A SELF-TEST IM BOARD REVIEW DAVID L. LONGWORTH, MD, JAMES K. STOLLER, MD, EDITORS ON A JONATHAN GLAUSER, MD CLINICAL Department of Emergency Medicine, Cleveland Clinic CASE

Cardiac arrhythmias, respiratory failure, and profound hypokalemia in a trauma patient

50-YEAR-OLD MAN, previously in excel- sounds. There was ecchymosis on his right A lent health, arrived at the emergency flank. department via helicopter, having been injured Extremities. The patient could not move at his job at a munitions factory. As he was his right arm, but otherwise moved his limbs placing 1 kilogram of propellant behind a 2- symmetrically. inch-thick transparent blast shield, it exploded, Oxygen saturation by pulse oximetry was throwing him 40 feet across the room. 92% on room air. Initially he was able to walk from the Past medical history was unremarkable. scene, but soon required help from coworkers. The emergency medical services crew arrived Imaging studies promptly and measured his heart rate at 122 Computed tomographic (CT) scans of the beats per minute, respiratory rate 28, and sys- head and abdomen and lateral cervical spine tolic blood pressure 88 mm Hg; the heart radiographs were normal. Radiographs of the His lab findings: monitor indicated he was in sinus rhythm. He right arm indicated a fractured radius, ulna, pH 6.84 had burns on his face and abdomen, with a and humeral condyles. A chest roentgeno- marked deformity of his right arm. He arrived gram revealed a small left apical pneumotho- bicarbonate 10 at the emergency department within 15 min- rax, consistent with the physical examination. lactate 21.8 utes of the event on a backboard with a cervi- cal collar in place. Arterial blood values potassium 3.5 •PCO2 35 mm Hg (normal 34–46) and falling Physical examination •PO2 (while receiving oxygen via a nonre- On arrival, his blood pressure was 170/110 breather mask at nearly 100% FIO2) 213 mm Hg, rectal temperature 29.5˚C (85.1˚F), mm Hg and heart rate 110 beats per minute, with ven- • Bicarbonate 10 mmol/L (normal 22–26) tricular bigeminy on the monitor. •pH 6.84 (normal 7.35–7.45) Head and neck examination revealed no scalp lacerations, but he had partial-thickness Chemistry profile and full-thickness burns with tattooing, multi- •Sodium 141 mmol/L (normal 135–146) ple superficial lacerations, and singed eyebrows. • Potassium 3.5 mmol/L (normal 3.5–5.0) His pupils were 4 mm and sluggishly reactive to • Chloride 107 mmol/L (normal 98–110) light. There were bilateral corneal burns. His • Blood urea 14 mg/dL (normal right tympanic membrane was ruptured. 10–25) Thorax. His breath sounds were dimin- • Lactate 21.8 mmol/L (normal 0.5–2.2) ished on the left side. His heart rhythm was • Anion gap 24 mmol/L (normal 8–16) regular with no murmur, gallop, or rub. Abdomen showed full-thickness and par- Complete blood count tial-thickness burns, with diminished bowel • Hemoglobin 10.2 g/dL (normal 13.5–17.0)

CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 68 • NUMBER 5 MAY 2001 401 Downloaded from www.ccjm.org on September 27, 2021. For personal use only. All other uses require permission. • Hematocrit 32.2% (normal 40.0–52.0) ❑ A central disease • White blood cell count 18.2 × 109/L (nor- ❑ Hypomagnesemia and hypocalcemia mal 4.0–10.0) ❑ Toxic exposure • Platelet count 197 × 109/L (normal 150–400). Causes of QT interval prolongation include all of the above; however, we can exclude The hypokalemia worsens, some of them in this patient. despite potassium replacement Hypothermia. This patient was hypother- Because the electrocardiogram exhibited mic, presumably because of his trauma. His ventricular ectopy with frequent premature rectal temperature of 29.5˚C could certainly ventricular contractions and nonsustained account for QT prolongation. ventricular tachycardia, a lidocaine infusion Hypokalemia. We know the patient had was started, and the patient was given three hypokalemia. The long QT interval associated 50-mmol ampules of sodium bicarbonate. with hypokalemia is probably due to a U wave, Ninety minutes later the patient’s potassi- which may be masked by ST-T abnormalities. um level had fallen to 2.9 mmol/L. An infu- T and U wave fusion may explain a prolonged sion of 50 mmol of potassium was started, to QT interval. run at 10 mmol/hour, along with two units of Central nervous system diseases that can red blood cells to be transfused over 2 hours. cause QT prolongation include subarachnoid One hour later, his blood pH was 7.36, PCO2 hemorrhage. Although this patient’s head 18 mm Hg, and potassium level 2.3 mmol/L. injury may have caused some blood to be pres- The remaining 40 mmol of potassium was ent in the subarachnoid space, there is no evi- rapidly infused over 30 minutes. Despite this dence that he suffered a primary subarachnoid potassium bolus, the potassium level fell fur- bleed, and his head CT was normal. ther to 1.5 mmol/L. Another 100 mmol of Hypomagnesemia and hypocalcemia potassium was infused over 30 minutes, and were not present: the patient’s magnesium his potassium rose to 4.2 mmol/L. level was 2.0 mg/dL and his calcium level was A chest tube was inserted to treat his 9.8 mg/dL. There was no pneumothorax, and he was taken to the oper- Toxic exposure that can cause QT prolon- sign that ating room for irrigation, debridement, and gation can be from drugs such as pheno- fasciotomies of his right upper extremity. He thiazines, tricyclic antidepressants, and other potassium recovered uneventfully from his injuries. His psychotropic drugs; class IA antiarrhythmics actually left his acid-base status stabilized and he required no (quinidine, disopyramide, procainamide); and further treatment for acidosis. class III antiarrhythmics (sotalol, amiodarone, body ibutilide, dofetilide). The patient had been tak- ■ WHAT CAN WE LEARN ing none of these. It can also be due to ethylene FROM THE ELECTROCARDIOGRAM? glycol or barium. He was not exposed to ethyl- ene glycol; we will consider barium below. The patient’s electrocardiogram showed a rate of 81 with sinus rhythm. The QT interval ■ WHAT ABOUT HIS ACIDOSIS? (406 ms) and QTc (470 ms) were prolonged— at a rate of 81 beats per minute a QT interval What are possible causes of the acidosis in of no more than 350 ms would be expected. 2 this patient? The electrocardiogram also showed ST ❑ depression in leads V1 through V5 and T- wave Renal failure flattening. ❑ Diabetic or ❑ Lactic acidosis What caused the prolonged QT interval in ❑ Toxic exposure 1 this patient? All of the above are possible causes of meta- ❑ Hypothermia bolic acidosis with a high anion gap, but we ❑ Hypokalemia can rule out most of them in this patient. He

