ, England Email: malaysianlim@yahoo.co.uk Jonathan Hendricks is a fairly common complication of renal insufficiency and may be a presenting complaint in undiagnosed renal disease. 2-4 Intercurrent or concomitant sepsis or dehydration can alter the potassium homeostasis dramatically and the serum potassium can be elevated to a dangerous level in a short time. 3 Case report The patient was a 49-year-old lady with recent above knee amputation of the right lower limb for peripheral vascular disease and gangrene. She was a non-smoker and the cause of her vascular disease had not been determined. She currently developed early gangrene of the left foot secondary to peripheral vascular disease and was awaiting definitive treatment. She did not have history of diabetes mellitus. The patient had end stage renal disease secondary to chronic glomerulonephritis. She was on haemodialysis three times a week. She presented to our department
Lim et al./extreme hyperkalaemia 229 with increasing shortness of breath and decreasing mobility with increased generalised weakness and lethargy on the day that she was due for her dialysis. There was no associated cardiac disease noted. Her blood pressure was 145/64 mmhg, pulse rate 64 beats per minute and oxygen saturation 100% (measured after supplemental oxygen of 5 L/min was given via a non-rebreathing mask). She was clinically dehydrated, lethargic and weak. Her peripheral veins were collapsed. She had an arteriovenous fistula in the left arm which was created during the last admission about three weeks earlier and a right internal jugular line for haemodialysis (this was also placed during her last admission). Her heart sounds and lung fields were normal. Her abdomen was soft and non-tender. She had a right above-knee amputation and the stump was healing well. The circulation in the left foot was critical with absent dorsalis pedis and posterior tibial pulses. There was wet gangrene in the left foot. Her initial electrocardiogram (ECG) was as shown in Figure 1. A diagnosis of hyperkalaemia was made and treatment initiated. Her initial blood gas whilst in the Emergency Department was as shown in Table 1. Her initial renal function and blood electrolytes whilst in the Emergency Department (confirmed blood sample not haemolysed and serum potassium was repeated) were Table 1. Arterial blood gas result whilst patient was in the Emergency Department. (Unfortunately the machine did not record any potassium result) Measurement Value Comment ph 7.267 pco 2 5.14 kpa po 2 24.93 kpa On 5 litres of oxygen per minute HCO 3 17.2 mmol/l Base excess - 9.1 mmol/l Oxygen saturation 99.4% Figure 1. The initial ECG showed an extremely widened QRS complex as well as an extremely tall 'T'wave. The 'p' waves were hardly discernable in the ECG.
230 Hong Kong j. emerg. med. Vol. 14(4) Oct 2007 as follows: urea 41.6 mmol/l; creatinine 383 µmol/l; sodium 128 mmol/l; and potassium 10.7 mmol/l. She was treated with two doses of intravenous calcium chloride (each dose was 10 ml of 10% calcium chloride) and two doses of intravenous insulin and dextrose combination (each dose consisted of intravenous soluble insulin 10 units and 50 ml of 50% dextrose solution). Calcium polystyrene sulfonate was also administered. The posttreatment ECG was as shown in Figure 2. The patient was transferred to the Department of Renal Medicine in another hospital where she underwent emergency haemodialysis. An initial blood sample obtained at the beginning of her dialysis revealed serum potassium of 10.1 mmol/l. Her serum potassium was normalised and the repeat ECG was as shown in Figure 3. She underwent a below-knee amputation for the gangrene of the left foot. She was discharged after 11 days in hospital. Figure 2. There was hardly any change in this post-treatment ECG when compared to Figure 1. Figure 3. The 'p' waves and QRS complexes were all normal after the serum potassium was normalised.
