Severe hypothermia in a patient with spinal cord injury without radiological abnormality.

We report a case of a 64-year-old caucasian male who was transported to the emergency department (ED) after being found unconscious on the side of the road. On arrival to the ED the patient went into ventricular fibrillation and advanced cardiac life support was started at that time. Thirty minutes into the resuscitation, after multiple rounds of code drugs and defibrillation attempts, the patient was found to be severely hypothermic with a rectal temperature of 24.9°C (76.9°F). Through the use of passive and active re-warming measures the patient's temperature increased enough to allow successful cardioversion and stabilization. Within minutes of cardiac stabilization the patient regained consciousness and was able to follow commands, but was found to be paralyzed from the neck down. Subsequent CT scans revealed no acute fractures, subluxations or acute spinal cord injury. This case represents the rare finding of severe hypothermia secondary to occult spinal cord injury. Case report was taken from case at Bayfront Hospital, St. Petersburg, Florida.

INTRODUCTION

Impaired thermoregulation is a known complication of high level spinal cord injury and side effects of hypothermia induced by such an injury may complicate trauma resuscitation. Hypothermia defined as a core temperature of <35°C are seen frequently in emergency departments (EDs) throughout the United States. Visits occurs mostly in a geographical and seasonal distribution but may also occur in the summer months without exposure to extreme temperatures. [1] The mortality rate for hypothermia in the United States approaches 700 per year with Florida accounting for on average six deaths per year. About 99% of the deaths occur in the months of November through February. [23]

Primary hypothermia caused by environmental cold water immersion and extreme cold temperatures is thought to be the most common cause of cold-related deaths. Secondary hypothermia is a low core temperature attributed to a variety of medical conditions, including spinal cord injury, and is overall more common than primary hypothermia. Mortality approaches 100% in some cases of secondary hypothermia. [4] Studies have shown that secondary hypothermia in trauma patients with a core temperature of less than 32°C (89.6°F) were ten times more likely to die than those with normothermia. [5]

This case illustrates a multifaceted and complex situation in which a trauma patient presents with multiple potential life-threatening injuries but also in full cardiac arrest due to secondary hypothermia from a rather rare cause of hypothermia, occult spinal cord injury.

CASE REPORT

A 64-year-old caucasian male with an unknown past medical history presented to the Bayfront Hospital ED in St. Petersburg, Florida, in early November. The average outside temperature that night was in the mid to upper 60s. The patient was initially found by local police officers lying unconscious in a ditch next to his bicycle. When EMS arrived on scene the patient was cold, unresponsive, GCS 3, covered in ants and without any other obvious signs of skeletal or traumatic injury. The patient was fully immobilized in a cervical collar and on a backboard prior to transport to the ED and was intubated secondary to his low GCS. The patient's vitals at the time showed sinus bradycardia at a rate of 30-40s, palpable pulse but an unobtainable blood pressure on multiple attempts.

At 08:22 the patient arrived at the ED and upon transfer to the trauma bed was noted to be in ventricular fibrillation. At that time AED pads were attached and advanced cardiac life support (ACLS) protocol was initiated. Trauma protocol labs were sent which consisted of CBC, CMP, serum cortisol, serum ETOH, amylase, TSH, cardiac enzymes, and a coagulation profile.

During the resuscitation the emergency room physician and trauma surgeon noted that the patient was very cold to the touch. A rectal temperature was performed but the temperature did not register. Per trauma protocol, the patient was being given warm IV fluids as well as warm humidified air via mechanical ventilation. It was not until 09:06 that the patient's temperature was accurately recorded to be 24.9°C (76.9°F). At approximately 09:22 the patient had been undergoing ACLS protocol for one hour and had been defibrillated 13 times and given five rounds of epinephrine, two rounds of atropine, and two rounds of amiodarone. With the patient still in ventricular fibrillation, it was decided to continue cardiopulmonary resuscitation with chest compressions and mechanical ventilation until the patient's core temperature increased. Supplemental active re-warming interventions including warm water lavage via OG tube and Foley catheter were started at that time.

The patient remained in ventricular fibrillation for more than three hours until 11:45, when his rectal temperature was 30.1°C (86.2°F) he was successfully converted into normal sinus rhythm at 66 bpm with a manual blood pressure of 180/120. As the patient's temperature continued to rise he went in and out of atrial fibrillation and sinus tachycardia but eventually returned and remained in normal sinus rhythm.

After cardiac stabilization, a complete secondary survey was performed that showed no other obvious signs of trauma or skeletal injury. A central line and arterial line was placed and he was started on a dopamine drip as his blood pressure decreased to 88/56. Once the patient's temperature reached 31.2°C (88.2°F) his OG and Foley catheter lavage were discontinued. The patient eventually became lucid and responsive to verbal commands. Although unable to remember the accident, or any events leading up to the accident, he did appropriately respond to some basic questions. It was at this that the patient's motor deficits were noticed as he was unable to feel anything from the neck down or move any of his extremities.

The patient underwent a scan of his head, neck, abdomen, and pelvis. The scans showed no head injury or C-spine fractures and noted only a small 1 mm broad-based disc bulge at the level of C5-6 and C6-7, moderately dilated loops of bowel consistent with an ileus and two small bilateral pleural effusions. Although a toxicology screen was not obtained, he did have an ETOH of 0.183 g/dl. The patient was transferred to the ICU, and subsequently underwent an MRI of his C-Spine which demonstrated diffuse edema of his cervical spine. After a prolonged hospital stay the patient's mental status did improve to baseline but his paralysis did not as he remained a tetraplegic. The patient was then transferred to a rehab facility for further care.