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TABLE 1 inappropriately ventilating for the degree of metabolic acidosis, as his PCO2 was 35 mm Hg, Categories of lactic acidosis and his first arterial blood gas measurements Type A did not indicate any degree of hypoxemia. Due to hypoperfusion, hypoxemia Causes: Cyanide, carbon monoxide, shock, pulmonary edema, Can methemoglobinemia methemoglobinemia, sulfhemoglobinemia, asphyxia, status explain the acidosis? asthmaticus The munitions industry uses a number of Type B nitrogenous compounds, including aromatic 1 Due to systemic illness (diabetes mellitus, malignancy, nitrates and ammonium nitrate, which carry pancreatitis, leukemia, sepsis, liver disease) the hazard of acute methemoglobinemia. TABLE 2 Due to (phenformin, ethanol, fructose, iron, isoniazid, 2 lists other toxins shown to cause methemo- strychnine) globinemia. 3 Due to congenital errors of metabolism or enzyme Symptoms and findings of methemoglo- deficiencies binemia parallel those of carbon monoxide to a certain extent. Methemoglobin levels of 10% to 15% can cause cyanosis; lev- els of 20% to 30% can cause headache, was not taking any and he had fatigue, and nausea; and levels of 50% to 60% not ingested any . Since there is also can cause metabolic lactic acidosis and dys- no evidence that he has renal insufficiency or rhythmias. Methemoglobinemia can be diag- any state that can lead to ketoacidosis, the nosed by a chocolate-brown color of blood acidosis must have been due to lactic acidosis after it has dried on filter paper.5 The classic or to a toxic substance to which he was slate-gray cyanosis may be masked by burns. If exposed during the explosion.1,2 One sub- methemoglobinemia is suspected, it is impor- stance used in the explosive industry that can tant to measure the methemoglobin level cause metabolic acidosis is . because this condition has specific therapy.6 Potassium With a lactate level of 28.8 mmol/L, the Patients with methemoglobinemia may should go up as patient clearly had lactic acidosis. TABLE 1 lists benefit from administration of methylene the general categories of lactic acidosis,3 and blue, exchange transfusion, or hyperbaric oxy- pH goes down TABLE 2 lists substances that can induce it. gen. Patients exposed to toxins that induce Since this patient does not have any history of methemoglobinemia should be decontami- systemic illness, specific ingestion, or a nated, including removing contaminated congenital error of metabolism, his lactic aci- clothing and flushing the skin. dosis must be of type A, ie, due to hypoperfu- This diagnosis was not looked for initially sion or hypoxemia. Of the various causes of in this patient. Presumptive therapy with hypoperfusion or hypoxemia, cyanide and car- methylene blue may induce central nervous bon monoxide poisoning are in the differen- system effects such as tremor, nausea, vomit- tial diagnosis for anyone sustaining a blast or ing, dizziness, and confusion—potential con- inhalation injury. founding effects. Our patient’s acidosis This patient was not hypotensive for very resolved with bicarbonate replacement and long. He did not have pulmonary edema or treatment of his injuries and did not require status asthmaticus. The possibility of met- specific therapy. His prompt recovery with hemoglobinemia, especially following expo- supportive care essentially rules out significant sure to explosives, is very strong.4 cyanide or carbon monoxide exposure. The acidemia resolved rapidly when the patient was given sodium bicarbonate, and ■ WHAT IS THE DANGER remained normalized as his vital signs stabi- FROM HYPOKALEMIA? lized. The anion gap resolved quickly as well. It appears that this laboratory abnormality can be Under experimental conditions, for every attributed to a period of hypoxemia or hypop- decline of 0.1 in the pH, the measured serum erfusion. There is no evidence that he was potassium level rises by 0.6 mmol/L, although

406 CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 68 • NUMBER 5 MAY 2001 Downloaded from www.ccjm.org on September 27, 2021. For personal use only. All other uses require permission. TABLE 2 Substances that can induce lactic acidosis

Substances that can induce hypotension, seizures, respiratory failure (PO2 < 35 mm Hg), hepatic failure, or renal failure Acetaminophen Ethylene glycol Papaverine Aspirin Fructose Phenformin Biguanides Iron Povidone-iodine ointment Carbon monoxide* Isoniazid Ritodrine Chloramphenicol Metformin Sorbitol/xylitol Streptozotocin Cyanide* Nalidixic acid Strychnine Epinephrine Nitroprusside Ethanol Norepinephrine

Substances that can cause methemoglobinemia* Nitrites (rapidly oxidize heme iron because of their high oxidation potential) Bismuth subnitrate, other nitrates (can be converted to nitrites by gut or skin bacteria and absorbed) Butyl, amyl, isobutyl nitrites (recreational agents) Nitroglycerin Silver nitrate Anilines (easily penetrate skin) Acetanilid Toluidine, nitrobenzenes (plastics, fungicides, dyes, paints, rubber) Potassium and sodium chlorates (matches, weed killers, mouthwash) Therapeutic agents Antimalarial agents Benzocaine Dapsone Hypokalemia Metoclopramide Nitroglycerin may be Phenacetin Sulfonamides spurious or due Contaminated well water (nitrates in fertilizers) to either depletion or *Classified as type A lactic acidosis redistribution this may not be seen with organic acidosis or ventricular tachycardias, AV dissociation, and acidemia. This patient, who had acidosis at the ultimately ventricular fibrillation. If the same time that his potassium level was 2.3 or patient is in sinus rhythm, the electrocardio- 1.5 mmol/L, had life-threatening hypokalemia. gram may show T-wave flattening, ST depres- The clinical effects of hypokalemia are a sion, and U waves. direct consequence of membrane hyperpolar- Skeletal muscle effects include paresthe- ization, ie, the membrane potential is made sia, muscle cramps, respiratory muscle paraly- more negative so that there is a shift in the sis, weakness, and lassitude. At potassium lev- membrane potential away from the threshold els below 2.5 mmol/L, muscle necrosis may level required to produce an action potential.7 develop, and at levels below 2.0 mmol/L, The major clinical effects of hypokalemia ascending paralysis may occur, although this is are in myocardial tissue, skeletal muscle, and unusual.8 the gastrointestinal system. Gastrointestinal effects commonly include Myocardial effects of hypokalemia nausea, vomiting, and paralytic ileus. Conscious include re-entrant and automatic atrial and patients may complain of constipation.