Lim et al./extreme hyperkalaemia 231 Discussion It is clear that the patient had hyperkalaemia secondary to end stage renal failure. This was further complicated by dehydration, sepsis and gangrene of the left foot. Hyperkalaemia is common in patients with chronic renal failure as more than 90% of the potassium load is excreted by the kidneys. 2,3,5 The mean serum potassium is usually higher than normal whilst the total body potassium is lower than normal in patients with end stage renal disease. 5 A serum potassium of up to 6 mmol/l is fairly well tolerated by patients with chronic renal failure. 2,3,5 However, these patients usually have difficulty in excreting the acute potassium load and hence it should be treated. 2,3,5 The classical ECG changes of hyperkalaemia may be graded as shown in Table 2. 4,6 The current recommendations for the management of acute hyperkalaemia with ECG changes include the followings: 7-9 A. For protection of the heart 1. Intravenous calcium chloride 10 ml 10% solution slow bolus 2. Intravenous calcium gluconate 10 ml 10% solution Calcium increases the threshold potential and hence restoring the normal gradient between the threshold potential and resting membrane potential; which is abnormally elevated in hyperkalaemia. It also antagonizes the neurological effect of hyperkalaemia. However, it does not have any effect on the serum potassium level. Intravenous calcium chloride is preferred as more ionised calcium is available for protection of the heart than an equivalent volume of calcium gluconate. The calcium in calcium chloride is also more rapidly available. However, calcium gluconate may be safer to use and is less irritant to blood vessels. Extravasation of calcium chloride may cause severe tissue necrosis. The effect of calcium starts within minutes and can last up to 60 minutes. It is contraindicated in patients with digitalis toxicity. Calcium preparations vary in the content of calcium: 10% calcium chloride 1g = 10 ml = 272 mg of calcium; 10% calcium gluconate 1g = 10 ml = 90 mg of calcium. Adverse effects (which may be worse with intravenous calcium chloride) of calcium administration include hypercalcaemia, cardiac arrhythmia, nausea and vomiting as well as localised reaction at injection sites especially if it is administered rapidly or if extravasation occurs. B. For shifting of potassium into the cells 1. Insulin with 50% dextrose combination (in the ratio of 2 units of insulin to 5 g of dextrose) 2. Intravenous sodium bicarbonate solution especially if the patient is in severe metabolic acidosis and if the patient is not in frank fluid overload 3. Nebulisation with salbutamol solution 10-20 mg As glucose enters the cells, it 'pulls' potassium, magnesium and phosphorus in with it. The onset of effect of this treatment usually starts in about 15-30 minutes and can last up to 2-3 hours. After an initial dose of 50 ml of 50% dextrose with insulin intravenously, a litre of 20% dextrose with 40-80 units of insulin may be given over the next 2-4 hours. This would obviously depend on the overall fluid status of Table 2. The correlation between ECG morphology and serum potassium level Serum potassium level (mmol/l) ECG changes 5.5-6.5 Peaking of T wave >6.5 Widening of QRS complex >7 Amplitude of P wave decreases, P-R interval increases >8 P wave disappears, sine wave appears 12-14 Ventricular fibrillation or asystole
232 Hong Kong j. emerg. med. Vol. 14(4) Oct 2007 the patient and one has to be careful not to fluid overload the patient. Extravasation of 50% dextrose may cause severe tissue necrosis and is irritant to the veins. The dose of insulin may be reduced as the effect of insulin is prolonged in patients with renal failure. The blood sugar level would have to be closely monitored. Intravenous sodium bicarbonate causes alkalosis that tends to reduce serum potassium levels. Its main indication is in the treatment of documented severe metabolic acidosis and hyperkalaemia-induced cardiac arrest. It is hypertonic and increases the serum concentration of sodium; hence it may aggravate fluid overload. The onset of action is usually within 15 minutes and its effect may last up to one hour. Nebulised salbutamol promotes cellular reuptake of potassium possibly via the cyclic AMP receptor cascade and hence can reduce serum potassium transiently. The onset of action is usually within 15-30 minutes and its effect can last 2-3 hours. C. Removal of potassium from the body 1. Haemodialysis 2. Cation exchange resin e.g. calcium polystyrene sulfonate (Resonium C) or sodium polystyrene sulfonate (Resonium A) Haemodialysis is the preferred option in this patient as the rate of removal of potassium from the body by cation exchange resin is rather slow. Cation exchange resin promotes the exchange of potassium for sodium in the gastrointestinal tract. Calcium polystyrene sulfonate binds with the potassium in the gut; forming an insoluble complex which cannot be absorbed whilst sodium polystyrene sulfonate exchanges gut potassium for sodium. Both calcium and sodium polystyrene sulfonate can cause gastrointestinal disturbance. Both calcium and sodium polystyrene sulfonate can potentially cause or aggravate sodium overload. The onset of action is usually delayed. It is clear that medical management alone would not lower the serum potassium to an acceptable level in these circumstances and hence there is a need for emergency haemodialysis. Conclusion Hyperkalaemia is a common complication in patients with chronic renal failure. Extreme hyperkalaemia, though not as common, is a deadly metabolic derangement that can be and must be expeditiously treated. References 1. Tran HA. Extreme hyperkalemia. South Med J 2005; 98(7):729-32. 2. Hylander B. Survival of extreme hyperkalemia. Acta Med Scand 1987;221(1):121-3. 3. Costa J, Crausman RS, Weinberg MS. Acute and chronic renal failure. J Am Podiatr Med Assoc 2004;94 (2):168-76. 4. Walbaum D, Kluth D. Clinical assessement of renal disease. Medicine 2007;35:353-8. 5. Gennari FJ, Segal AS. Hyperkalemia: An adaptive response in chronic renal insufficiency. Kidney Int 2002;62(1):1-9. 6. Lim YH, Anantharaman V. Pseudo myocardial infarct- -electrocardiographic pattern in a patient with diabetic ketoacidosis. Singapore Med J 1998;39(11):504-6. 7. Mahoney BA, Smith WA, Lo DS, Tsoi K, Tonelli M, Clase CM. Emergency interventions for hyperkalaemia. Cochrane Database Syst Rev 2005;(2):CD003235. 8. Ahee P, Crowe AV. The management of hyperkalaemia in the emergency department. J Accid Emerg Med 2000; 17(3):188-91. 9. Alfonzo AV, Isles C, Geddes C, Deighan C. Potassium disorders--clinical spectrum and emergency management. Resuscitation 2006;70(1):10-25.