Page 110 - Journal of Special Operations Medicine - Summer 2015
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plasma within 6 hours.  Depending on when the test   hours to determine the peak CK level and trend change
                               8
          is performed, the  potential for false measurements  is   over time.
          significant and thus it is difficult to make clinical judg-
          ments based on their readings. It is for these reasons that   Electrolyte abnormalities in rhabdomyolysis are often
          urine myoglobin measurements may provide more pre-  transient and are corrected with fluid therapy. The ex-
          dictable and reliable diagnostic findings. A colorimetric   ception  to  this  is  severe  hyperkalemia;  in  the  absence
          urine dipstick test (qualitative) does not differentiate   of laboratory values, an electrocardiogram (ECG) may
          between hemoglobin and myoglobin. If the dipstick is   provide an available diagnostic tool to identify this co-
          positive but urine microscopy shows no red blood cells   morbidity. Peaked T waves on ECG are indicative of a
          (RBCs), myoglobinuria secondary to rhabdomyolysis   hyperkalemic state. A patient with this finding should
          should be suspected. Depending on hydration level and   be monitored  closely for arrhythmia  and may benefit
          urinary output, myoglobinuria may be sporadic. Urine   from specific hyperkalemia treatment (Figure 2).
          dipstick findings are not definitive and are positive in
          less than 50% of patients with rhabdomyolysis; a nor-  Figure 2  ECG featuring peak T waves indicative of
          mal test result does not rule out this condition. 10  hyperkalemia.

          Finally, the release of cellular contents can cause hyper-
          kalemia (high potassium level). This excess potassium
          can cause life-threatening dysrhythmias and potentially
          death if not recognized in a timely manner. The clini-
          cally significant influx of potassium outside of the cell
          occurs in 10% to 40% of cases.  In addition, hypokale-
                                     11
          mia (low potassium level) can also play a significant role
          in rhabdomyolysis. Hypokalemia in itself can result in
          decreased vascular flow to muscles, contributing to the
          potential for myocyte damage. 12
                                                             Aggressive and early fluid therapy is important to pre-
                                                             vent rhabdomyolysis-associated renal failure. Additional
          Treatment
                                                             interventions to promote urine production and prevent
          Providing supportive care through the ABCs, ensuring   kidney failure, including the use of diuretics (mannitol,
          adequate hydration, accurate recording of fluid input/  furosemide) and bicarbonate, have not shown any clear
          output, and identifying and correcting the cause of the   benefit. Despite a lack of quality evidence, many clini-
          rhabdomyolysis (e.g., trauma, dehydration, infection,   cians still dogmatically use urine alkalization. These
          or toxins) all form the basis of care. The cornerstone   decisions  are  best  determined  on  a  case-by-case  basis
          of treatment revolves around the expansion of extra-  under close hospital monitoring, due to the potential
          cellular volume through the use of intravenous fluids,   for worsening electrolyte imbalance and for kidney fail-
          typically normal saline or Ringer’s lactate. Although   ure.  Despite appropriate fluid therapy, approximately
                                                                4,5
          there is no clearly superior specific fluid therapy, ret-  10% to 50% of  rhabdomyolysis patients  progress to
          rospective studies have shown that early fluid interven-  acute renal failure. Some of those patients may go on to
          tions are associated with improved outcomes. 5,13  Fluid   require hemodialysis.
          therapy increases intravascular volume, which, in turn,
          increases the glomerular filtration rate, oxygen delivery,   Case Resolution
          and dilutes myoglobin in the renal tubules. A reasonable
          start would be an initial bolus of 1–2L of normal sa-  With the limited resources you have available, you have
          line, followed by an infusion at a rate of 200–500mL/h.   identified muscle weakness and renal involvement in
          This rate can be adjusted to maintain a urine output of   this patient, and these represent significant abnormali-
          at least 200mL/h or 2–4mL/kg/h. For monitoring pur-  ties. Given your preliminary results, additional labora-
                                       5
          poses, a Foley catheter and an urometer may be help-  tory testing and monitoring is warranted. You decide to
          ful, if available. Otherwise, the urine should be collected   evacuate this patient to the nearest hospital facility. As
          and measured. Crystalloid requirements may be quite   you organize transportation to the nearest hospital, you
          large depending on the degree of rhabdomyolysis and   decide to initiate intravenous fluid therapy with 0.9%
          myocyte damage. In patients with CK levels of 15,000   normal saline. You start with a 1L bolus and continue
          U/L or higher, volumes of fluid measuring 6L or more   with an infusion of 300mL/h. You do not have a Foley
          may be required in adults to maintain adequate urinary   catheter, but you begin to roughly measure his urinary
          output over 24 hours.  Laboratory tests, including mea-  output by having him urinate into a bottle of known
                             5
          suring of CK levels, should be repeated every 6 to 12   volume. You call back to higher medical  authority to


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