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■ HYPOKALEMIA: Potassium redistribution is clearly what A DIAGNOSTIC APPROACH is going on in this patient. The major causes of potassium redistribution are: What is the probable cause of this •Alkalemia with increased plasma bicar- 3 patient’s low potassium measurements? bonate. This can be dismissed as the patient is not alkalemic and does not have an elevated ❑ Spurious hypokalemia plasma bicarbonate level. ❑ True potassium depletion • Insulin excess (endogenous or exoge- ❑ Potassium redistribution nous). This does not apply to this patient either. Spurious hypokalemia. In some cases the •Beta-adrenergic antagonists, which this patient actually has a normal serum potassium patient does not use. level, but the level in the blood sample • Drugs and toxins such as theophylline, declines by the time the laboratory measures barium, toluene, and calcium channel it. This occurs in two specific instances. blockers. The patient is not taking theo- • If the patient has received insulin within phylline or calcium channel blockers; how- the past 15 to 20 minutes, the insulin may ever, barium and toluene have to be strong- transiently drive down the serum potassium, ly considered. representing redistribution. • In leukemic patients with white blood How do drugs and toxic substances counts of 100 to 250 × 109/L, the white blood induce hypokalemia? cells may metabolize the potassium in the Some drugs and substances can induce serum. hypokalemia by causing actual potassium loss. Neither of these situations existed in this Others, however, cause potassium redistribu- case. tion (TABLE 3). In the latter group, substances (Pseudohyperkalemia, representing an such as theophylline, beta-2 agonists, and thy- artificially elevated plasma potassium from roid hormone drive potassium into cells via Potassium hemolysis, prolonged use of a tourniquet, or the sodium-potassium ATPase pump. Others, replacement marked leukocytosis or thrombocytosis is such as barium and chloroquine, lower serum much more common than pseudohypo- potassium by blocking potassium channels may be kalemia.) and preventing potassium from getting out of ineffective if True potassium depletion can develop the cells via osmosis. In these cases, although from either chronic extrarenal or renal losses. potassium cannot exit the cell, it continues to magnesium is Extrarenal loss of potassium associated with be pumped in via the ATP-dependent sodi- low acidosis can be caused by prolonged fasting, um-potassium pump, and although the total diarrhea, GI fistulas, and villous adenomas of body store of potassium remains normal, the the rectum. Renal causes of potassium loss extracellular potassium level may drop precip- include certain primary proximal types of itously.9 renal tubular acidosis, diabetic ketoacidosis, The two toxic substances that lower ureterosigmoidostomy, loop diuretics, and car- serum potassium and warrant serious consider- bonic anhydrase inhibitors. ation are toluene and barium, both of which We can dismiss these conditions, as the are used in the explosives industry.10–12 patient has not been chronically ill, is not tak- ing a diuretic, and has no known history of ■ CAN TOLUENE ACCOUNT renal disease or diabetes. He has no history of FOR HIS HYPOKALEMIA? anything that would cause gastrointestinal potassium loss, and he has no history of surgi- Toluene is used in the explosives industry, cal procedures such as ureterosigmoidostomy. especially in the early phases of manufactur- Finally, he simply has not had time to lose ing. Specifically, it is used with sulfuric acid or potassium—the hypokalemia developed nitric acid at 100˚C to produce the aromatic acutely and with no evidence that potassium nitrates dinitrotoluene and trinitrotoluene actually left his body. (TNT).