DISCUSSION

Hypothermia is defined as a core temperature of less than 35°C (95°F). Mild hypothermia is defined as a temperature 32-35°C, moderate 28-32°C, and severe <28°C. Hypothermia is further delineated into primary and secondary causes. Primary hypothermia is caused by accidental or environmental exposure such as cold water immersion and extreme cold outdoor temperatures. Secondary hypothermia is seen more commonly in the general population and can be caused by medical conditions that lowers the body's temperature set point, i.e. severe cerebrovascular disease, infection, endocrine dysfunction, hypothalamic dysfunction, peritonitis, pancreatitis, medications, and in our case spinal cord injury. [1-5]

Thermoregulatory dysfunction has been reported in high spinal cord injuries but the reports referencing immediate autonomic dysreflexia following trauma are not well described in the literature. Most of the reported cases discussing thermoregulatory dysfunction and autonomic dysreflexia in patients with high spinal cord injury mostly discuss observed temperature elevations. [6]

After a spinal cord injury above the major splanchnic sympathetic outflow (T4-T6), it is common for partial poikilothermia to occur secondary to the lack of hypothalamic control over the sympathetic nervous system. This impairment occurs because of the interruption of neuronal pathways between the periphery and the hypothalamus, the resultant deficit is the inability to shiver when it is cold and the lack of proper blood vessel vasodilation or vasoconstriction to certain environmental stimuli, which normally keeps the body at an ambient temperature. [7] The lack of hypothalamic control results in depressed heat regulation, accounting for only a 10-15% increase in core temperature compared to a normal increase of 200-500%. [8]

Due to our patient's high spinal cord injury and complete tetraplegia, he most likely lost all form of heat regulation usually governed by an intact spinal cord pathway and hypothalamic feedback. This explains our patient's partial poikilothermia and resultant inability to keep his core body temperature above the ambient temperature which was in the mid to upper sixties that night.

Re-warming the hypothermic patient is the mainstay of treatment regardless of the primary cause and is the only means to return cardiac stabilization following dysrhythmias such as ventricular fibrillation. Re-warming can take place by using three different mechanisms; passive external, active external, and active internal warming. Active external warming with blankets has been shown to increase temperatures by 1°C-2°C/h, active internal warming with warm humidified air by 1°C-1.5°C/h and active internal warming with infusion of warm fluid into gastric, colonic, pleural, peritoneal or pericardial cavities by 2°C-2.5°C/h. [910] From initial presentation to cardiac stabilization, our patient was re-warmed at a rate of 2.13°C/h using the described passive and active re-warming methods stated earlier. Another option to re-warming that was not addressed in our case was the use of cardiopulmonary bypass in the setting of prolonged CPR. This option can increase re-warming at rates up to 10°C per hour. In the case of all resuscitations in the hypothermic patient, they should not be considered unsuccessful until the patient has a core temperature of 32°C. [11]

Sometimes it is difficult to determine who is deemed appropriate to re-warm to a core temperature of 32°C before terminating resuscitation efforts. Current recommendations suggest that all lifesaving procedures should be initiated unless the victim is obviously dead (eg, rigor mortis, decomposition, hemisection, decapitation) or have ominous signs of a grave prognosis regardless of efforts which include potassium levels >10 meq/L, temperature <12°C, pH <6.5 and a fibrinogen level <50 mg/dl. [12]

The evidence of the patient's paralysis was not apparent until he woke up following successful cardioversion and re-warming. No radiologic abnormalities were seen except the small 1-mm broad-based bulge seen at level C5-6 and C6-7. The MRI done later that day demonstrated diffuse spinal cord edema which finally explained his injuries. This type of injury is most commonly seen in children and is termed a spinal cord injury without radiological abnormality or spinal cord injury without radiological abnormality (SCIWORA). SCIWORA is defined as the occurrence of acute traumatic myelopathy despite normal plain radiographs and normal computed tomographic (CT) studies. It is most described and discovered in the pediatric population and thought to be due to the mismatch in the elasticity of the tissue of the vertebral column and spinal cord. [13] SCIWORA in adults is very rare and most of these injuries are often missed initially and diagnosis is often delayed because these injuries tend to occur in the multi-trauma patient. [14] For the most part, SCIWORA in adolescents and adults are less severe because most of them present as incomplete paralysis with transient symptoms and a delayed onset and should always be suspected in patients that have a neurological deficits and apparently normal x-rays and/or CT scans. [13] The use of steroids is controversial but has shown some long-term benefit and is recommended as a treatment “option.” The National Acute Spinal Cord Injury Study (NASCIS) trials showed no statistical difference between methylprednisolone sodium succinate (MPSS) and placebo in terms of neurological recovery at one year, but the post-hoc analyses of subgroups did. The NASCIS III study found that in patients treated earlier than 3 hours after injury, the administration of methylprednisolone for 24 h was best. The dose, if considered, consists of a high dose methylprednisone bolus of 30 mg/kg IV within 8 h of the injury as well as an infusion of 5.4 mg/kg/h for the next 23 h. [15-17]

CONCLUSION

It is evident from this case report that even though hypothermia can occur from many different causes, it is still treated the same until its underlying cause can be identified. Current trauma protocol, using warm saline and warm humidified air during mechanical ventilation, allows prompt treatment in those patients who are not initially discovered to be hypothermic. This case also highlights the complexity of the trauma patient and the multiple conditions that can present and mask other conditions. This case was ultimately caused by an occult spinal cord injury after the patient fell from his bicycle. This injury is classified as a SCIWORA and in adults is a condition that is rare. To have this condition causing severe hypothermia with cardiopulmonary arrest makes it an even more rare occurrence.