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TABLE 2  Stages of Hypothermia                     medevac times, including tail-to-tail handoffs, as well as iatro-
           Measured Core Temperature   Clinical Assessment   genic interventions such as cold IV fluids and paralytics, and
           Mild: 32°C–35°C (89.6°F–95°F) Stage 1: Conscious, shivering  DKA are powerful contributors to hypothermia.
           Moderate: 28°C–31.9°C   Stage 2: Confused, shivering
           (82.4°F–89.6°F)                                   This patient exhibited multiple pathophysiologic manifesta-
                                   Stage 3: Unconscious, not   tions of hypothermia, including life-threatening arrhythmias,
                                   shivering, vital signs present  electrolyte abnormalities, and decreased oxygen delivery. Dur-
           Severe: <28°C (82.4°F)                            ing the rewarming phase of resuscitation, the patient exhib-
                                   Stage 4: Unconscious, vital signs
                                   absent                    ited rewarming shock, hyperkalemia, and difficult-to-control
                                                             blood glucose levels.
          a temperature probe in the distal esophagus or specialized
          instruments placed in the nasopharyngeal space or snuggly   The cardiopulmonary effects  of hypothermia  vary. Blood
          against the tympanic membrane can achieve accurate core   pressure can remain stable due to peripheral vasoconstriction
          temperatures. In expeditionary settings, an initial intermedi-  shunting intravascular volume to the core. However, hypoten-
          ate measurement by forehead Tempa Dot thermometer (3M)   sion  can  occur  secondary  to  hypothermia-induced  arrhyth-
          or the sublingual route followed by core measurement by the   mias. The most common arrhythmia in hypothermic patients
          rectal or esophageal route are accepted methods. 1
                                                             is atrial fibrillation, followed by ventricular tachycardia (in-
                                                             cluding ventricular fibrillation). Bradycardia can be seen. The
          In contrast to induced hypothermia in patients after cardiac ar-  patient in this report had a combination of these arrhythmias.
          rest or who are undergoing cardiac bypass, accidental and iat-  Rewarming shock, a phrase coined to describe hypotension
          rogenic hypothermia can be life threatening owing to multiple   and hemodynamic instability due to acidosis from oxygen con-
          pathophysiologic  derangements.  Hypothermia,  not  intended   sumption (Vo ) and oxygen delivery (Do ) mismatch, was ex-
          as medical therapy, can be caused by environmental and non-  hibited by our patient. Vo /Do  mismatch during reperfusion
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          environmental factors. Table 3 lists causes of nonenvironmen-  is worsened by shivering, which increases oxygen demand.
          tal hypothermia. In Afghanistan in the winter, as demonstrated   Reperfusion during rewarming also contributes to a systemic
          in the case reported here, it is challenging to maintain the ther-  inflammatory  response  syndrome–induced  vasodilatory  re-
          mal neutral zone during care in prolonged field settings and en   sponse. This combination of decreased cardiac output from
          route. The outside temperature on the ground on the day of   acidosis in the setting of vasoplegia leads to cardiogenic shock
          admission of this patient was −5°C (23°F). Convective cooling   combined with distributive shock.
          was exacerbated during the almost 12-hour combined rotary
          wing and ground transportation. His prolonged medevac, in-  Hypothermia affects renal and metabolic systems, leading to
          terrupted by heat-losing interventions such as intubations and   electrolyte disturbances such as hypokalemia (hypothermia
          medicine administration, ultimately brought his core tempera-  shifts potassium into cells), hypocalcemia, hypomagnesemia,
          ture to 31°C (87.8°F).
                                                             and hypophosphatemia.  In addition, cold diuresis can worsen
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                                                             hypokalemia. Because our patient had concomitant DKA and
          TABLE 3  Nonenvironmental Causes of Hypothermia    acute kidney injury, he was hyperkalemic. Potassium stasis
           Cold intravenous fluids                           was challenging during his rewarming and resuscitation, and
           Paralytic medications                             vigilance for hypokalemia was required while he was undergo-
           Endocrine                                         ing insulin infusion therapy.
             Hypothyroidism
             Hypopituitarism
             Hypoglycemia                                    A left shift of the oxyhemoglobin dissociation curve is caused
             Diabetic ketoacidosis                           by hypothermia, whereas a right shift occurs in acidosis from
           Neurologic                                        DKA and increased lactate (Figure 3). This discordance likely
             Cerebrovascular accidents                       contributed to our patient’s survival. A left shift leads to de-
           Infections                                        creased oxygen delivery, which is deleterious in the setting of
           Antipsychotic medications                         already-hypoxic tissues. Our patient’s pH was 6.681 as a re-
           Alcohol                                           sult of ketoacidosis, respiratory acidosis, and chloride-liberal
                                                             fluid resuscitation, which resulted in a right shift. Just as hypo-
          Although the patient was normothermic initially at the Role   thermia increases hemoglobin’s oxygen affinity (and decreases
          1 facility, he was near the threshold for hypothermia, likely   oxygen delivery), his acidosis decreased hemoglobin’s oxygen
          as a result of his DKA. Furthermore, his ability to shiver was   affinity (and increased oxygen delivery). This patient had
          reduced from cold IV fluids and the use of paralytics. Before   mildly increased lactate level (2.8mmol/L)), which also con-
          paralysis, his core temperature likely dropped below the point   tributed to his acidosis. His base deficit (−30mEq/L) was the
          when shivering was possible: stage 3 hypothermia. In addi-  lowest the authors have ever calculated. In large case series,
          tion, the patient was subjected to nonenvironmental causes of   when a discordance between initial measured lactic acid and
          hypothermia. DKA is a known cause of nonenvironmental hy-  base deficit exists in critical care patients, the base deficit does
          pothermia and results from the inability of adenosine triphos-  not predict mortality. 4
          phate to use glucose in the patient with highly insulin-resistant
          DKA. Impaired glucose use leads to a lack of substrate for heat   Hypothermia deserves respect when considering use of para-
          production. In one case series spanning 7 years, DKA was the   lytics. In addition to the reduction in our patient’s ability to
          most common cause of nonenvironmental hypothermia.  Non-  maintain core temperature through shivering, paralytics have
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          environmental causes of hypothermia are important factors   altered pharmacokinetics and pharmacodynamics in hypo-
          to consider when transporting patients in expeditionary set-  thermia. Depolarizing agents such as succinylcholine are more
          tings. The winter environment in Afghanistan and prolonged   potent and have prolonged duration in hypothermic patients


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