408 CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 68 • NUMBER 5 MAY 2001 Downloaded from www.ccjm.org on September 27, 2021. For personal use only. All other uses require permission. Toluene is also a major ingredient of air- TABLE 3 plane glue and may be an additive in unlead- ed gasoline. Toluene has been mainly Substances that lower described in persons who sniff glue or spray serum potassium levels paint to produce euphoria. Substances that can cause spurious hypokalemia Insulin Diagnosis of toluene intoxication Symptoms of toluene intoxication include Substances that can cause true potassium depletion muscle weakness, quadriparesis, and a variety Acetazolamide Amphotericin B of gastrointestinal complaints including Antibiotics in high doses abdominal pain, nausea, vomiting, and Ampicillin hematemesis.13 Neuropsychiatric signs may Carbenicillin predominate and include altered mental sta- Nafcillin tus, cerebellar signs, , Penicillin headache, dizziness, and syncope. Confusion and coma have been reported, as have dys- Carbonic anhydrase inhibitors rhythmias and myocardial infarction.14 Cathartics Factors pointing to toluene intoxication Dextrose in this patient include hypokalemia, high Licorice, carbenoxalone, gossypol anion gap metabolic acidosis, and possible Loop diuretics Oral hypoglycemics exposure in his work. However, other factors Osmotic diuretics argue against toluene intoxication in this Salicylates patient: Sodium polystyrene sulfonate • The muscle weakness in toluene intoxica- Steroids tion generally spares respiratory and central Strychnine muscles. Sympathomimetics •Toluene intoxication is generally associat- Thiazide diuretics ed with chronic, not acute, exposure or abuse. Vitamin B12 •Toluene is used at an earlier stage of man- Substances that can cause potassium redistribution ufacturing than this patient was exposed to. Barium (soluble salts) •Toluene tends not to cause as acute a drop Beta-adrenergic agonists in serum potassium levels as in this patient, Bicarbonate since it causes potassium wasting through a Chloroquine mechanism of renal tubular acidosis, which Insulin (possibly) entails more of a potassium loss rather than a Theophylline (in overdose) potassium redistribution. Thyroid hormone This patient’s presentation is therefore not Toluene Verapamil (in overdose) consistent with acute toluene intoxication.

■ CAN BARIUM PRODUCE THIS PICTURE? used in fireworks and in explosives, and bari- um nitrate is commonly used in manufactur- Barium is a divalent alkaline earth with ing TNT. A chronic form of barium poisoning a molecular weight of 137. With such a high called baritosis has also been reported and rep- molecular weight, it is not readily penetrated resents a chronic and benign pneumoconiosis. by x-rays, and so it is used as a contrast agent The hypokalemia of barium poisoning, as for radiographic studies in the form of barium discussed above, entails potassium redistribu- sulfate, which is insoluble. tion. Barium reduces potassium efflux from Barium poisoning results from ingestion or muscle cells by blocking potassium channels inhalation of the acid salts,15 most often and has no proven activity on the sodium- rodenticides such as barium carbonate or bari- potassium ATP-dependent pump. Therefore, um hydroxide. Of note: barium chlorate is the continued activity of the ion pump com-

