Cardiac Arrhythmias, Respiratory Failure, and Profound Hypokalemia in a Trauma Patient
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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 nitrogen 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 nervous system 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 alcoholic ketoacidosis ❑ 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 CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 68 • NUMBER 5 MAY 2001 405 Downloaded from www.ccjm.org on September 27, 2021. For personal use only. All other uses require permission. IM BOARD REVIEW GLAUSER 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 toxins (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 poisoning 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 medications and he had fatigue, and nausea; and levels of 50% to 60% not ingested any poisons. 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 toluene. 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 toxin 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.