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LETTER TO THE EDITOR

Hyperkalemic Cardiac Arrest with Hypertonic Mannitol Infusion: The Strong Ion Difference Revisited

Department of Anesthesiology and Critical Care, Columbia Presbyterian Hospital, New York, New York, bergid2002{at}yahoo.com

To the Editor:

Since first described by Scharfetter et al. in 1960 (1), hypertonic mannitol has been used in neuroanesthesia to reduce intracranial pressure and volume during cerebral aneurysm clippings. Several case reports have described patients becoming hyperkalemic during hypertonic mannitol infusions, with adverse effects on cardiac rhythm (2,3). A patient of mine had a 37-min cardiac arrest during a hypertonic mannitol infusion, possibly caused by hyperkalemia secondary to the hypertonic mannitol.

A previously healthy 41-yr-old male presented for elective craniotomy and clipping of a left middle cerebral aneurysm. Anesthetic induction, intubation of the trachea, and insertion of a radial arterial catheter proceeded uneventfully. His preoperative electrocardiogram (ECG) showed normal sinus rhythm at 81 bpm with a normal QRS duration and QT interval. It is customary at our institution to infuse 200 gm of 20% mannitol and to decrease end-tidal CO₂ to 20 mm Hg during aneurysm clippings. Both of these were initiated shortly after skin incision.

Approximately 40 min after we had initiated the mannitol infusion, with nearly 120 gm infused, the patient’s ECG had peaking of the T-waves and an increased QRS duration. We stopped the mannitol infusion. The ECG rapidly progressed to a sine-wave ventricular tachycardia that soon deteriorated into coarse ventricular fibrillation. We initiated cardiopulmonary resuscitation (CPR) with chest compressions and made three attempts at electrical defibrillation. These attempts were futile, and asystole ensued. During the resuscitation, we gave the patient boluses of epinephrine, calcium, vasopressin, and bicarbonate. The initial blood gas drawn approximately 10 min into the code showed pH 7.48, Paco₂ 18 mm Hg, Pao₂ 60 mm Hg, bicarbonate 12 mEq and base excess of –10. His sodium was 116 mEq, potassium 7.5 mEq, and calcium 3.5 mEq. After 37 min of CPR, we administered a bolus of insulin and dextrose, which resulted in the patient regaining a native rhythm for several heart beats, before deteriorating into asystole once again. We repeated the bolus of insulin and dextrose. Again the patient returned to native sinus rhythm, which was sustained. His blood gas showed a pH 7.18, a Paco₂ 46 mm Hg, a Pao₂ 203 mm Hg, a bicarbonate 17 mEq, and a base excess of –10. His sodium was 135 mEq, potassium 3.9 mEq, and calcium 6.5 mEq.

The surgery was aborted, and the scalp was closed. Echocardiogram showed global hypokinesis, with no other cardiac aberrancies. The patient was cooled overnight to 33°C. After we tracheally extubated him on postoperative Day 1, we found no neurologic deficits other than amnesia of the entire previous day. Two weeks later, the patient underwent an uneventful aneurysm clipping, this time without the use of mannitol.

Manninen et al. (4) showed that low dose mannitol (1 gm/kg) caused a slight decrease in plasma potassium, whereas high dose (2 gm/kg) mannitol caused a significant increase in plasma potassium. Possible mechanisms by which hypertonic mannitol causes an increase in serum potassium include (a) a dilutional acidosis due to expansion of extracellular fluid and dilution of bicarbonate (5), (b) hemolysis due to red blood cell crenation directly by mannitol, and (c) a "solvent drag phenomena" whereby potassium-rich intracellular fluid shifts out of cells due to the body’s attempt to maintain isotonicity while undergoing a hypertonic infusion (4,6).

The strong ion difference (SID), also known as the "physicochemical approach" developed by Stewart in the 1980s (7), may explain the development of hyperkalemia in response to hypertonic infusions. Osmotic diuretics limit passive reabsorption of water in the proximal tubule and descending loop of Henle. Passive reabsorption of water normally follows the active reabsorption of sodium. Osmotic diuretics reduce Na⁺ reabsorption by increasing urine flow rates, decreasing the contact time between fluid and the tubular epithelium. The difference between strong cations and strong anions, (Na⁺ + K⁺ + Mg⁺ + Ca²⁺) – (Cl^– + lactate), is the SID. Osmotic diuresis decreases sodium reabsorbtion, decreasing the SID. Stewart’s model shows that a decrease in SID increases H₂O dissociation, increasing the concentration of H⁺. Hyperkalemia is the expected physiological response to increased H⁺ concentration.

REFERENCES

1. Scharfetter V, Hunziker A, Buhlmann A. Zur osmotherapie der intrakraniellen drucksteigerung. Schweizerische Medizinische Wochenschrift 1960;90:342.[Medline]
2. Seto A, Murakami M, Fukuyama H, et al. Ventricular tachycardia caused by hyperkalemia after administration of hypertonic mannitol. Anesthesiology 2000;93:1359–61.[Web of Science][Medline]
3. Hirota K, Hara T, Hosoi S, et al. Two cases of hyperkalemia after administration of hypertonic mannitol during craniotomy. J Anesth 2005;19:75–7.[Medline]
4. Manninen PH, Lam AM, Gelb AW, Brown SC. The effect of high-dose mannitol on serum and urine electrolytes and osmolality in neurosurgical patients. Can J Anaesth 1987;34:442–6.[Web of Science][Medline]
5. Winters RW, Scaglione PR, Nahas GG, et al. The mechanism of acidosis produced by hyperosmotic infusions. J Clin Invest 1964;43:647–658.[Web of Science][Medline]
6. Makoff DL, da Silva JA, Rosenbaum BJ, et al. Hypertonic expansion: acid-base and electrolyte changes. Am J Physiol 1970;218:1201–7.[Free Full Text]
7. Stewart PA. Modern quantitative acid-base chemistry. Can J Physiol Pharmacol 1983;61:1444–61.[Web of Science][Medline]

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