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bined with blocked potassium efflux results in theoretic risk of potassium overshoot, since extracellular hypokalemia and intracellular the total-body store of potassium is normal, potassium accumulation. Since muscle but potassium replacement seems to be well accounts for 44% of body mass, the serum tolerated. The serum potassium level must rise potassium level can drop quite precipitously, high enough to displace barium from the and as it does, so does the transmembrane potassium channels. With potassium replace- ionic diffusion potential, to less than 60 mV. ment, symptoms generally abate by 24 hours At this membrane potential the muscle is and patients are usually ambulatory by 48 unexcitable and paralysis ensues.16 hours. If hypertension, paralysis, or QT prolon- Diagnosis of barium intoxication gation exist, cardiac monitoring is indicated. Laboratory abnormalities with barium intoxi- Dysrhythmias secondary to barium poisoning cation are rhabdomyolysis, hypophosphat- should be treated with potassium—not with emia, and potentially severe hypokalemia. lidocaine or procainamide. This patient was Potassium levels as low as 0.3 to 0.8 mmol/L given lidocaine, but it was not known at the have been reported.17 time what the etiology of his ventricular dys- Other manifestations of barium poisoning rhythmias was. Lidocaine was discontinued include hypertension, cardiac dysrhythmias, with potassium replacement. The diagnosis of and gastrointestinal toxicity. Perioral pares- barium poisoning was not made until his thesia, tingling in the face and hands, abdom- hypokalemia was addressed. Hypertension inal cramps, diarrhea, and intractable vomit- should be treated with nitroglycerin in gener- ing may develop within minutes. Central ner- al. Intravenous magnesium sulfate poses a risk vous system signs of barium poisoning include if precipitating barium sulfate in the renal mydriasis, anxiety, headache, confusion, calyces. myoclonus, trismus, and seizures. Barium can Gastric lavage with sodium sulfate or cause ventricular tachydysrhythmias, QT pro- potassium sulfate may have a role if the mech- longation, congestive heart failure, and asys- anism was ingestion of barium, since the sul- Both toluene tole. Sensation is preserved, as is level of con- fate ions bind to the barium ions, which pre- and barium are sciousness. The weakness may not correlate cipitate as nontoxic barium sulfate. Activated with the degree of hypokalemia documented charcoal is ineffective in adsorbing barium. used in by the laboratory. Hemodialysis may shorten the half-life of bar- explosives The differential diagnosis of barium poi- ium but is generally unnecessary. soning includes various diseases that may induce paralysis, including familial hypo- ■ WHICH LABORATORY TESTS kalemic periodic paralysis, thyrotoxic periodic CAN CONFIRM THE DIAGNOSIS? paralysis, Guillain-Barré syndrome, gastroen- teritis, botulism, diphtheria, paralytic shellfish What further laboratory tests might be poisoning, , and neu- 4 indicated for this patient? rotoxic . This patient’s clinical presentation and ❑ Serum barium levels exposure in the explosive industry are consis- ❑ Tests for methemoglobinemia tent with and characteristic of barium intoxi- ❑ Tests for toluene toxicity cation. The most likely barium salt that he ❑ Thyroid function tests would have been exposed to is either barium nitrate or barium chlorate. Barium levels can confirm the diagnosis of barium toxicity. The normal range for Treatment of barium poisoning serum barium is 3 to 29 µg/dL. This patient Treatment involves aggressive potassium had a serum barium level of 133 µg/dL. Since replacement, since paralysis is due to he was treated appropriately with potassium hypokalemia, not to the barium per se.18 replenishment, his high barium level did not Patients may need as much as 400 mmol of change his course of therapy. Abdominal potassium over the first 24 hours. There is a roentgenograms may reveal ingested barium,

410 CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 68 • NUMBER 5 MAY 2001 Downloaded from www.ccjm.org on September 27, 2021. For personal use only. All other uses require permission. although this patient’s exposure appears to Thyroid function tests. The patient had have been by inhalation and through skin hypothermia, paralysis, and hypokalemia, all absorption via his burns. of which are indications for checking thyroid Tests for methemoglobinemia. This function at some point. Hypothyroidism is patient did not sustain clinically significant always in the differential diagnosis of methemoglobinemia, although testing in this hypothermia. Hyperthyroidism can be associ- situation may be warranted.19 ated with periodic paralysis and as noted earli- Urinary DNAT. Another test to consider er, development of hypokalemia via the sodi- in anyone who works in the munitions indus- um-potassium ATPase pump. try is urine screening for 2,6-dinitroamino- toluene (DNAT). By industry standards this is ■ DIAGNOSIS the screen most often used routinely for ongo- ing monitoring of toluene toxicity, although • Barium poisoning with acute hypokalemia in this patient’s case it would be of little emer- due to potassium redistribution gency use. •Type A lactic acidosis due to transient Serum magnesium is generally important hypoxemia or hypoperfusion to check because the patient may be refracto- • QT prolongation due to hypothermia, to ry to potassium replacement if he is hypomag- barium exposure, and perhaps also to nesemic. hypokalemia.

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